UMLS:C0020175 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Target Concepts:

Query: UMLS:C0020175 (hunger)
5,670 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leptin is a hormone involved in body weight and hunger regulation, and may contribute to the inverse relationship between cigarette smoking and body weight. Leptin levels, body mass indices (BMIs), and hunger ratings were determined in 22 nonsmokers (12 male, 10 female) and 19 cigarette smokers (11 male, 8 female). Smokers were tested after ad lib smoking and following a 24-h smoking abstinence period; nonsmokers came to the laboratory once. Leptin levels were not different among the groups. Hunger ratings, however, were higher after smoking abstinence compared to after ad lib smoking and nonsmokers (Ps<.05); levels of hunger did not differ between ad lib smokers and nonsmokers. Men reported higher hunger levels than did women, but women had higher serum leptin levels than did men, regardless of smoking condition (P<.05). Leptin levels were correlated with BMI (P<.05) among smokers only. This first study on leptin responses in female smokers suggests that leptin levels do not change following a 24-h smoking abstinence period and that leptin may not contribute to increased hunger following smoking abstinence.
...
PMID:Leptin, hunger, and body weight: Influence of gender, tobacco smoking, and smoking abstinence. 1521 36

The peripheral physiological and central nervous mechanisms contributing to the control of eating present formidable challenges to experimental analysis. One of the most productive approaches to these challenges has been endocrinological. This review introduces the endocrine control of eating by considering three hormonal signals that have been hypothesized to control hunger or satiation, cholecystokinin CCK, leptin, and ghrelin. The roles of these molecules in humans and in rodents are considered against a set of criteria established in classical endocrinology for establishing physiological endocrine action. It is concluded that according to these criteria, CCK's satiating action in humans is the best-established physiological endocrine action. In contrast, support for endocrine actions of leptin in satiation and of ghrelin in hunger is incomplete, and areas urgently requiring further research are identified. Finally, a review of work on these three hormones suggests the utility of a new conceptual scheme for understanding the endocrine control of eating. This scheme distinguishes between endocrine, in which the stimuli for hormonal secretion and the effect of secretion on eating are tightly coupled, and endocrine effects, in which one or both of these links is uncoupled. The implications of this concept for research design and interpretation of data are discussed. A vast literature links endocrine systems to the control of eating behavior [Geary, N. Hunger and satiation. In: Martini, L., ed. Encyclopedia of endocrine diseases. San Diego, CA: Academic Press, 2004, in press.]. This is fortunate for ingestive science. Endocrinology is a well-developed discipline with an impressive armamentarium of intellectual and technical tools. In contrast, ingestive science, i.e., the study of eating, drinking, and drug use, is at a more rudimentary stage of development. My general thesis here is that the adaptation and application of some of the well-accepted intellectual tools of endocrinology is likely to accelerate progress in ingestive science. The organization of the review is threefold. First, the treatment of endocrine controls of eating is selective. Just three hormones, CCK, leptin, and ghrelin, are considered. It is not clear that these are the three most important endocrine controls of eating, but they are each certainly interesting candidates, and comparisons among them are instructive. Second, I argue for the utility of the application of classical endocrine criteria for the identification of physiological effects of hormones, as adapted to eating behavior. This is done by introducing these criteria, considering each hormone's status with respect to them, and identifying the areas where relevant evidence is currently available or is lacking. Third, I argue for the utility of making explicit the distinction between endocrine actions, in which the stimuli for hormonal secretion and the effect of secretion on eating are tightly coupled, and endocrine actions, in which these links are uncoupled. This concept is assembled inductively in the course of the review.
...
PMID:Endocrine controls of eating: CCK, leptin, and ghrelin. 1523 77

To examine leptin's role in human appetite regulation, we studied recombinant methionyl human leptin's effects on satiation and satiety in a model of leptin insufficiency, lipodystrophy. Eight females with hypoleptinemia and lipodystrophy were given sc injections of A-100 (maximal dose, 200% of that predicted to normalize serum leptin) for 4 months. Satiation and satiety were determined before and again during leptin treatment. Satiation was measured as the time to voluntary cessation of eating from a standardized food array after a 12-h fast. Satiety was determined as the time to hunger sufficient to consume a full meal after consumption of a standardized preload. During leptin treatment, satiation time decreased (41.2 +/- 18.2 to 19.5 +/- 10.6 min; P = 0.01), satiety time increased (62.9 +/- 64.8 to 137.8 +/- 91.6 min; P = 0.04), energy consumed to produce satiation decreased (2034 +/- 405 to 1135 +/- 432 kcal or 8.5 +/- 1.7 to 4.7 +/- 1.8 MJ; P < 0.01), and the amount of food desired in the postabsorptive state decreased (P < 0.02). Ghrelin concentrations also decreased during leptin administration (284.3 +/- 127.9 to 140.6 +/- 104.5 pmol/liter; P < 0.002). We conclude that increased leptin in patients with lipodystrophy results in less caloric, shorter, more satiating meals and longer-lived satiety. These data support the hypothesis that leptin plays an important, permissive role in human appetite regulation.
...
PMID:Effects of exogenous leptin on satiety and satiation in patients with lipodystrophy and leptin insufficiency. 1535 17

