leptin and Helicobacter-Infections

Obesity is an important public health problem worldwide. It increases the risk of many chronic diseases such as diabetes and cardiovascular diseases. Meanwhile, obesity is a major risk factor for several types of cancer including gastric cancer. Possible mechanisms linking obesity with gastric cancer may include obesity associated gastro-oesophageal reflux, insulin resistance, altered levels of adiponectin, leptin, ghrelin, and an abnormally increased blood level of insulin-like growth factor (IGF). Helicobacter pylori (H. pylori) infection is a well-recognized risk factor for peptic ulcer and gastric cancer. Recent studies have revealed an increased prevalence of H. pylori infection in obese patients, providing another clue for the increased incidence of gastric cancer in obese population. If this connection can be confirmed in animal models and a large cohort of patients, then eradicating H. pylori together with life style modification in obese individuals may help prevent the development of gastric cancer in the increasingly obese population.

Topics: Adiponectin; Animals; Gastroenteritis; Gastroesophageal Reflux; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation; Insulin Resistance; Insulin-Like Growth Factor I; Leptin; Obesity; Risk Factors; Signal Transduction; Stomach Neoplasms

Helicobacter pylori (H. pylori) infection is reported to be associated with many extragastrointestinal manifestations, such as hematological diseases [idiopathic thrombocytopenic purpura (ITP) and unexplained iron deficiency anemia (IDA)], cardiovascular diseases (ischemic heart diseases), neurological disorders (stroke, Parkinson's disease, Alzheimer's disease), obesity and skin disorders. Among these, the best evidence so far is in ITP and unexplained IDA, with high-quality studies showing the improvement of IDA and ITP after H. pylori eradication. The evidence of its association with coronary artery disease is weak and many of the results may be erroneous. The role of H. pylori infection in affecting serum leptin and ghrelin levels has attracted a lot of attention recently and available data to date have been conflicting. There have also been many uncontrolled, small sample studies suggesting an association between H. pylori infection and neurological disorders or chronic urticaria. However, more studies are required to clarify such proposed causal links.

Topics: Anemia, Iron-Deficiency; Cardiovascular Diseases; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Nervous System Diseases; Obesity; Purpura, Thrombocytopenic, Idiopathic

Ghrelin and leptin are newly discovered, still very mysterious, hormones. Beside the energy balance, they regulate endocrine and immune system, growth and maturate processes. Fluctuations of both hormones concentration are observed in many gastrointestinal tract diseases. In this publication is presented current knowledge about meaning ghrelin and leptin in choosen diseases, like malabsorption syndromes, inflammatory diseases and tumors of gastrointestinal tract.

Topics: Energy Metabolism; Gastroenteritis; Gastrointestinal Diseases; Gastrointestinal Tract; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin

To evaluate the influence of Helicobacter pylori infection on the gastric regulation of food intake and body weight.. H. pylori infection leads to a decrease of circulating ghrelin through a reduction of ghrelin-producing cells in the gastric mucosa and increases the amount of gastric leptin with no effect on circulating leptin levels. Eradication of H. pylori reverses the abnormal regulation of gastric hormone secretion. This finding is suggested to favor weight gain after H. pylori eradication and points to the potential effect of H. pylori in the pathophysiology of obesity.. H. pylori has an influence on the release of gastric hormones and therefore plays a role in the regulation of body weight, hunger and satiety.

Topics: Appetite; Body Weight; Eating; Gastric Mucosa; Gastritis; Ghrelin; Helicobacter Infections; Helicobacter pylori; Homeostasis; Humans; Leptin

Topics: Animals; Body Mass Index; Body Weight; Female; Gastritis; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Mice; Obesity; Pepsinogens; Rats

Topics: Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Obesity; Risk Factors

Topics: Animals; Body Mass Index; Cholesterol; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Obesity

Topics: Animals; Body Mass Index; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Hyperlipidemias; Leptin; Obesity

Helicobacter pylori are bacteria that have coevolved with humans to be transmitted from person to person and to persistently colonize the stomach. Their population structure is a model for the ecology of the indigenous microbiota. A well-choreographed equilibrium between bacterial effectors and host responses permits microbial persistence and health of the host but confers risk of serious diseases, including peptic ulceration and gastric neoplasia.

Topics: Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation; Leptin; Peptide Hormones; Stomach; Stomach Diseases; Virulence

Topics: Animals; Gastric Acid; Gastric Mucosa; Gastritis; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Lipid Metabolism; Nitric Oxide; Peptide Hormones; Stomach Diseases

Topics: Animals; Body Mass Index; Body Weight; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Obesity; RNA, Messenger

This study aimed to analyze the influence of H. pylori infection on insulin resistance and metabolic syndrome (MS) by multivariate analysis of a community-based cohort study. From January 2013 to February 2014,811 subjects were enrolled in a community-based cohort study from the northeastern region of Taiwan. All subjects received a demographic survey and blood tests, including an H. pylori antibody test, liver biochemistry tests, lipid profiles, sugar/insulin levels for Homeostatic model assessment (HOMA-IR index), and measurements of adipokines and inflammatory cytokines. A total of 264 men and 547 women were included in this study. The mean age was 59.2 ± 12.7 years. Subjects seropositive for H. pylori antibodies exhibited higher rates of hypertension, an increased incidence of a HOMA-IR index > 2.5 and a higher level of tumor necrosis factor-α than those without H. pylori antibodies. We found a significant difference in the presence of H. pylori antibodies between subjects with MS and those without MS (76.7% vs. 53.7%, p = 0.007) among subjects < 50 y/o. A HOMA-IR index >2.5, H. pylori antibody presence and leptin were predictors for MS in subjects < 50 y/o. The estimated odds ratio of MS for a subject with H. pylori antibodies was 3.717 (95% CI = 1.086-12.719) times that of a subject without H. pylori antibodies. In addition, no difference in H. pylori antibody status was detected for MS prediction in subjects that were ≧ 50 y/o (p = 0.861). In conclusion, subjects with H. pylori antibodies had a higher incidence of a HOMA-IR >2.5 than those without H pylori antibodies. For subjects aged < 50 y/o, the H. pylori antibody was a predictor for MS.

Topics: Age Factors; Aged; Antibodies, Bacterial; Case-Control Studies; Female; Helicobacter Infections; Helicobacter pylori; Humans; Hypertension; Insulin Resistance; Leptin; Male; Metabolic Syndrome; Middle Aged; Taiwan

Appetite and energy expenditure are regulated in part by ghrelin and leptin produced in the gastric mucosa, which may be modified by H. pylori colonization. We prospectively evaluated the effect of H. pylori eradication on meal-associated changes in serum ghrelin and leptin levels, and body weight.. Veterans referred for upper GI endoscopy were evaluated at baseline and ≥8 weeks after endoscopy, and H. pylori status and body weight were ascertained. During the first visit in all subjects, and during subsequent visits in the initially H. pylori-positive subjects and controls, blood was collected after an overnight fast and 1 h after a standard high protein meal, and levels of eight hormones determined.. Of 92 enrolled subjects, 38 were H. pylori-negative, 44 H. pylori-positive, and 10 were indeterminate. Among 23 H. pylori-positive subjects who completed evaluation after treatment, 21 were eradicated, and 2 failed eradication. After a median of seven months following eradication, six hormones related to energy homeostasis showed no significant differences, but post-prandial acylated ghrelin levels were nearly six-fold higher than pre-eradication (p=0.005), and median integrated leptin levels also increased (20%) significantly (p<0.001). BMI significantly increased (5 ± 2%; p=0.008) over 18 months in the initially H. pylori-positive individuals, but was not significantly changed in those who were H. pylori-negative or indeterminant at baseline.. Circulating meal-associated leptin and ghrelin levels and BMI changed significantly after H. pylori eradication, providing direct evidence that H. pylori colonization is involved in ghrelin and leptin regulation, with consequent effects on body morphometry.

Topics: Aged; Amoxicillin; Anti-Bacterial Agents; Body Mass Index; Clarithromycin; Drug Therapy, Combination; Female; Food; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Middle Aged; Proton Pump Inhibitors

Melatonin (MT) and its precursor L-tryptophan (TRP) are implicated in the protection of gastric mucosa against aspirin-induced lesions and in the acceleration of healing of idiopathic gastro-duodenal ulcers, but no information is available whether these agents are also effective in healing of gastroduodenal ulcers accompanied by Helicobacter pylori (H. pylori) infection. In this study three groups A, B and C, each including 7 H. pylori-positive patients with gastric ulcers and 7 H. pylori-positive patients with duodenal ulcers, aging 28-50 years, were randomly assigned for the treatment with omeprazole 20 mg twice daily combined with placebo (group A), MT administered in a dose of 5 mg twice daily (group B) or TRP applied in a dose of 250 mg twice daily (group C). All patients underwent routine endoscopy at day 0 during which the gastric mucosa was evaluated and gastric biopsies were taken for the presence of H. pylori and histopathological evaluation. The rate of ulcer healing was determined by gastroduodenoscopy at day 0, 7, 14 and 21 after the initiation of the therapy. Plasma MT, gastrin, ghrelin and leptin were measured by specific RIA. At day 21, all ulcers were healed in patients of groups B and C but only 3 out of 7 in group A of gastric ulcers and 3 out of 7 in duodenal ulcers. Initial plasma MT showed similar low levels in all three groups but it increased several folds above initial values in ulcer patients at day 7, 14 and 21. Plasma gastrin and leptin levels showed a significant rise over initial values in patients treated with omeprazole and placebo, MT or TRP while plasma ghrelin levels were not significantly affected by these treatments. We conclude that MT or TRP added to omeprazole treatment, significantly accelerates healing rate of H. pylori infected chronic gastroduodenal ulcers over that obtained with omeprazole alone and this likely depends upon the significant rise in plasma MT and possibly also in leptin levels, both hormones involved in the mechanism of gastroprotection and ulcer healing.

