leptin and Hepatitis--Viral--Human

Adipokines are polypeptides secreted in the adipose tissue in a regulated manner. While some of these molecules are expressed only by adipocytes, resident and infiltrating macrophages and components of the vascular stroma markedly contribute to expression of other adipokines. As a result, adipose tissue inflammation is associated with a modification in the pattern of adipokine secretion. Leptin, adiponectin, and resistin are the best-studied molecules in this class, but cytokines such as tumor necrosis factor or interleukin-6 are also secreted at high levels by the adipose tissue. Several other molecules have been recently identified and are actively investigated. Adipokines interfere with hepatic injury associated with fatty infiltration, differentially modulating steatosis, inflammation, and fibrosis. Several studies have investigated plasma levels of adiponectin in patients with nonalcoholic fatty liver disease, to establish correlations with the underlying state of insulin resistance and with the type and severity of hepatic damage. Hepatitis C is another disease where adipokines may represent a link between viral infection, steatosis, and metabolic disturbances. Identification of the mediators secreted by expanded adipose tissue and their pathogenic role is pivotal in consideration of the alarming increase in the prevalence of obesity and of the detrimental role that this condition exerts on the course of liver diseases.

Topics: Adipocytes; Adipokines; Adiponectin; Adipose Tissue; Apelin; Fatty Liver; Hepatic Stellate Cells; Hepatitis, Viral, Human; Humans; Intercellular Signaling Peptides and Proteins; Leptin; Liver; Liver Cirrhosis; Liver Diseases; Nicotinamide Phosphoribosyltransferase; Obesity; Resistin; Retinol-Binding Proteins, Plasma; Tumor Necrosis Factor-alpha

Recent reports suggest that adipokines are potent modulators of inflammation. We tested the hypothesis that the decreased food intake and the acute liver disease might be associated with changes of serum ghrelin, adipokines and insulin levels.. Fasting ghrelin, adiponectin, leptin, resistin and insulin were measured in 25 children suffering from acute viral hepatitis, caused by either hepatitis A or Epstein-Barr viruses. The age of the patients ranged from 2.2 to 17.2 years (mean: 10.4 years); 10 male and 15 female. Samples for hormones and liver function tests were drawn at 08 : 00 to 09 : 00 h after an overnight fast. The first samples were collected in the morning after the day of admission, the second samples after 2 months of recovery.. Ghrelin and adiponectin levels were significantly higher during hepatitis than after recovery (831.4+/-276.44 vs. 736.21+/-274.91 pg/ml, P<0.0001; and 22.91+/-12.93 vs. 15.16+/-8.81 microg/ml, P<0.001, respectively). Adiponectin levels correlated significantly with age-specific and sex-specific body mass index-matched percentile values as well (P=0.0062). Linear regression analysis confirmed that there was a significant association of changes in serum ghrelin and resistin levels and the severity of hepatitis (P=0.005; P<0.05). We could verify a marginal relationship of the changes of serum leptin and the severity of the disease (P=0.0646).. This study confirms that there are significant changes in serum levels of ghrelin, and adipokines in disease-associated malnutrition and acute hepatitis.

Topics: Acute Disease; Adipokines; Adolescent; Child; Child, Preschool; Epstein-Barr Virus Infections; Fasting; Female; Ghrelin; Hepatitis A; Hepatitis, Viral, Human; Humans; Leptin; Male; Resistin

The aim of the present study was to investigate serum leptin levels in relation to anthropometric features in patients with liver cirrhosis (LC) and chronic viral hepatitis (CVH), and to determine the effect of the severity and aetiology of the LC on serum leptin levels.. Forty-nine patients with LC, 32 patients with CVH and 69 control subjects were age, body mass index (BMI) and sex-matched and included in the study. Plasma glucose, serum leptin and insulin levels were determined. Insulin resistance was assessed using homoeostasis model assessment (HOMA). Body composition was estimated by skinfold thickness.. Female patients with Child-A LC had higher levels of leptin, and female and male patients with Child-A LC had higher absolute leptin (leptin/BFM) levels compared to patients with Child-C LC and control subjects. Serum leptin levels of the patients with alcohol LC were higher than the control subjects, but the absolute leptin levels were comparable. When alcoholic and post-viral hepatitis cirrhotic patients were compared with each other on an aetiologic basis, there was no significant difference between them in leptin and absolute leptin levels. There were significant correlations between leptin and BMI, body fat percentage (BFP), BFM (body fat mass) in all three groups in both sexes.. These data suggest that the physiologic correlations among serum leptin level, sex, BMI and BFM were well preserved in patients with chronic liver disease. Patients with alcohol LC had higher leptin levels. In early stages of liver disease, leptin levels and absolute leptin levels are higher than in normal subjects. However, in advanced stages of the disease the significant decline in leptin levels and similar levels of leptin expressed in relation to BFM compared to control subjects predominantly represent the expression of fat mass.

