leptin and Dehydration

Evidence synthesizing the effects of acute body water losses on various markers of glycemic regulation, appetite, metabolism, and stress is lacking. Thus, the purpose of this review was to summarize the response of various hormonal changes involved in these physiologic functions to dehydration. A comprehensive literature search for peer-reviewed research in the databases PubMed, Scopus, CINAHL, and SportDiscus was conducted. Studies were included if they contained samples of adults (>18 years) and experimentally induced dehydration as measured by acute body mass loss. Twenty-one articles were eligible for inclusion. Findings suggested cortisol is significantly elevated with hypohydration (standard mean difference [SMD] = 1.12, 95% CI [0.583, 1.67],

Topics: Adolescent; Adult; alpha-Amylases; Appetite; Blood Glucose; Caloric Restriction; Dehydration; Female; Ghrelin; Humans; Hydrocortisone; Leptin; Male; Peptide YY; Stress, Physiological; Testosterone; Young Adult

Dehydration in rodents induces anorexia. In humans however, the role of dehydration in energy intake is controversial. This study investigated the effect of extreme fluid restriction on acute energy intake during and after exercise-induced dehydration. Eight physically active participants performed two exercise sessions to induce dehydration. After the exercise, the men were allowed to either rehydrate for 2 h or were maintained in a hypohydrated state, in a randomized manner. After 2 h, they were given cereal bars ad libitum for 1 h. Blood and saliva samples of the participants were collected before the exercise session, after the exercise session, after rehydration, and after the meal. Post-exercise energy intake differed between hypohydrated (1430 ± 210 kcal) and rehydrated (2190 ± 780 kcal) trials (

Topics: Adult; Biomarkers; Cross-Over Studies; Dehydration; Drinking; Eating; Energy Intake; Exercise; Ghrelin; Humans; Leptin; Male; Organism Hydration Status; Peptide YY; Salivation; Time Factors; Young Adult

It has now been established that exercise performed under various environmental conditions may affect acute energy intake and appetite-related hormones. The exact mechanism linking acute energy intake and exercise remains unknown, although indirect evidence suggests a possible role for hydration status. Therefore, the purpose of this study was to investigate the interaction of exercise and hydration status on subsequent energy intake and appetite-related hormones.. In a randomized, counterbalanced design, 10 physically active males completed three experimental trials in a fasted state: exercise when hydrated (0%-1% of body mass), exercise when dehydrated (-1% to -2% of body mass), and a hydrated resting control. Exercise consisted of treadmill running for 45 min at 70% VO2peak. Participants were then given access to a buffet-style breakfast from which they could consume ad libitum. Blood was sampled regularly during trials for appetite-related hormones.. There were no significant differences in total energy intake between trials (P = 0.491); however, relative energy intake was significantly higher in the control (4839 ± 415 kJ, P < 0.001) compared to hydrated (1749 ± 403 kJ) and dehydrated exercise (1656 ± 413 kJ) conditions. Exercise performed in a dehydrated state resulted in significantly lower concentrations of ghrelin compared with control (P = 0.045) and hydrated exercise conditions (P = 0.014).. Exercise significantly decreased relative energy intake compared with resting control; however, energy intake (relative and total) was no different between the exercise conditions (dehydrated vs hydrated). Despite similar energy intake between trials, exercise in a dehydrated state resulted in a significantly lower concentration of ghrelin, a hormone responsible for stimulating appetite.

Topics: Analysis of Variance; Appetite; Blood Glucose; Dehydration; Energy Intake; Exercise; Fasting; Ghrelin; Humans; Insulin; Leptin; Male; Pancreatic Polypeptide; Peptide YY; Surveys and Questionnaires; Young Adult

Physiological systems responsible for water homeostasis and energy metabolism are interconnected. This study hypothesized altered responses to dehydration including thirst, ad libitum water intake, and copeptin in men with obesity.. Forty-two men (22 lean and 20 with obesity) were stimulated by a 2-hour hypertonic saline infusion and a 24-hour water deprivation. In each dehydrating condition, thirst, ad libitum water intake after dehydration, and urinary and hormonal responses including copeptin were assessed.. After each dehydration condition, ad libitum water intake was similar between both groups (p > 0.05); however, those with obesity reported feeling less thirsty (p < 0.05) and had decreased copeptin response and higher urinary sodium concentrations when stressed (p < 0.05). Angiotensin II, aldosterone, atrial and brain natriuretic peptides, and apelin concentrations did not differ by adiposity group and did not explain the different thirst or copeptin responses in men with obesity. However, leptin was associated with copeptin response in lean individuals during the hypertonic saline infusion (p < 0.05), but the relationship was diminished in those with obesity.. Diminished thirst and copeptin responses are part of the obesity phenotype and may be influenced by leptin. Adiposity may impact pathways regulating thirst and vasopressin release, warranting further investigation.