Topics: Adult; Anti-Infective Agents; Anti-Ulcer Agents; Drug Therapy, Combination; Duodenal Ulcer; Gastric Mucosa; Gastrins; Gastroscopy; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Mucosa; Leptin; Melatonin; Middle Aged; Omeprazole; Stomach Ulcer; Treatment Outcome; Tryptophan; Wound Healing

Helicobacter pylori (H. pylori) is a common gastric infection associated with extragastric conditions. The association between H. pylori infection and obesity is unclear. H. pylori may affect gut hormones involved in food intake and energy expenditure. The aim of this study is to evaluate ghrelin/obestatin balance and leptin in obese subjects with H. pylori infection.. Sixty healthy volunteers were divided into: obese and non-obese groups. Each group was divided into H. Pylori positive or H. pylori negative. Anthropometric parameters, H. pylori status, serum glucose, insulin level, and lipid profile were estimated with calculation of Homeostasis Model Assessment Insulin Resistance (HOMA-IR). Serum levels of ghrelin, obestatin, and leptin were evaluated.. Significant increase was found in serum glucose, insulin and HOMA-IR ratio in obese subjects with positive H. pylori as compared to other groups. H. pylori positive obese subjects showed significantly increased ghrelin, ghrelin/obestatin balance, and leptin with a significant decrease in obestatin as compared to negative subjects. Ghrelin/obestatin ratio positively correlated with weight, body mass index, waist, glucose, insulin, HOMA-IR, leptin, cholesterol, triglycerides, low density cholesterol and also with H. pylori antigen in the same group.. It can be concluded that ghrelin, obestatin, and leptin are affected by presence of H. pylori seropositivity in obese subjects. The higher ghrelin levels and ghrelin/obestatin ratio with lowered obestatin could be considered as a gastro-protective effect against inflammation induced by H. pylori.

Topics: Adult; Cardiovascular Diseases; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Metabolic Diseases; Middle Aged; Obesity; Risk

Helicobacter pylori (H. pylori) infection may induce inflammatory cytokines or adipokines that influence bone turnover and bone fracture risk. This study aimed to evaluate the association among H. pylori infection, adipokines, and 10-year fracture risk using the Fracture Risk Assessment Tool scale. From August 2013 to February 2016, a community-based cohort was surveyed by Keelung Chang-Gung Memorial Hospital. Subjects were included if they were older than 40 years and not pregnant. All participants underwent a standardized questionnaire survey, physical examination, urea breath test, and blood tests. A total of 2,689 participants (1,792 women) were included in this cross-sectional study. In both sexes, participants with a high fracture risk were older and had higher adiponectin values than participants without a high fracture risk (mean age, female: 72.9 ± 5.6 vs. 55.8 ± 7.3 years, P < 0.0001; male: 78.9 ± 4.7 vs. 58.1 ± 8.9 years, P < 0.001) (adiponectin, female: 10.8 ± 6.3 vs. 8.7 ± 5.2 ng/ml, P < 0.001; male: 9.7 ± 6.1 vs. 5.5 ± 3.8 ng/ml, P < 0.001). Adiponectin was correlated with high fracture risk in both sexes, but H. pylori infection and leptin was not. In logistic regression analysis, adiponectin could not predict high fracture risk when adjusting the factor of body mass index (BMI) in men group. In conclusion, H. pylori infection and leptin could not predict 10-year fracture risk in either sex. Adiponectin was correlated with bone fracture risk in both sexes and the correlation might be from the influence of BMI.

Topics: Adiponectin; Aged; Cross-Sectional Studies; Female; Fractures, Bone; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Middle Aged

Topics: Adolescent; Age Factors; Appetite Regulation; Biomarkers; Breath Tests; Case-Control Studies; Child; Child, Preschool; Cross-Sectional Studies; Energy Metabolism; Enzyme-Linked Immunosorbent Assay; Female; Ghrelin; Helicobacter Infections; Helicobacter pylori; Homeostasis; Host-Pathogen Interactions; Humans; Leptin; Linear Models; Male; Mexico; Multivariate Analysis

Helicobacter pylori is associated with gastrointestinal diseases such as gastritis, peptic ulcers, malignancy and lymphoma, and extra-gastrointestinal conditions. H. pylori infection is negatively associated with children's growth. Chronic inflammation of the stomach that results in the loss of appetite and, dysregulation of neuroendocrine hormones such as leptin, and ghrelin are the probable reasons of this negative association. The objective of this study is to determine the serum levels of leptin, ghrelin, and IGF-1 in H. pylori-infected children and their relations with growth.. A hundred and sixty-one school children aged between 6 and 14 years were selected randomly from five primary schools representing a cross section of population. Demographic and sociocultural characteristics, and anthropometric measurements were recorded. Serum H. pylori IgG, insulin-like growth factor-1, leptin, and ghrelin levels were measured in all children. The children were grouped according to the nutritional status and Helicobacter pylori seropositivity. Nutritional indices were compared among groups in association with serum leptin, ghrelin, and insulin-like growth factor-1 levels.. H. pylori IgG positivity was found in 34.2%, and 14.9% of children were malnourished. H. pylori seropositivity was significantly higher in older ages (10.32 ± 2.26 vs 9.53 ± 2.36 years, p = .036), and body weight and height Z scores were significantly lower in H. pylori-seropositive children (-0.33 ± 1.08 vs 0.04 ± 1.26, p = .044 and 0.13 ± 0.92 vs 0.23 ± 0.91, p = .018 respectively). H. pylori seropositivity was found to be an independent risk factor for shorter body height (p = .01). Serum leptin, ghrelin, and IGF-1 levels were not associated with H. pylori IgG seropositivity (0.35 vs 0.55 ng/mL, p = .3; 3267.4 ± 753.0 vs 2808.3 ± 911.4 pg/mL, p = .06; 470 ± 176 vs 521 ± 179 ng/mL, p = .32, respectively).. Children infected with H. pylori are prone to short stature. This effect seems to be independent of neuroendocrine hormones.

Topics: Adolescent; Anthropometry; Child; Cross-Sectional Studies; Demography; Female; Ghrelin; Helicobacter Infections; Humans; Insulin-Like Growth Factor I; Leptin; Male; Nutritional Status; Schools; Serum; Students

Helicobacter pylori have been shown to influence physiological regulation of metabolic hormones involved in food intake, energy expenditure and body mass. It has been proposed that inducing H. pylori-induced gastric atrophy damages hormone-producing endocrine cells localized in gastric mucosal layers and therefore alter their concentrations. In a recent study, we provided additional proof in mice under controlled conditions that H. pylori and gut microbiota indeed affects circulating metabolic gut hormones and energy homeostasis. In this addendum, we presented data from follow-up investigations that demonstrated H. pylori and gut microbiota-associated modulation of metabolic gut hormones was independent and precedes H. pylori-induced histopathological changes in the gut of H. pylori-infected mice. Thus, H. pylori-associated argumentation of energy homeostasis is not caused by injury to endocrine cells in gastric mucosa.

Topics: Animals; Energy Metabolism; Gastric Mucosa; Gastrointestinal Microbiome; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Insulin; Leptin; Mice; Peptide YY

The associations between Helicobacter pylori infection, serum vitamin D level, and metabolic syndrome (MS) are controversial. The present community-based study aimed to investigate the effect of H pylori infection and serum vitamin D deficiency on MS development.Individuals from the northeastern region of Taiwan were enrolled in a community-based study from March, 2014 to August, 2015. All participants completed a demographic survey and underwent the urea breath test (UBT) to detect H pylori infection as well as blood tests to determine levels of vitamin D, adiponectin, leptin, and high-sensitivity C-reactive protein. The ATP III criteria for MS were used in this study.A total of 792 men and 1321 women were enrolled. The mean age was 56.4 ± 13.0 years. After adjusting for age and sex, the estimated odds of MS development for a UBT-positive subject were 1.503 (95% confidence interval [CI]: 1.206-1.872, P < 0.001) when compared to a UBT-negative subject. For participants with vitamin D deficiency (<20 ng/mL), the odds of MS development were 1.423 (95% CI: 1.029-1.967, P = 0.033) when compared to those with sufficient vitamin D level (>30 ng/mL). For participants with both H pylori infection and vitamin D deficiency, the odds of MS development were 2.140 (95% CI: 1.348-3.398, P = 0.001) when compared to subjects without H pylori infection and with sufficient vitamin D levels.H pylori infection and vitamin D deficiency could be predictors of MS. For individuals with both H pylori infection and vitamin D deficiency, the odds of MS development were 2.140 when compared to individuals without H pylori infection and with sufficient vitamin D levels.