Ghrelin, a gut-brain peptide that signals hunger, is normally suppressed after meals. Subnormal suppression of postprandial ghrelin, previously noted in obese, insulin-resistant individuals, may contribute to increased food intake. Given the ethnic disparities in obesity and obesity-related cardiovascular morbidity in the United States, the present study compared a single postprandial ghrelin measure in 43 women (22 white, 21 black). Each completed a rigorously controlled 4-d dietary intervention designed to maintain weight and constant daily sodium and potassium intake (220 mEq Na, 40 mEq K). Two hours after consuming a test meal of identical content, blood samples were drawn to assess postprandial ghrelin, leptin, and norepinephrine; resting cardiovascular function was measured; and a 24-h urinary cortisol sample was obtained. Independent of body mass index, postprandial ghrelin was significantly higher in black vs. white women, and higher ghrelin was associated with higher cortisol in blacks, who failed to show the expected inverse relation between ghrelin and central obesity seen in whites. Higher ghrelin was correlated with higher blood pressure but lower norepinephrine in obese women. These findings suggest subnormal postprandial ghrelin suppression (or faster ghrelin rebound) in black women, especially the obese, that might play a role in their increased prevalence of obesity and cardiovascular disorders.
...
PMID:Postprandial ghrelin is elevated in black compared with white women. 1535 47

The worldwide increase in the incidence of obesity is a consequence of a positive energy balance, with energy intake exceeding expenditure. The signalling systems that underlie appetite control are complex, and the present review highlights our current understanding of key components of these systems. The pattern of eating in obesity ranges from over-eating associated with binge-eating disorder to the absence of binge-eating. The present review also examines evidence of defects in signalling that differentiate these sub-types. The signalling network underlying hunger, satiety and metabolic status includes the hormonal signals leptin and insulin from energy stores, and cholecystokinin, glucagon-like peptide-1, ghrelin and peptide YY3-36 from the gastrointestinal tract, as well as neuronal influences via the vagus nerve from the digestive tract. This information is routed to specific nuclei of the hypothalamus and brain stem, such as the arcuate nucleus and the solitary tract nucleus respectively, which in turn activate distinct neuronal networks. Of the numerous neuropeptides in the brain, neuropeptide Y, agouti gene-related peptide and orexin stimulate appetite, while melanocortins and alpha-melanocortin-stimulating hormone are involved in satiety. Of the many gastrointestinal peptides, ghrelin is the only appetite-stimulating hormone, whereas cholecystokinin, glucagon-like peptide-1 and peptide YY3-36 promote satiety. Adipose tissue provides signals about energy storage levels to the brain through leptin, adiponectin and resistin. Binge-eating has been related to a dysfunction in the ghrelin signalling system. Moreover, changes in gastric capacity are observed, and as gastric capacity is increased, so satiety signals arising from gastric and post-gastric cues are reduced. Understanding the host of neuropeptides and peptide hormones through which hunger and satiety operate should lead to novel therapeutic approaches for obesity; potential therapeutic strategies are highlighted.
...
PMID:Peripheral and central signals in the control of eating in normal, obese and binge-eating human subjects. 1538 23