Topics: Body Weight; Dehydration; Drinking; Glycopeptides; Humans; Leptin; Male; Obesity; Saline Solution, Hypertonic; Thirst

The lateral hypothalamic area (LHA) is essential for ingestive behavior but it remains unclear how LHA neurons coordinate feeding vs. drinking. Most LHA populations promote food and water consumption but LHA neurotensin (Nts) neurons preferentially induce water intake while suppressing feeding. We identified two molecularly and projection-specified subpopulations of LHA Nts neurons that are positioned to coordinate either feeding or drinking. One subpopulation co-expresses the long form of the leptin receptor (LepRb) and is activated by the anorectic hormone leptin (Nts

Topics: Animal Feed; Animals; Brain; Colchicine; Dehydration; Feeding Behavior; Female; Genotype; Green Fluorescent Proteins; Hypothalamic Area, Lateral; Leptin; Male; Mesencephalon; Mice; Mice, Inbred C57BL; Neurons; Neurotensin; Neurotransmitter Agents; Water

The involvement of plasma leptin in the adaptation of dromedary camels to harsh conditions such as food or water shortages was studied through 2 experiments. In experiment 1, fourteen female camels were either fed at 68% of maintenance energy requirements (MER) during 112d (n=4) or overfed at 134% of MER during the first 56d and then underfed at 17% of MER the next 56d (OV-UN, n=5), or underfed and then overfed for the same durations and energy intake levels (UN-OV, n=5). Weekly plasma samples showed that leptin, glucose and non-esterified fatty acid (NEFA) concentrations were significantly modulated by energy intake level. NEFA increased sharply but transiently in underfed camels of the UN-OV or OV-UN groups, whereas glucose and leptin concentrations decreased with underfeeding and increased with overfeeding with more significant effects in camels that were previously overfed or underfed, respectively. In experiment 2 twelve female camels were either normally watered (n=6) or dehydrated (n=6) during 23d and then rehydrated during 4d. Dehydration specifically increased blood hematocrit, plasma NEFA and glucose whereas leptin decreased slightly. For both experiments, leptinemia was positively related to hump adipocyte volume. Taken together these results provide new data for a better understanding of lipid and energy metabolism in camels.

Topics: Adipocytes; Animals; Blood Glucose; Blood Proteins; Body Weight; Camelus; Cell Size; Dehydration; Fatty Acids, Nonesterified; Female; Food Deprivation; Hematocrit; Leptin

Food-restricted animals present metabolic adaptations that facilitate food-seeking behavior and decelerate energy utilization by reducing the hypothalamus-pituitary-thyroid (HPT) axis function. Stress by dehydration induces an anorexic behavior in rats, loss of weight and reduced food intake when compared to ad libitum fed animals, however these alterations are accompanied by HPT axis changes such as increased serum thyrotropin levels and enhanced expression of thyrotropin-releasing hormone (TRH) in the paraventricular nucleus of the hypothalamus, which is considered as anorexigenic peptide. In contrast, a pair-fed group conformed by forced-food-restricted animals (FFR) (eating the exact same amount of food as dehydration-induced anorexic rats--DIA rats) present decreased TRH mRNA levels. NPY synthesis in the arcuate nucleus and orexin-expressing neurons from the lateral hypothalamic area (LHA) are activated during food restriction. These brain structures project into PVN, suggesting that NPY and orexins are possible factors involved in TRHergic neuron activation in DIA rats. Leptin signaling is another likely factor to be involved in TRH differential expression. Therefore, to gain more insight into the regulation of the feeding behavior in the experimental models, we analyzed Y1, Y5, Ox1-R and Ob-R(b) mRNA levels in PVN and prepro-orexin in LHA, since their signaling to the PVN might be altering TRH synthesis and feeding in DIA animals. Prepro-orexinergic cells were activated in FFR animals; Ox1-R and Y1 expression was reduced in FFR vs. controls or DIA group. Compensatory changes in PVN receptor expression of some feeding-related peptides in anorexic rats may alter TRHergic neural response to energy demands.