Topics: Adiponectin; Adult; Aged; Breath Tests; C-Reactive Protein; Female; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Metabolic Syndrome; Middle Aged; Taiwan; Urea; Vitamin D; Vitamin D Deficiency

Wstęp. Peptydy produkowane w przewodzie pokarmowym, tkance tłuszczowej i w mózgu odgrywają ważną rolę w wydzielaniu hormonu wzrostu (GH) oraz regulacji przyjmowania posiłków. Zgodnie z hipotezą molekularnego podobieństwa antygeny mikroorganizmów bytujących w przewodzie pokarmowym mogą stać się mechanizmem spustowym dla produkcji przeciwciał, które reagują krzyżowo z peptydami regulatorowymi i modyfikują ich działanie. Celem pracy była ocena stężenia greliny, leptyny, oreksynyA i αMSH oraz poziomu przeciwciał skierowanych przeciwko wymienionym peptydom u dzieci z idiopatycznym niedoborem wzrostu (ISS) i niedoborem GH (GHD) w odniesieniu do infekcji Helicobacter pylori (H.pylori) i zasiedlenia Candida albicans (C.albicans). Materiał i metody. Analiza obejmowała 89 dzieci z niedoborem wzrostu (w wieku 10,24±3,52 lat): 64 z ISS i 25 z GHD oraz 36 dzieci prawidłowego wzrostu (grupa kontrolna) (w wieku 11,41±2,72 lat). U każdego dziecka oceniono w surowicy stężenie greliny, leptyny, oreksynyA i αMSH (alpha-melanocyte-stimulating hormone), poziom przeciwciał IgG skierowanych przeciwko wymienionym peptydom oraz przeciwko H.pylori, zaś obecność C.albicans na podstawie badania próbki kału. Grupa kontrolna została dobrana tak, aby częstość występowania infekcji H.pylori i zasiedlenia C.albicans była podobna do grupy badanej. Wyniki. Poziom przeciwciał IgG przeciwko grelinie i leptynie był znamiennie wyższy w grupie ISS niż w grupie kontrolnej. Stężenie greliny było istotnie wyższe u dzieci z GHD niż w grupie kontrolnej, zaś stężenie leptyny (jak również wskaźnik masy ciała) istotnie niższe w grupie ISS niż w grupach GHD i kontrolnej. Nie wykazano różnic pomiędzy grupami w odniesieniu do stężenia oreksynyA i αMSH ani przeciwciał skierowanych przeciwko nim. Wnioski. Podwyższony poziom przeciwciał skierowanych przeciwko grelinie i leptynie u dzieci z ISS jest związany z upośledzeniem wzrastania i gorszymi przyrostami masy ciała, prawdopodobnie poprzez modyfikację aktywności greliny i leptyny. Możliwe, że te przeciwciała reagują krzyżowo z peptydami na skutek molekularnego podobieństwa między wymienionymi peptydami a H.pylori i C.albicans, jednak potrzebne są dalsze badania wyjaśniające tę kwestię.

Topics: Adolescent; alpha-MSH; Autoantibodies; Candida albicans; Candidiasis; Child; Female; Ghrelin; Growth Disorders; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Orexins

Helicobacter pylori (H. pylori) infection and eradication therapy have been known to influence gastric ghrelin and leptin secretion, which may lead to weight gain. However, the exact relationship between plasma ghrelin/leptin levels and H. pylori infection has remained controversial. The aim of this study was to investigate plasma ghrelin and leptin levels in H. pylori-positive and -negative patients, to compare the two levels of the hormones before and after H. pylori eradication, and to examine the correlation between body mass index (BMI) and active ghrelin or leptin levels, as well as that between atrophic pattern and active ghrelin or leptin levels.. Seventy-two H. pylori-positive patients who underwent upper gastrointestinal endoscopy, 46 diagnosed as having peptic ulcer and 26 as atrophic gastritis, were enrolled. Control samples were obtained from 15 healthy H. pylori-negative volunteers. The extent of atrophic change of the gastric mucosa was assessed endoscopically. Body weight was measured and blood was collected before and 12 weeks after H. pylori eradication therapy. Blood samples were taken between 8 and 10 AM after an overnight fast.. Plasma ghrelin levels were significantly lower in H. pylori-positive patients than in H. pylori-negative patients. In particular, plasma active ghrelin levels were significantly lower in patients with gastritis compared with patients with peptic ulcer. Plasma ghrelin levels decreased after H. pylori eradication in both peptic ulcer and gastritis patients, while plasma leptin levels increased only in peptic ulcer patients. Plasma leptin levels and BMI were positively correlated, and active ghrelin levels and atrophic pattern were weakly negatively correlated in peptic ulcer patients.. H. pylori infection and eradication therapy may affect circulating ghrelin/leptin levels. This finding suggests a relationship between gastric mucosal injury induced by H. pylori infection and changes in plasma ghrelin and leptin levels.

Topics: Adult; Aged; Amoxicillin; Anti-Bacterial Agents; Anti-Ulcer Agents; Biopsy; Body Mass Index; Body Weight; Case-Control Studies; Clarithromycin; Drug Therapy, Combination; Endoscopy, Digestive System; Female; Gastric Mucosa; Gastritis, Atrophic; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Lansoprazole; Leptin; Male; Middle Aged; Peptic Ulcer

Helicobacter pylori, is an invariably commensal resident of the gut microbiome associated with gastric ulcer in adults. In addition, these patients also suffered from a low grade inflammation that activates the immune system and thus increased shunting of energy to host defense mechanisms. To assess whether a H. pylori infection could affect growth in early life, we determined the expression levels of selected metabolic gut hormones in germ free (GF) and specific pathogen-free (SPF) mice with and without the presence of H. pylori. Despite H. pylori-infected (SPFH) mice display alteration in host metabolism (elevated levels of leptin, insulin and peptide YY) compared to non-infected SPF mice, their growth curves remained the same. SPFH mice also displayed increased level of eotaxin-1. Interestingly, GF mice infected with H. pylori (GFH) also displayed increased levels of ghrelin and PYY. However, in contrast to SPFH mice, GFH showed reduced weight gain and malnutrition. These preliminary findings show that exposure to H. pylori alters host metabolism early in life; but the commensal microbiota in SPF mice can attenuate the growth retarding effect from H. pylori observed in GF mice. Further investigations of possible additional side effects of H. pylori are highly warranted.

Topics: Animals; Body Mass Index; Chemokine CCL11; Energy Metabolism; Ghrelin; Helicobacter Infections; Helicobacter pylori; Host-Pathogen Interactions; Humans; Insulin; Intestine, Large; Leptin; Mice, Inbred C57BL; Microbiota; Models, Biological; Peptide Hormones; Peptide YY; Specific Pathogen-Free Organisms; Weight Gain

Helicobacter pylori (H. pylori) -induced gastric inflammation impacts the functions of leptin- and ghrelin-producing cells in the gastroduodenum. Inflammation resulting from H. pylori sensing via Toll-like receptors (TLRs) and the associated downstream signaling largely remain ambiguous. Here, we investigated the role of gut hormones, pro-inflammatory cytokines and single nucleotide polymorphisms (SNPs) associated with TLR 4p14 in H. pylori disease in 30 subjects with non-ulcer dyspepsia (NUD), 40 with peptic ulcer disease (PUD) and 15 with gastric cancer (GC) subjects positive and negative for H. pylori infection. The level of pro-inflammatory cytokines was directly proportional to the severity of gastritis, and disease status influenced the levels of gut hormones and pro-inflammatory cytokines. TLR-1 SNPs rs4833095 and TLR-10 SNPs rs10004195 and were directly associated with H. pylori disease, and were up-regulated in the presence of H. pylori in a genotype-independent manner. We concluded that TLR-1 rs4833095 and TLR10 rs10004195 confer susceptibility to development of gastroduodenal disease, especially GC in H.pylori disease.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Chromosomes, Human, Pair 4; Cytokines; Female; Genetic Predisposition to Disease; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Middle Aged; Polymorphism, Single Nucleotide; Receptor, Insulin; Stomach Neoplasms; Toll-Like Receptor 1; Toll-Like Receptor 10; Young Adult

Many of peptides synthesized in gastrointestinal tract (GI) and adipose tissues, regulate growth and food intake. The GI microflora is an antigenic source. Based on the molecular mimicry hypothesis, intestinal microbe-derived antigens may trigger the production of autoantibodies cross-reacting with some neuropeptides.. The aim of the study was to assess whether in idiopathic short stature (ISS) children with Candida albicans (C.albicans) colonisation and/or Helicobacter pylori (H.pylori) infection the autoantibodies (in positive levels) against selected neuropeptides [anti-NP Abs(+)]: ghrelin, leptin, orexin A, αMSH are more prevalent than in Controls.. The study group comprised 64 children with ISS and 36 children with normal height (Controls). In each child, IgG antibodies against H.pylori, ghrelin, leptin, orexin A and αMSH were assessed in serum, while presence of C.albicans - in stool samples.. The higher prevalence of anti-NP Abs(+) in ISS children with C.albicans and/or H.pylori than in normal height children with the colonization in question (34.4% vs 21.1%, p<0.01) was found. The prevalence of anti-NP Abs(+) in groups of children without C.albicans and H.pylori were low, anti-NP Abs(+) were detected in 9.4% of ISS children only, while in Controls they were not found.. In short children with C.albicans and/or H.pylori the incidence of autoantibodies against selected neuropeptides is high. It probably is connected with molecular mimicry between antigens of these microbiota and the mentioned peptides. It is tempting to speculate that presence of cross-reacting autoantibodies against regulatory neuropeptides may results in worse growth velocity. However, further studies are necessary to elucidate this issue.