Topics: Adult; Aged; Anthropometry; Blood Glucose; Body Mass Index; Female; Hepatitis, Chronic; Hepatitis, Viral, Human; Humans; Hypoglycemic Agents; Insulin; Leptin; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Risk Factors; Severity of Illness Index

The presence of steatosis is a common histological finding in patients with chronic hepatitis C (CHC). The causes of the severity of this condition are not yet clear, although both metabolic and viral factors supposedly are involved. In this study our aim was to examine the possible influence that leptin levels, hepatitis C virus (HCV) RNA levels, and hepatitis G virus (HGV) infection have on the severity of steatosis and on the presence and degree of fibrosis in patients with CHC.. One hundred eighty-two CHC patients with histological findings of steatosis were chosen from among a cohort of patients referred to our center for staging of liver disease. Among them 48 CHC patients were accurately selected so as to rule out possible confounding factors for the presence of steatosis (diabetes mellitus, hyperlipemia, obesity, alcohol). Leptin levels, HCV RNA levels, and HCV genotype, and the presence of HGV RNA were assessed in these patients and related to histological findings.. We found that leptin levels in CHC patients were similar to those in healthy subjects. No relationship was found between leptin levels and severity of steatosis. HCV RNA levels, HCV genotype, and the presence of HGV infection were no different among CHC patients with various degrees of steatosis. Leptin was not related to different degrees of fibrosis, whereas higher viral load was the only parameter associated to higher fibrosis scores.. These findings suggest that the degree of steatosis in patients with CHC does not seem to depend on serum leptin levels or on viral factors, at least as far as HCV viremia and genotype and HGV infection are concerned. The severity of fibrosis does not seem to be influenced by leptin levels, whereas HCV viral load does seem to play some role.

Topics: Adult; Case-Control Studies; Fatty Liver; Female; Flaviviridae; Hepacivirus; Hepatitis C, Chronic; Hepatitis, Viral, Human; Humans; Leptin; Liver; Liver Cirrhosis; Male; Middle Aged; RNA, Viral; Severity of Illness Index; Viral Load

Leptin is a peptide hormone that mainly regulates food intake and energy expenditure of human body. A close correlation between serum leptin levels and the percentage of body fat stores is well known. Nonalcoholic steatohepatitis (NASH) is a common disorder which causes serum liver enzyme elevation. In this study, the serum leptin levels were investigated in patients with NASH to determine a possible role in the pathogenesis and in patients with chronic viral hepatitis to ascertain the effect of hepatic inflammation on serum leptin level.. Forty-nine patients (38 men, 11 women) with NASH diagnosed by biopsy, 32 patients with biopsy-proven chronic viral hepatitis (21 men and 11 women), and 30 healthy adults (17 men, 13 women) enrolled in the study. Fasting blood samples were obtained, and serum leptin levels were measured by ELISA. Body mass index (BMI) was calculated for all subjects, and serum insulin, C-peptide, and lipoprotein levels were also detected.. The mean serum leptin levels (+/-SEM) were 6.62 +/- 0.71, 4.24 +/- 1.0, and 4.02 +/- 0.46 ng/ml in NASH, chronic hepatitis, and the control group, respectively. Mean serum leptin level in the NASH group was significantly higher than those in the other groups tested. BMI was also slightly higher in the NASH group when compared to the other groups (26.7 +/- 0.3, 23.7 +/- 0.6, and 24.6 +/- 0.3, respectively). There was a significant correlation between BMI and serum leptin levels when all the subjects were evaluated together (NASH, hepatitis, and control groups, r = 0.337, p = 0.012) but not in the NASH group when evaluated alone (r = 0.238, p = 0.1). Of the predisposing factors for NASH, obesity was observed in 24% of patients and hyperlipidemia in 67%. Serum cholesterol and triglyceride levels were significantly higher in the NASH group than those in controls (p < 0.05). It has been detected that most of these patients consumed high amounts of fat in their dietary habits.. The serum leptin levels were significantly higher in patients with NASH, while they were not affected by chronic hepatitis. This elevation is out of proportion to BMI of these patients and may be related to hyperlipidemia in most. Elevated serum leptin levels, therefore, may promote hepatic steatosis and steatohepatitis.

Topics: Adult; Body Composition; Body Mass Index; Case-Control Studies; Causality; Dietary Fats; Enzyme-Linked Immunosorbent Assay; Fatty Liver; Female; Hepatitis, Viral, Human; Humans; Hyperlipidemias; Leptin; Male; Obesity