Topics: Animals; Anorexia; Dehydration; Feeding Behavior; Gene Expression Regulation; Hypothalamo-Hypophyseal System; Intracellular Signaling Peptides and Proteins; Leptin; Male; Malnutrition; Neurons; Neuropeptide Y; Neuropeptides; Orexin Receptors; Orexins; Paraventricular Hypothalamic Nucleus; Pituitary-Adrenal System; Rats; Rats, Wistar; Receptors, G-Protein-Coupled; Receptors, Neuropeptide; Receptors, Neuropeptide Y; Signal Transduction; Thyrotropin; Thyrotropin-Releasing Hormone

Topics: Animals; Carotid Artery, External; Corticosterone; Dehydration; Disease Models, Animal; Disease Progression; Hypothalamus; Infarction, Middle Cerebral Artery; Ischemia; Leptin; Osmolar Concentration; Pharyngeal Muscles; Postoperative Complications; Rats; Reproducibility of Results; Thyrotropin; Tongue; Weight Loss

The present study was designed to compare the effect of leptin on acute colonic inflammation with that of acute stress exposure, which acts via the hypothalamic-pituitary-adrenal (HPA) axis. Sprague-Dawley rats of both sexes were administered intrarectally with acetic acid. Either leptin (10 microg/kg; i.p.) or saline was injected immediately before and 6 h after the induction of colitis. A group of rats was exposed to water avoidance stress (WAS) for 30 min at the 6th h of colitis induction. RU-486 (2 mg/kg; i.p.), a glucocorticoid receptor antagonist, was injected intraperitoneally, at 12 and 1 h before the initial leptin injection, and at 1 h before the second leptin injection or exposure to WAS. Rats were decapitated at 24 h and the distal 8 cm of the colon were removed for macroscopic and microscopic scoring, determination of tissue wet weight index (WI) and tissue myeloperoxidase activity (MPO). Acetic acid-induced colitis significantly increased macroscopic and microscopic damage scores, WI and MPO, compared to control group. Exposure to acute WAS or treatment with leptin reduced the elevations in damage scores, WI and MPO induced by colitis, but no additive inhibitory effect was observed when WAS and leptin were applied together. RU-486 treatment reversed the inhibitory effects of leptin or WAS on colonic inflammation. Our results demonstrate that exogenous leptin mimics the effects of HPA axis activation on colitis-induced inflammatory process. The results also suggest that the anti-inflammatory effect of leptin involves a tissue neutrophil-dependent mechanism and is dependent on the release of glucocorticoids.

Topics: Acetic Acid; Animals; Anti-Inflammatory Agents; Colitis; Colon; Dehydration; Female; Glucocorticoids; Inflammation; Leptin; Male; Peroxidase; Rats; Rats, Sprague-Dawley

We have investigated the hormonal and hypothalamic neuropeptidergic substrates of dehydration-associated anorexia. In situ hybridization and hormone analyses of anorexic and paired food-restricted rats revealed two distinct profiles. First, both groups had the characteristic gene expression and endocrine signatures usually associated with starvation: increased neuropeptide Y and decreased proopiomelanocortin and neurotensin mRNAs in the arcuate nucleus (ARH); increased circulating glucocorticoid but reduced leptin and insulin. Dehydrated animals are strongly anorexic despite these attributes, showing that the output of leptin- and insulin-sensitive ARH neurons that ordinarily stimulate eating must be inhibited. The second pattern occurred only in anorexic animals and had two components: (1) reduced corticotropin-releasing hormone (CRH) mRNA in the neuroendocrine paraventricular nucleus (PVH) and (2) increased CRH and neurotensin mRNAs in the lateral hypothalamic (LHA) and retrochiasmatic areas. However, neither corticosterone nor suppressed PVH CRH gene expression is required for anorexia after dehydration because PVH CRH mRNA in dehydrated adrenalectomized animals is unchanged from euhydrated adrenalectomized controls. We also showed that LHA CRH mRNA was strongly correlated with the intensity of anorexia, increased LHA CRH gene expression preceded the onset of anorexia, and dehydrated adrenalectomized animals (which also develop anorexia) had elevated LHA CRH gene expression with a distribution pattern similar to intact animals. Finally, we identified specific efferents from the CRH-containing region of the LHA to the PVH, thereby providing a neuroanatomical framework for the integration by the PVH of neuropeptidergic signals from the ARH and the LHA. Together, these observations suggest that CRH and neurotensin neurons in the LHA constitute a novel anatomical substrate for their well known anorexic effects.

Topics: Adrenalectomy; Adrenocorticotropic Hormone; Animals; Anorexia; Arcuate Nucleus of Hypothalamus; Axonal Transport; Body Weight; Corticosterone; Corticotropin-Releasing Hormone; Dehydration; Food Deprivation; Gene Expression Regulation; Hypothalamic Area, Lateral; Insulin; Leptin; Male; Neuropeptide Y; Neuropeptides; Neurotensin; Paraventricular Hypothalamic Nucleus; Phytohemagglutinins; Pro-Opiomelanocortin; Proteins; Rats; Rats, Sprague-Dawley; RNA, Messenger; Thymus Gland; Time Factors; Transcription, Genetic