Topics: Adolescent; alpha-MSH; Autoantibodies; Candida albicans; Candidiasis; Carrier State; Child; Child, Preschool; Cross Reactions; Female; Ghrelin; Growth Disorders; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Molecular Mimicry; Neuropeptides; Orexins

There is an inverse secular trend between the incidence of obesity and gastric colonization with Helicobacter pylori, a bacterium that can affect the secretion of gastric hormones that relate to energy homeostasis. H. pylori strains that carry the cag pathogenicity island (PAI) interact more intimately with gastric epithelial cells and trigger more extensive host responses than cag(-) strains. We hypothesized that gastric colonization with H. pylori strains differing in cag PAI status exert distinct effects on metabolic and inflammatory phenotypes.. To test this hypothesis, we examined metabolic and inflammatory markers in db/db mice and mice with diet-induced obesity experimentally infected with isogenic forms of H. pylori strain 26695: the cag PAI wild-type and its cag PAI mutant strain 99-305. H. pylori colonization decreased fasting blood glucose levels, increased levels of leptin, improved glucose tolerance, and suppressed weight gain. A response found in both wild-type and mutant H. pylori strain-infected mice included decreased white adipose tissue macrophages (ATM) and increased adipose tissue regulatory T cells (Treg) cells. Gene expression analyses demonstrated upregulation of gastric PPAR γ-responsive genes (i.e., CD36 and FABP4) in H. pylori-infected mice. The loss of PPAR γ in immune and epithelial cells in mice impaired the ability of H. pylori to favorably modulate glucose homeostasis and ATM infiltration during high fat feeding.. Gastric infection with some commensal strains of H. pylori ameliorates glucose homeostasis in mice through a PPAR γ-dependent mechanism and modulates macrophage and Treg cell infiltration into the abdominal white adipose tissue.

Topics: Adipose Tissue; Animals; Blood Glucose; Body Weight; CD36 Antigens; Enzyme-Linked Immunosorbent Assay; Fatty Acid-Binding Proteins; Flow Cytometry; Gastric Mucosa; Gene Expression Profiling; Genomic Islands; Ghrelin; Helicobacter Infections; Helicobacter pylori; Homeostasis; Insulin; Leptin; Macrophages; Mice; Obesity; PPAR gamma; T-Lymphocytes, Regulatory

It was suggested that gastric colonization with Helicobacter pylori (H. pylori) was associated with suboptimal nutrition and growth in childhood. Furthermore, several studies indicated a relationship between H. pylori colonization and alterations in the circulating levels of growth-related molecules (GRM). Accordingly, in this study, we investigate the effect of H. pylori infection on GRMs and on the growth of healthy school children, taking into consideration the effect of their economic status (ES) and anthropometric indices of their parents.. To acquire sociodemographic and anthropometric nutritional parameters and to detect H. pylori-specific serum IgG antibodies and growth-related molecules, we evaluated a total of 473 children attending four different primary and secondary schools in Istanbul. Subsequently, we assessed the effect of H. pylori on growth-related parameters (weight for age SDS, height for age SDS, BMI SDS, TSF, and waist-to-hip ratio) and on GRMs (leptin, ghrelin, and insulin-like growth factor-1 (IGF-1)), controlling for age, gender, family income, household crowding (HC), breastfeeding, maternal and paternal BMI SDS, and midparental height SDS with complex statistical models.. Of the 473 children (275 F/198 M, age 6-15 years; mean: 10.3 ± 0.1 years), 161 (34%) were H. pylori-positive. The prevalence of H. pylori was significantly higher in lower economic status (ES) groups, in children living in crowded houses, and in older age groups. Using simple statistical models, we did not find any significant associations between H. pylori infection and the growth parameters. However, in complex models for height for age SDS and for weight for age SDS, there was a significant interaction between H. pylori infection status and ES. Whereas in H. pylori-positive subjects, mid-income family children were both taller and heavier than the low-income group, there was no such an association in H. pylori-negative subjects. Among biochemical parameters, only ghrelin levels were associated with H. pylori infection in all models. Leptin levels were associated with HC in girls, whereas none of the parameters was significantly associated with leptin levels in boys. For IGF-1 levels, for boys, age and maternal BMI, and for girls, age and HC were significantly associated with IGF-1 levels.. We suggest that H. pylori may impair growth significantly only in susceptible children where unfavorable socioeconomic conditions facilitate its action, probably through mechanisms, at least in part, involving growth-related molecules.

Topics: Adolescent; Anthropometry; Antibodies, Bacterial; Body Height; Body Mass Index; Body Weight; Child; Female; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Insulin-Like Growth Factor I; Leptin; Male; Schools; Socioeconomic Factors; Students; Turkey

Topics: Adult; Atherosclerosis; Biomarkers; Blood Glucose; Body Fat Distribution; CD40 Ligand; Female; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Middle Aged; Oxidative Stress; Peptic Ulcer; Prognosis

Obesity is associated with gastroesophageal reflux disease (GERD). Leptin is a hormone which controls appetite and energy homeostasis. Alterations of its level in humans have been linked with obesity and related carcinogenesis. We postulated that the leptin level in plasma or tissues might be different according to the phenotype of GERD. We evaluated this hormone in patients with non-erosive reflux disease (NERD) and reflux esophagitis (RE) with demographic characteristics to confirm the postulation.. The patients with typical GERD symptoms such as acid regurgitation and heartburn were prospectively enrolled and evaluated. The demographic data included body mass index, waist circumference, smoking, and the consumption of coffee. Rapid urease test was done to evaluate the status of Helicobacter pylori infection. We measured plasma leptin level along with the tissue level, which was obtained from the fundus of stomach.. A total of 44 patients were evaluated (RE 20 cases, NERD 24 cases). No demographic data was different between the two groups, except waist circumference (mean 88.6 cm in RE, 80.9 cm in NERD, p=0.006), smoking (45% in RE, 12.5% in NERD, p=0.021) and coffee consumption (85% in RE, 50% in NERD, p=0.025). The level of plasma leptin was not different between the two groups. The level of tissue leptin was also not different between the two groups with an increasing tendency in RE (mean 32.5 ng/mL vs. 28.0 ng/mL in NERD).. We could not find any association between plasma and tissue leptin levels and the phenotype of GERD. However, increasing tendency in RE could afford to further studies in near future.

Topics: Adult; Aged; Body Mass Index; Coffee; Female; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Middle Aged; Obesity; Phenotype; Smoking; Waist Circumference

Bacterial infection can trigger the development of functional GI disease. Here, we investigate the role of the gut-brain axis in gastric dysfunction during and after chronic H. pylori infection. Control and chronically H. pylori-infected Balb/c mice were studied before and 2 mo after bacterial eradication. Gastric motility and emptying were investigated using videofluoroscopy image analysis. Gastric mechanical viscerosensitivity was assessed by cardioautonomic responses to distension. Feeding patterns were recorded by a computer-assisted system. Plasma leptin, ghrelin, and CCK levels were measured using ELISA. IL-1beta, TNF-alpha, proopiomelanocortin (POMC), and neuropeptide Y mRNAs were assessed by in situ hybridizations on frozen brain sections. Gastric inflammation was assessed by histology and immunohistochemistry. As shown previously, H. pylori-infected mice ate more frequently than controls but consumed less food per bout, maintaining normal body weight. Abnormal feeding behavior was accompanied by elevated plasma ghrelin and postprandial CCK, higher TNF-alpha (median eminence), and lower POMC (arcuate nucleus) mRNA. Infected mice displayed delayed gastric emptying and visceral hypersensitivity. Eradication therapy normalized gastric emptying and improved gastric sensitivity but had no effect on eating behavior. This was accompanied by persistently increased TNF-alpha in the brain and gastric CD3(+) T-cell counts. In conclusion, chronic H. pylori infection in mice alters gastric emptying and mechanosensitivity, which improve after bacterial eradication. A feeding pattern reminiscent of early satiety persists after H. pylori eradication and is accompanied by increased TNF-alpha in the brain. The results support a role for altered gut-brain pathways in the maintenance of postinfective gut dysfunction.

Topics: Animals; Autonomic Nervous System; Brain; CD3 Complex; Cell Count; Feeding Behavior; Female; Gastritis; Gastrointestinal Motility; Gastrointestinal Tract; Ghrelin; Heart Rate; Helicobacter Infections; Helicobacter pylori; In Situ Hybridization; Leptin; Mice; Mice, Inbred BALB C; Receptors, Cholecystokinin

Both ghrelin and leptin are important appetite hormones secreted from the stomach. We examined whether demographic background, Helicobacter pylori infection, or its related gastritis severity could be associated with circulating ghrelin and leptin levels.. This study prospectively enrolled 341 dyspeptic patients (196 females, 145 males), who had received endoscopy to provide the gastric specimens over both antrum and corpus for histology reviewed by the updated Sydney's system. The fasting blood sample of each patient was obtained for total ghrelin and leptin analysis.. Without H. pylori infection, there were similar ghrelin levels between female and male patients. In the H. pylori-infected patients, the males had lower plasma ghrelin levels than females (1053 vs. 1419 pg/mL, p < .001). Only in males, not in females, the H. pylori infection and its related acute and chronic inflammation scores were significantly associated with a lower ghrelin level (p < or = .04). The multivariate regression disclosed that only the chronic inflammation score independently related to a lower ghrelin level. Only in males, the ghrelin levels ranked in a downward trend for the gastritis feature as with limited-gastritis, with antrum-predominant gastritis, and with corpus-gastritis (1236, 1101, and 977 pg/mL). Leptin level was not related to H. pylori-related gastritis, but positively related to body mass index.. There should be a gender difference to circulating total ghrelin levels, but not leptin levels, in response to H. pylori infection and its related chronic gastritis.

Topics: Adult; Aged; Body Mass Index; Chronic Disease; Female; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Middle Aged; Prospective Studies; Sex Characteristics

Serological screening for gastric cancer (GC) may reduce mortality. However, optimal serum markers for advanced gastric precursor lesions are lacking.. To evaluate in a case-control study whether serum leptin levels correlate with intestinal metaplasia (IM) and can serve as a tool to identify patients at high risk for GC.. Cases were patients with a previous diagnosis of IM or dysplasia, controls were patients without such a diagnosis. All patients underwent endoscopy. Fasting serum was collected for the measurement of leptin, pepsinogens I/II, gastrin, and Helicobacter pylori. Receiver operating characteristic (ROC) curves and their area under the curve (AUC) were provided to compare serum leptin levels with other serological markers.. One hundred nineteen cases and 98 controls were included. In cases, the median leptin levels were 116.6 pg/mL versus 81.9 pg/mL in controls (p = .01). After adjustment for age, sex and BMI, leptin levels remained higher in cases than in controls (p < .005). In multivariate analysis, male sex (p = .002), age (<0.001), low pepsinogen levels (p = .004) and high leptin levels (p = .04) were independent markers for the presence of IM. In addition, a ROC curve including age, sex and pepsinogen I levels had an AUC of 0.79 (95% CI (0.73-0.85)). Adding serum leptin levels increased the AUC to 0.81 (95% CI (0.75-0.86)).. High leptin levels are associated with an increased risk of IM. Moreover, serum leptin levels are a significant independent marker for the presence of IM. However, in combination with the serological test for pepsinogen I the additional value of serum leptin levels is rather limited.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Biomarkers; Case-Control Studies; Female; Helicobacter Infections; Helicobacter pylori; Humans; Intestines; Leptin; Male; Metaplasia; Middle Aged; Risk Factors; Stomach Neoplasms; Young Adult

To determine the effect of Helicobacter pylori (H. pylori) eradication on blood levels of soluble CD40 ligand, leptin, oxidative stress and body composition in patients with dyspepsia infected with H. pylori.. The infection of H. pylori was based on the presence of both (14)C urea breath test (UBT) and histology. Patients were given triple eradication therapy for 14 days and at 3 months after the treatment, (14)C UBT was reinstituted. Fasting glucose, leptin, body composition, soluble CD40 ligand, total oxidant status (TOS) were studied before and at 3 months after the treatment.. In 33 subjects, H. pylori infection was successfully eradicated. sCD40L, and TOS levels were significantly decreased after H. pylori eradication. The percentage of body fat and body fat mass significantly decreased whereas the fat free mass (FFM) increased after eradication. However, eradication of the organism yielded no differences in leptin levels.. These findings suggest that H. pylori eradication reduces the sCD40L and oxidative stress, fat mass with a significant increase in fat free mass. Thus, eradication of H. pylori infection not only improves ulcer healing, but may also reduce the presumed atherosclerosis risk.

Topics: Adult; Anti-Bacterial Agents; Atherosclerosis; Body Fat Distribution; CD40 Ligand; Drug Therapy, Combination; Female; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Oxidative Stress; Peptic Ulcer; Prospective Studies; Risk Factors; Young Adult

Helicobacter pylori, and the chronic gastric inflammation that it causes, may compromise the function and survival of ghrelin-producing cells, resulting in a decrease of circulating ghrelin levels. This finding raises the possibility that the infection might affect growth in children by reducing the ghrelin production.. To determine baseline circulating levels of ghrelin and leptin in prepubertal children with and without H. pylori infection and to evaluate the long-term effects of H. pylori eradication on circulating levels of ghrelin and leptin as well as on body composition.. Thirty children with H. pylori-associated gastritis, 35 children with H. pylori-negative gastric mucosa, and 20 healthy controls were studied.. At baseline, while leptin levels were significantly lower in H. pylori-positive patients, ghrelin concentrations did not differ among the three study groups. However, a significant inverse correlation between ghrelin concentrations and histological severity of gastritis was found. Eradication of the organism was associated with a progressive decrease in ghrelin concentrations over baseline at both 6- and 12-month follow-ups. SDS-body mass index (BMI), lean and fat mass, as well as leptin concentrations, significantly increased over baseline at both follow-ups.. In prepubertal children, serum ghrelin concentrations are inversely related to the severity of H. pylori-associated gastritis. In these youngsters, long-term eradication of H. pylori infection is associated with a significant increase in BMI, lean and fat mass along with a significant decrease in circulating ghrelin levels and an increase in leptin levels.

Topics: Anti-Bacterial Agents; Body Composition; Body Mass Index; Child; Child Development; Child, Preschool; Female; Follow-Up Studies; Gastritis; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Insulin-Like Growth Factor I; Leptin; Male

A vaccine against Helicobacter pylori would be a desirable alternative to antibiotic therapy. Vaccination has been shown to be effective in animal models but the mechanism of protection is poorly understood. Previous studies investigating the gene expression in stomachs of vaccinated mice showed changes in adipokine expression correlated to a protective response. In this study, we investigate a well-characterized adipokine-leptin, and reveal an important role for leptin receptor signaling in vaccine-induced protection.. Leptin receptor signaling-deficient (C57BL/Ks Lepr(db)), wild-type C57BL/Ks m littermates and C57BL/6 mice were vaccinated, and then challenged with H. pylori. Levels of bacterial colonization, antibody levels, and gastric infiltrates were compared. The local gene expression pattern in the stomach of leptin receptor signaling-deficient and wild-type mice was also compared using microarrays.. Interestingly, while vaccinated wild-type lean C57BL/6 and C57BL/Ks m mice were able to significantly reduce colonization compared to controls, vaccinated obese C57BL/Ks Lepr(db) were not. All mice responded to vaccination, i.e. developed infiltrates predominantly of T lymphocytes in the gastric mucosa, and made H. pylori-specific antibodies. A comparison of expression profiles in protected C57BL/6 and nonprotected C57BL/Ks Lepr(db) mice revealed a subset of inflammation-related genes that were more strongly expressed in nonprotected mice.. Our data suggest that functional leptin receptor signaling is required for mediating an effective protective response against H. pylori.

Topics: Animals; Bacterial Vaccines; Gastritis; Helicobacter Infections; Helicobacter pylori; Leptin; Mice; Mice, Inbred C57BL; Microarray Analysis; Receptors, Cell Surface; Receptors, Leptin; Signal Transduction

Leptin and ghrelin, hormones involved in human energy homeostasis, are both produced in the stomach.. We sought to determine whether the presence of Helicobacter pylori affects gastric and systemic levels of leptin and ghrelin.. We consecutively enrolled 256 patients referred for upper endoscopy at a Veterans Affairs outpatient endoscopy center.. We obtained fasting serum, fundic and antral biopsies, and gastric juice. Based on histological, biochemical, and serological assays, patients were categorized as H. pylori+ or H. pylori-. Leptin and total ghrelin levels in serum, gastric biopsies, and gastric juice were determined by specific ELISAs.. Of the 256 subjects, 120 were H. pylori+ and 96 were H. pylori-; 40 patients of indeterminate status were excluded. Serum and fundic leptin levels correlated with body mass index in the H. pylori+ (r = 0.35; P < 0.0001 and r = 0.35; P < 0.0001, respectively) and H. pylori- (r = 0.65; P < 0.0001 and r = 0.41; P < 0.0001, respectively) groups, but H. pylori+ subjects had significantly lower serum leptin levels [median 2.2 ng/ml (interquartile range 0.9-4.6) vs. 4.0 ng/ml (1.7-7.2); P = 0.0003]. Serum ghrelin levels were similar in the H. pylori+ and H. pylori- groups [median 1651 pg/ml (interquartile range 845-2247) vs. 1629 pg/ml (992-2886); P = 0.23]. H. pylori status did not significantly affect gastric biopsy leptin and ghrelin levels. Ghrelin levels in gastric juice varied over 4 log(10) (<80-776,000 pg/ml) and correlated with gastric juice pH in the H. pylori+ group (r = 0.68; P < 0.0001).. These findings provide evidence that H. pylori status affects leptin and ghrelin homeostasis, presumably via intragastric interactions.

Topics: Adult; Aged; Disease Progression; Gastric Juice; Gastric Mucosa; Ghrelin; Helicobacter Infections; Helicobacter pylori; Homeostasis; Humans; Leptin; Male; Middle Aged; Prospective Studies; Stomach; Stomach Diseases

Gastrointestinal parasites have evolved with humans and colonize many asymptomatic subjects. We investigated the influence of microbial gastrointestinal colonization on the nutritional status of rural Amerindians (40 males and 61 females). Helicobacter pylori was detected by 13C-breath test, and intestinal parasites were detected in fecal specimens. Body morphometry and bioelectrical impedance measurements were measured. Although Amerindians showed low height and weight for age, they had an adequate body mass index, morphometric parameters, and cell mass. Intestinal parasites were detected in 99% of the subjects, with no detrimental effect on nutritional parameters. Helicobacter pylori was present in 82% of adults and half the children, and was positively correlated with improved nutritional status. Despite the high prevalence of gastrointestinal microbes often associated with disease, the studied population of Amerindians had a body morphometry and composition indicative of good nutritional status, and improved in children positive for gastric H. pylori.

Topics: Adolescent; Adult; Aged; Body Composition; Body Mass Index; Child; Child, Preschool; Female; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Diseases, Parasitic; Leptin; Male; Middle Aged; Nutritional Status

The purpose of this study was to examine the changes in gastric ghrelin and leptin with respect to Helicobacter pylori infection and whether such changes affect the plasma levels of leptin and ghrelin. In addition, we examined the relationship between changes in gastric mucosal ghrelin and leptin levels and gastrointestinal symptoms. Sixty-three patients diagnosed with chronic gastritis were enrolled in the study. Twenty-nine patients were Helicobacter pylori negative and 34 were Helicobacter pylori positive. Expression of ghrelin and leptin mRNA in the gastric mucosa was measured using endoscopic biopsies from the fundus. Plasma levels of ghrelin and leptin were measured by radioimmunoassay. Expression of leptin mRNA in the gastric mucosa was significantly higher in Helicobacter pylori-positive patients than in negative patients (0.38 +/- 0.17 vs. 0.24 +/- 0.12, p = 0.039). The expression of ghrelin was lower in positive patients than in the negative group, although this difference was not significant (p = 0.07). However, there was no significant difference in plasma leptin and ghrelin levels. Gastric mucosal ghrelin mRNA expression was significantly lower in patients with dyspepsia than in those without (0.15 +/- 0.11 vs. 0.23 +/- 0.20, p = 0.05). Helicobacter pylori infection and gastrointestinal symptoms could be associated with leptin and ghrelin expression in the gastric mucosa.

Topics: Adult; Aged; Biomarkers; Biopsy; Diagnosis, Differential; Female; Gastric Mucosa; Gastritis; Gastroscopy; Gene Expression; Ghrelin; Growth Hormone; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Middle Aged; Peptide Hormones; Polymerase Chain Reaction; Prognosis; Radioimmunoassay; RNA, Messenger; Severity of Illness Index; Surveys and Questionnaires

Family unit is generally accepted as one of the contributors to Helicobacter pylori infection that is most frequently acquired in childhood, so it seems logical to diagnose and treat this infection in childhood. This study was designed to assess H. pylori prevalence in children from shepherd families having contacts with sheep.. This study involved 146 children (58 M/88 F, age 6-17 years; mean: 10.2 years) from families living in Polish Tatra Mountains with contact (group A, n=58) or without contact with sheep (group B, n=88). H. pylori status was determined by (13)C-urea breath test and was compared to 141 age- and gender-matched urban controls (group C). In both groups of mountain children, the anti-H. pylori and anti-CagA IgG were measured by ELISA and serum gastrin, ghrelin and leptin concentrations by RIA.. The H. pylori prevalence in group A was significantly higher (58.6%) than that in group B (21.6%) and urban controls (26%). Serum gastrin concentrations were significantly higher in H. pylori-positive than in H. pylori-negative mountain children (52.2+/-5.8 pmol/L versus 22.7+/-2.1 pmol/L), while serum ghrelin and leptin concentrations were significantly lower in H. pylori-infected (741+/-112 pg/mL and 3.6+/-0.8 ng/mL) than in non-infected children (1323+/-104 pg/mL and 8.6+/-2.4 ng/mL).. Children with sheep contact show about twice higher H. pylori prevalence and higher serum gastrin but lower ghrelin and leptin levels than those without H. pylori infection. Considering almost 100% positive 13C-urea breath test in sheep, it is reasonable to propose that H. pylori infection in shepherd children may originate from sheep and the infection might, therefore, be considered as zoonosis.

Topics: Adolescent; Agricultural Workers' Diseases; Animal Husbandry; Animals; Breath Tests; Child; Female; Gastrins; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Parents; Peptide Hormones; Poland; Prevalence; Seroepidemiologic Studies; Sheep; Urea

Recently, gastric Helicobacter pylori (H. pylori) colonization has been shown to affect the expression of leptin and ghrelin, hormones that control appetite and satiety. Gastric leptin, produced by chief and parietal cells and released in response to meals, may play a role in weight gain after eradication of H. pylori infection, whereas ghrelin, produced by X/A-like enteroendocrine cells in oxyntic gland, is released during fasting, and suppressed by feeding and leptin. Whether either that H. pylori genes represent microbial contributions to the complement of thrifty genes of humans, or that H. pylori disappearance plays a role in adiposity remains to be determined. Simply, ghrelin-leptin might tango in body weight regulation, gastric inflammation, and gastric motility. In the current review about the possible role of ghrelin in gastric inflammation, we found that high serum albumin condition decreased ghrelin expression, whereas serum albumin deprivation significantly increased ghrelin expression, however, of which regulation was abolished after H. pylori infection. Ghrelin significantly attenuated the inflammatory stimuli imposed after H. pylori, shown with inactivation of phospho-extracellular signal-regulated kinase (p-ERK) and nuclear factor-kappaB (NF-kappaB)-DNA binding activities. Conclusively, besides orexigenic and weight gaining actions of gastric hormone, ghrelin, it likely endows the stomach the protective effect from exogenous damages.

Topics: Amino Acid Sequence; Appetite Stimulants; Gastritis; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Insulin-Like Growth Factor I; Leptin; Mitogen-Activated Protein Kinases; Molecular Sequence Data; Neurosecretory Systems; NF-kappa B; Peptide Hormones; Signal Transduction; Weight Gain

The aim of the study was to investigate the relationship between gastritis and leptin and ghrelin in elderly patients. Patients older than 75 years undergoing an endoscopy were included. We reported data on nutritional status and Helicobacter pylori infection diagnosis (serology, 13C-urea breath test, culture, histology, and polymerase chain reaction on gastric biopsies). Gastric messenger RNA expression of leptin and ghrelin were quantified by real-time polymerase chain reaction. Sixty-two patients were included (84.7 +/- 5.2 years). H. pylori infection was associated with decreased gastric expression of leptin (p = .021), ghrelin (p =.002), and plasma ghrelin levels (p = .018). Atrophy was associated with decreased gastric leptin (p = .007) and ghrelin (p = .02). H. pylori infection correlated negatively with patient energy intake (r = -0.36; p = .001) and body mass index (r = -0.34; p = .018). The negative association between ghrelin and H. pylori infection may be related to a higher prevalence of atrophy and raises the possibility that H. pylori may be contributing to undernutrition in some older people.

Topics: Aged; Aged, 80 and over; Aging; Body Mass Index; Endoscopy, Gastrointestinal; Energy Intake; Female; Gastric Mucosa; Gastritis, Atrophic; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Nutritional Status; Peptide Hormones; Polymerase Chain Reaction; RNA, Messenger; Severity of Illness Index; Stomach

Ghrelin and leptin are endogenous peptides that have been implicated in the control of food intake, energy homeostasis and body weight gain. Although the stomach is the major source of circulating ghrelin and partly contributes also to plasma leptin, controversy exists over the influence of gastric Helicobacter pylori (Hp) infection on the ghrelin and leptin release. To resolve this controversy, plasma immunoreactive ghrelin and leptin levels were determined in Hp-positive and Hp negative children (N=60) and in adults (N=120) and daily concentrations of these hormones were measured at 2 h intervals before and after meals. Serum levels of ghrelin and leptin as well as gastrin were measured by RIA. Hp status was assessed using (13)C-urea breath test (UBT) and serology. Children with negative UBT showed significantly higher basal serum levels of ghrelin and lower concentrations of leptin than those with positive UBT. Adults without Hp infection also showed significantly higher fasting serum levels of ghrelin and lower levels of leptin than those in Hp infected subjects. In adults, especially without Hp infection, plasma levels of ghrelin showed a marked rise before the meal and sudden decrease following the food intake, while plasma leptin did not showed significant meal-related alterations, but in general its level was significantly higher in Hp positive than Hp negative subjects. Serum gastrin concentrations were significantly elevated in both Hp positive children and adults and these levels were significantly lower in Hp negative subjects. We conclude that Hp infection in children and adults causes a marked reduction in plasma levels of ghrelin, while increasing plasma levels of leptin and gastrin. These alterations in plasma levels of gastric originated appetite-controlling hormones in Hp infected children and adults may contribute to the alterations of the appetite and dyspeptic symptoms observed in these subjects.

Topics: Adolescent; Adult; Child; Eating; Female; Gastrins; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-8; Leptin; Male; Middle Aged; Tumor Necrosis Factor-alpha

To determine the concentrations of leptin in plasma and gastric fundic mucosa in humans, with reference to Helicobacter pylori (H pylori) infection, and their association with gastric mucosal levels of interleukin (IL)-1beta, IL-6 and IL-8.. Plasma leptin concentrations were determined in 135 outpatients with non-ulcer dyspepsia, consisting of 95 H pylori-infected and 40 uninfected subjects, and 13 patients before and after cure of the infection with anti-H pylori regimen. Using biopsy samples that were endoscopically obtained from the middle corpus along the greater curvature, gastric leptin contents were measured by radioimmunoassay and the mucosal concentrations of IL-1beta, IL-6 and IL-8 were measured by enzyme linked immunosorbent assay. We also analysed the expression of leptin in the fundic mucosa by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry.. The mucosal levels of leptin in the fundic mucosa of H pylori-infected patients were significantly higher than those of uninfected patients. The amount of gastric leptin correlated positively with the mucosal levels of IL-1beta and IL-6, but not IL-8. Circulating leptin correlated with body mass index, but not with H pylori status, and there was no change in plasma leptin levels following cure of the infection. Leptin immunoreactive cells were noted in the lower half of the fundic glands, and its expression of messenger ribonucleic acid in the oxyntic mucosa was detected by RT-PCR.. Leptin production is enhanced in H pylori-infected gastric mucosa. Gastric leptin may be involved in immune and inflammatory response during H pylori infection, through interaction with proinflammatory cytokines.

Topics: Adult; Aged; Aged, 80 and over; Female; Gastric Fundus; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-1; Interleukin-6; Interleukin-8; Leptin; Male; Middle Aged; RNA, Messenger

Eradication of Helicobacter pylori improves clinical symptoms and quality of life in patients with peptic ulcer.. To investigate the effect of eradication of H. pylori on body mass index and incidence of hyperlipidaemia in patients with peptic ulcer.. The study population comprised 50 patients (42 men, 8 women; mean age, 51 years; 28 gastric ulcer, 22 duodenal ulcer) who underwent physical and blood examination before and 1 year after undergoing eradication therapy and 100 sex- and age-matched control subjects. Body mass index, total cholesterol and triglyceride were measured before and 1 year after therapy.. The eradication therapy group showed a significant increase in body mass index (22.7+/-2.5 kg/m2 before eradication versus 23.6+/-2.6 kg/m2 after eradication, p < 0.01), serum total cholesterol (204.1+/-33.2 mg/dL versus 221.2+/-38.8 mg/dL, p < 0.01), and triglyceride. Additionally, the eradication therapy group showed a significant increase in the incidence of hypercholesterolemia (30% versus 58%, p<0.01), hypertriglyceridaemia (28% versus 44%, p < 0.01) and obesity (12% versus 22%, p <0.05) 12 months after therapy.. Our findings show that eradication of H. pylori significantly increases the incidence of hyperlipidaemia and obesity in patients with peptic ulcer.

Topics: Adult; Aged; Body Mass Index; Breath Tests; Comorbidity; Female; Helicobacter Infections; Helicobacter pylori; Humans; Hyperlipidemias; Leptin; Male; Middle Aged; Obesity; Peptic Ulcer; Quality of Life

Helicobacter pylori infection may decrease serum ghrelin and increase gastric leptin levels, which may, in turn, decrease body mass index.. To determine whether H. pylori seropositivity is associated with body mass index.. Serum H. pylori and cytotoxin-associated gene product A (CagA) antibody levels were measured on 6724 adult participants of the third National Health and Nutrition Examination Survey (1988-91). We evaluated the association between H. pylori/CagA antibody status [both negative (-/-), H. pylori-positive/CagA-negative (+/-), or both positive (+/+)] and body mass index, adjusting for sociodemographic factors. We also investigated whether H. pylori/cytotoxin-associated gene product A antibody status was associated with fasting serum leptin levels.. H. pylori/CagA antibody status was not associated with obesity (body mass index > or = 30 kg/m(2)) [adjusted odds ratio (OR) 1.2, 95% CI: 0.9-1.6 comparing (+/+) to (-/-) and adjusted OR 1.1, 95% CI: 0.8-1.5 comparing (+/-) to (-/-)], overweight (body mass index 25 to <30 kg/m(2)) [adjusted OR 1.0, 95% CI: 0.7-1.2 comparing (+/+) to (-/-) and adjusted OR 1.0, 95% CI: 0.8-1.3 comparing (+/-) to (-/-)], or fasting serum leptin level in the USA population.. H. pylori seropositivity and CagA antibody status are not associated with body mass index or fasting serum leptin level.

Topics: Adult; Aged; Antigens, Bacterial; Bacterial Proteins; Body Mass Index; Enzyme-Linked Immunosorbent Assay; Epidemiologic Methods; Female; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Middle Aged; Obesity; United States

Ghrelin, an endogenous ligand for growth hormone secretagogue receptor, influences appetite, energy balance, gastric motility and acid secretion. The stomach is the main source of circulating ghrelin. There are inconsistent reports on the influence of Helicobacter pylori (H pylori) infection on circulating ghrelin levels. We sought to elucidate the relationship between ghrelin and various peptides in plasma, with special reference to H pylori.. Plasma ghrelin levels were measured by radioimmunoassay in 89 subjects who were referred for upper gastrointestinal endoscopy, consisting of 42 H pylori infected and 47 uninfected ones. Plasma gastrin, somatostatin, leptin, insulin-like growth hormone 1 (IGF-1) and chromogranin A concentrations were also measured. Twelve patients were treated with anti- H pylori regimen.. Ghrelin circulating levels were greatly decreased in H pylori-positive than negative individuals (194.2+/-90.2 fmol/mL and 250.4+/-84.1 respectively, P<0.05), but did not significantly alter following the cure of infection (176.5+/-79.5 vs 191.3+/-120.4). There was a significant negative correlation between circulating ghrelin and leptin levels, as well as body mass index, for the whole and uninfected population, but not in H pylori-infected patients. Plasma ghrelin concentrations correlated positively with IGF-1 in H pylori-negative group and negatively with chromogranin A in the infected group. There were no significant correlations among circulating levels of ghrelin, gastrin and somatostatin irrespective of H pylori status.. H pylori infection influences plasma ghrelin dynamics and its interaction with diverse bioactive peptides involved in energy balance, growth and neuroendocrine function.

Topics: Adult; Aged; Energy Metabolism; Female; Gastrins; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Insulin-Like Growth Factor I; Leptin; Male; Middle Aged; Neurosecretory Systems; Peptide Hormones

Obesity is an important public health problem in the United States. Because of its potential effects on gastric leptin homeostasis, Helicobacter pylori may play a role in regulating body weight. The authors' aim in this study was to examine the association between H. pylori colonization and overweight status. Nonpregnant participants in the Third National Health and Nutrition Examination Survey (1988-1994) aged > or = 20 years who had had H. pylori testing performed and body mass index (weight (kg)/height (m2)) measured were studied. Overweight was defined as a body mass index greater than or equal to 25. On the basis of serologic results, the participants were categorized into three H. pylori status groups: H. pylori-positive and cytotoxin-associated gene A (cagA)-positive (H. pylori+ cagA+), H. pylori-positive and cagA-negative (H. pylori+ cagA-), and H. pylori-negative (H. pylori-). Of the 7,003 subjects with complete body mass index and H. pylori data, 2,634 (weighted percentage, 22.9%) were H. pylori+ cagA+, 1,385 (15.1%) were H. pylori+ cagA-, and 2,984 (62.0%) were H. pylori-. The adjusted odds of being overweight were 1.17 (95% confidence interval: 0.98, 1.39; p = 0.075) for the H. pylori+ cagA+ group and 0.99 (95% confidence interval: 0.80, 1.22; p = 0.92) for the H. pylori+ cagA- group in comparison with H. pylori- subjects. Serum leptin levels did not differ significantly between the three H. pylori groups. In this US population-based study, there was no significant association between H. pylori colonization, cagA+ strains of H. pylori, and being overweight.

Topics: Adult; Antigens, Bacterial; Bacterial Proteins; Body Mass Index; Confounding Factors, Epidemiologic; Cross-Sectional Studies; Female; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Middle Aged; Nutrition Surveys; Obesity; United States

Ghrelin stimulates growth hormone and has orexigenic and adipogenic effects. Plasma ghrelin levels are reduced in obesity and possibly in Helicobacter pylori infection.. To investigate whether there was a relation between H. pylori infection, body mass index (BMI) and serum ghrelin or leptin levels.. University students undergoing an annual health check-up were invited to participate. H. pylori status was based on the presence of specific IgG H. pylori antibodies in urine. Fasting serum ghrelin, leptin levels, and pepsinogen I and II levels were measured by enzyme immunoassay (EIA).. Eight hundred and one students volunteered. There was no significant difference in the height and BMI between those with and without H. pylori infection. The population of ghrelin study consisted of 132 (66 H. pylori-positive and 66 H. pylori-negative) students matched for age, sex, and BMI. The ghrelin level in the H. pylori-positive group was significantly lower (median 55 pmol/l) compared to the H. pylori-negative group (103 pmol/l) (p < .00001). Leptin, triglyceride, total cholesterol, and HDL-cholesterol were not different between the two groups, whereas LDL-cholesterol levels were significantly higher (106 versus 100 mg/dl) (p = .03) in the H. pylori-positive group. Leptin levels correlated with the BMI (r = 0.53) (p < .00001). Among H. pylori-positive subjects, ghrelin correlated only with pepsinogen I levels (r = 0.26, p = .04).. H. pylori infection was associated with a reduction in circulating ghrelin levels independent of sex and BMI.

Topics: Adolescent; Adult; Body Mass Index; Case-Control Studies; Female; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Pepsinogen A; Peptide Hormones; Prevalence

To determine the concentrations of leptin and ghrelin, which have opposite effects on appetite, energy expenditure, and weight control, in the plasma of patients with Crohn's disease (CD), which is often associated with weight loss and malnutrition.. Plasma leptin and ghrelin 'concentrations were determined in 28 outpatients with CD by radioimmunoassay. Age- and sex-matched controls with and without Helicobacter pylori (H pylori) infection (28 for each) were enrolled in the study. Circulating levels of these hormones were assessed with respect to CD activity, disease localization and medical treatment.. There were no significant differences in ghrelin levels between CD patients and H pylori-negative controls. However, circulating ghrelin levels were significantly lower in H pylori-infected subjects than in CD patients and uninfected controls. Plasma leptin levels were comparable among the groups. Localization and medication profile had no significant impact on circulating ghrelin and leptin levels.. Apart from H pylori infection, CD itself has no significant influence on circulating ghrelin and leptin levels in the outpatients who were mostly in inactive state.

Topics: Adolescent; Adult; Case-Control Studies; Crohn Disease; Female; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Malnutrition; Middle Aged; Peptide Hormones; Weight Loss

In the Western world, the incidence of oesophageal adenocarcinoma has increased over the last 30 years coinciding with a decrease in the prevalence of Helicobacter pylori. Trends of increasing oesophageal adenocarcinoma can be linked causally to increasing gastro-oesophageal reflux disease (GORD) which can be linked to an increasingly obese population. However, there is no plausible biological mechanism of association between H. pylori, obesity, and GORD. Ghrelin, a peptide produced in the stomach, which regulates appetite, food intake, and body composition, was studied in H. pylori positive asymptomatic subjects.. Plasma ghrelin, leptin, and gastrin were measured for six hours after an overnight fast, before and after cure of H. pylori in 10 subjects. Twenty four hour intragastric acidity was also assessed.. After cure, median (95% confidence intervals) integrated plasma ghrelin increased from 1160.5 (765.5-1451) pg/ml x h to 1910.4 (1675.6-2395.6) pg/ml x h (p=0.002, Wilcoxon's rank sum test), a 75% increase. This was associated with a 14% increase in 24 hour intragastric acidity (p=0.006) and non-significant changes in leptin and gastrin. There was a significant positive correlation between plasma ghrelin and intragastric acidity (r(s) 0.44, p=0.05, Spearman's rank correlation).. After H. pylori cure, plasma ghrelin increased profoundly in asymptomatic subjects. This could lead to increased appetite and weight gain, and contribute to the increasing obesity seen in Western populations where H. pylori prevalence is low. This plausible biological mechanism links H pylori, through increasing obesity and GORD, to the increase in oesophageal adenocarcinoma observed in the West.

Topics: Adenocarcinoma; Adult; Esophageal Neoplasms; Female; Gastric Acidity Determination; Gastrins; Gastroesophageal Reflux; Ghrelin; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Peptide Hormones; Radioimmunoassay

Our recent histochemical studies have revealed the marked increase of myofibroblasts in the Helicobacter pylori-infected Mongolian gerbil fundic mucosa, while the mediators, which facilitate the conversion of fibroblasts to the myofibroblasts have remained unknown.. The present study was undertaken to clarify the alteration of leptin in the control and H. pylori-infected Mongolian gerbil stomach. The effector sites of rebamipide were also investigated in relation to leptin.. The localization of leptin was investigated by the indirect immunofluorescence. Plasma leptin levels were determined by ELISA method. The localization of 3H-rebamipide binding sites was investigated by autoradiography.. Serum leptin content in H. pylori-infected Mongolian gerbils was significantly increased. The presence of leptin immunoreactivity was recognized in the endothelial cells of the microcirculatory network and very weakly in the glandular cells in the control group, while in the H. pylori-infected group leptin was markedly recognized in the mesenchymal cells. Rebamipide bound to the fibroblasts and surface mucous cells and decreased the leptin immunoreactivity in the gastric mucosa.. Leptin was mostly found in the mesenchymal cells. Rebamipide administration brought about the decrease of leptin in the gastric mucosaof the H. pylori-infected gerbils.

Topics: Alanine; Animals; Anti-Ulcer Agents; Autoradiography; Cell Differentiation; Fibroblasts; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Immunohistochemistry; Leptin; Quinolones

Topics: Adolescent; Anti-Bacterial Agents; Body Mass Index; Child; Drug Therapy, Combination; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male

Leptin regulates feeding behaviour and therefore may be a mediator of anorexia associated with acute and chronic inflammation. Recently, leptin mRNA and leptin protein were found in the gastric epithelium.. The aim of the present study was to examine the effect of Helicobacter pylori infection on gastric leptin expression to investigate the pathophysiological role of gastric leptin.. Surgically resected human stomach tissues were subjected to immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR) to check for the presence of leptin in the human gastric epithelium. A total of 201 H pylori positive patients with chronic gastritis underwent eradication therapy for H pylori and were examined for the effect of infection cure in terms of body mass index (BMI) and serum leptin levels. Biopsy specimens from the gastric fundic mucosa were obtained from 40 of the 201 patients before and three months after eradication therapy. These samples were subjected to quantitative RT-PCR to examine the effect of eradication therapy on leptin expression in the gastric fundic mucosa.. Leptin immunoreactive cells were detected in the lower half of the gastric fundic glands and a leptin PCR product was also found in the gastric fundic mucosa. H pylori infection significantly increased gastric leptin expression. In addition, cure of H pylori infection significantly reduced gastric leptin expression, with a concomitant increase in BMI. In contrast, serum leptin levels did not change significantly after cure of H pylori infection.. Leptin is present in the human gastric mucosa. Gastric leptin may play a role in weight gain after eradication of H pylori infection. Gastric leptin may have a local rather than systemic action.

Topics: Adult; Amoxicillin; Anti-Ulcer Agents; Biomarkers; Biopsy; Body Mass Index; Case-Control Studies; Clarithromycin; Drug Therapy, Combination; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Middle Aged; Omeprazole; Reverse Transcriptase Polymerase Chain Reaction; Statistics, Nonparametric; Stomach Neoplasms

Topics: Body Mass Index; Female; Helicobacter Infections; Humans; Leptin; Male; Middle Aged; Obesity

Leptin, a protein product of obese gene expressed primarily by adipocytes, provides feedback information on the size of energy stores to central OB receptors controlling the food intake, energy expenditure and body weight homeostasis. It has recently been detected in the rat stomach, especially after cholecystokinin (CCK) administration and in human stomach infected with Helicobacter pylori, but its role in gastric secretory functions in humans has not been revealed. This study was designed to determine the involvement of leptin in the control of basal, CCK- and meal-induced gastric H+ secretion and plasma gastrin and CCK levels in humans before and after an eradication of H. pylori.. Two groups (A and B) of subjects were used; group A (n = 7), for comparison of the effects of CCK and leptin on basal gastric H+ and plasma hormone (leptin, gastrin and CCK) levels, and group B (n = 6), for studies on the involvement of leptin in gastric secretory and plasma hormonal responses to vagal stimulation and gastric peptone meal before and after H. pylori eradication.. In H. pylori-positive subjects, CCK (12-200 pmol kg(-1) h(-1)) given i.v. caused a dose-dependent increase of gastric H+ accompanied by a dose-dependent rise in plasma CCK and leptin levels. In contrast, leptin administered i.v. in graded doses (5-80 pmol kg(-1) h(-1)) resulted in a gradual inhibition of basal gastric H+ secretion and in adose-dependent increment in plasma leptin accompanied by an increase in plasma gastrin without alteration of plasma CCK level. Following eradication of H. pylori by 1-week triple therapy in group B patients, the infusion of CCK produced a significantly smaller increase in gastric H+ secretion and significantly smaller rise in plasma leptin as compared to those before the eradication. Cephalic phase stimulation of gastric secretion induced by modified sham-feeding in group B H. pylori-positive subjects increased gastric H+ secretion to about 40% of pentagastrin maximum without affecting plasma leptin, gastrin, or CCK level, while gastric peptone meal resulted in the increase in gastric H+ response reaching about 70% of pentagastrin maximum accompanied by a marked rise in plasma leptin, gastrin and CCK. The treatment with a standard dose of leptin (20 pmol kg(-1) h(-1)) failed to affect sham-feeding-induced gastric H+ secretion but reduced significantly the peptone meal-stimulated H+ secretion, while raising plasma gastrin in response to this meal. Plasma CCK under basal conditions and after sham-feeding was not affected, but plasma CCK response to gastric meal was significantly reduced by leptin infusion. Eradication of H. pylori did not affect basal or sham-feeding-induced H+ secretion but resulted in a significant fall in gastric meal-induced H+ and plasma leptin, gastrin and CCK levels.. 1) The gastric meal and CCK enhance the release of leptin in H. pylori-positive patients and this leptin is capable of inhibiting basal and meal-stimulated gastric H+ secretion, while raising plasma gastrin and reducing the plasma CCK levels, and 2) the eradication of H. pylori reduces the postprandial gastric H+ and plasmagastrin responses as well as the release of leptin in response to CCK and meal.

Topics: Adult; Cholecystokinin; Eating; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male

Leptin, a newly discovered weight-reducing hormone, is mainly produced in fat cells. Recently, this hormone has been reported to be produced in rat gastric mucosa cells. In the present study we analyzed the localization and expression of leptin and its receptors in normal human gastric mucosa and in patients with Helicobacter pylori-associated gastritis.. Plasma leptin levels and gastric mucosa leptin content were determined in 39 patients with dyspepsia. Cellular localization of leptin and of the signaling receptor (Ob-RL) were assessed by immunohistochemistry. Reverse transcriptase polymerase chain reaction (RT-PCR) for leptin receptor isoforms was performed on gastric epithelial cells isolated by laser-capture-microdissection.. Leptin content of the corpus gastric mucosa in H. pylori-positive patients was significantly increased (4.6+/-1.2. n = 15) as compared with the H. pylori-negative group (27.5+/-0.5 pg/mg, n = 24, P = 0.006). The presence of leptin immunoreactivity was shown in the lower half of corpus epithelial glands. By RT-PCR no leptin mRNA was detectable in human gastric tissue. In contrast, expression of both Ob-R(L) and the leptin receptor isoforms could be detected in gastric epithelial cells. Leptin receptor protein was detected throughout the mucosa.. Leptin itself is stored and secreted but not produced in human gastric mucosa. The functional receptor and all isoforms are present in human gastric mucosa. H. pylori-associated gastritis leads to significant increases in local leptin concentration in the gastric corpus.

Topics: Analysis of Variance; Biopsy; Carrier Proteins; Endoscopy, Gastrointestinal; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Leptin; Male; Middle Aged; Receptors, Cell Surface; Receptors, Leptin; Reverse Transcriptase Polymerase Chain Reaction; RNA