A unique subset of individuals termed metabolically obese but normal weight (MONW) has been identified. These young women are potentially at increased risk for development of the metabolic syndrome despite their young age and normal body mass index. We seek to determine metabolic and behavioral factors that could potentially distinguish MONW women from young women with a normal metabolic profile.Ninety-six women were classified as MONW (n = 12) or non-MONW (n = 84) based on a cut point of insulin sensitivity (as estimated by the homeostasis model assessment). Potentially distinguishing phenotypes between groups measured included serum lipids, ghrelin, leptin, adiponectin, body composition and body fat distribution, resting and physical activity energy expenditure, peak oxygen uptake, dietary intake, dietary behavior, and family history and lifestyle variables. Despite a similar body mass index between groups, MONW women showed higher percent body fat, lower fat-free mass, lower physical activity energy expenditure, and lower peak oxygen uptake than non-MONW women. Plasma cholesterol level was higher in MONW women, whereas no differences were noted for other blood lipids, ghrelin, leptin, adiponectin, and resting energy expenditure. MONW women had lower dietary restraint scores than non-MONW women, but no differences were noted in disinhibition, hunger, and dietary intake. Stepwise regression analysis performed on all subjects showed that 33.5% of the unique variance of the homeostasis model assessment was explained with the variables of percentage of body fat (17.1%), level of dietary restraint (10.4%), and age (6%). Both metabolic and dietary behavioral variables contribute to the deleterious metabolic profile of MONW women. They display lower insulin sensitivity due potentially to a cluster of sedentary behavior patterns that contribute to their higher adiposity. Furthermore, cognitive attitudes toward food (i.e. dietary restraint) and concomitant lifestyle behaviors may play a role in regulating insulin sensitivity in MONW women.
...
PMID:Metabolic and behavioral characteristics of metabolically obese but normal-weight women. 1547 99

This study aimed to verify the serum leptin concentration during the terrestrial phase of the Southern elephant seal (Mirounga leonina) on Elephant Island (South Shetlands, Antarctica). Sera from 25 adult Southern elephant seals were analyzed. Leptin concentration was determined using the 125I radioimmunoassay method. Total protein, triglycerides, and cholesterol concentration were measured by spectrophotometric methods. Seals were grouped by sex and their physiological status (reproducing or molting seals). In reproducing seals, serum concentrations of leptin, total protein, triglycerides, and cholesterol were, respectively, 9.33+/-1.97 ng/ml, 6.87+/-0.09 g/dl, 98.26+/-2.12 mg/dl, and 232.17+/-41.18 mg/dl in males and 5.30+/-1.36 ng/ml, 6.44+/-0.29 g/dl, 109.01+/-3.34 mg/dl, and 219.20+/-26.65 in females (mean+/-1 SD). In molting seals, these values were 2.35+/-1.51 ng/ml, 7.42+/-0.25 mg/dl, 321.10+/-20.01 mg/dl, and 244.66+/-22.24 mg/dl in males and 2.94+/-1.89 ng/ml, 7.88+/-0.46 mg/dl, 197.54 mg/dl, and 224.55+/-16.70 mg/dl in females. In both males and females, there were no significant differences (P>0.05) in total protein and cholesterol concentration between reproducing and molting seals. However, both males and females showed higher leptin concentration (P<0.05) and lower triglyceride concentration (P<0.05) in the reproductive period than in the molt period. In the reproductive period, it was expected that the Southern elephant seal shows an inhibited hunger sensation, mobilizes stored energy, and stimulates the HPG axis. Results from the present study support this hypothesis and suggest that this strategy may be effected by the hormonal stimulation of leptin.
...
PMID:Serum leptin concentration during the terrestrial phase of the Southern elephant seal Mirounga leonina (Carnivora: Phocidae). 1550 91

Leptin is a nutritionally regulated hormone that may modulate neuroendocrine function during caloric deficit. We hypothesized that administration of low-dose leptin would prevent changes in neuroendocrine function resulting from short-term caloric restriction. We administered physiologic doses of r-metHuLeptin [(0.05 mg/kg sc daily or identical placebo in divided doses (0800, 1400, 2000, and 0200 h)] to 17 healthy, normal-weight, reproductive-aged women during a 4-d fast. Leptin levels were lower in the placebo-treated group during fasting (3.3 +/- 0.2 vs. 9.6 +/- 1.0 ng/ml, P < 0.001, placebo vs. leptin-treated at end of study). Fat mass decreased more in the leptin than the placebo-treated group (-0.6 +/- 0.1 vs. -0.2 +/- 0.1 kg, P = 0.03). Both overnight LH area (38.9 +/- 21.5 vs. 1.2 +/- 11.1 microIU/ml.min, P = 0.05) and LH peak width increased (15.8 +/- 7.1 vs. -2.3 +/- 6.7 min, P = 0.06) and LH pulsatility decreased (-2.0 +/- 0.9 vs. 1.0 +/- 0.8 peaks/12 h, P = 0.03) more in the leptin vs. placebo group. LH pulse regularity was higher in the leptin-treated group (P = 0.02). Twenty-four-hour mean TSH decreased more in the placebo than the leptin-treated group, respectively (-1.06 +/- 0.27 vs. -0.32 +/- 0.18 microIU/ml, P = 0.03). No differences in 24-h mean GH, cortisol, IGF binding protein-1, and IGF-I were observed between the groups. Hunger was inversely related to leptin levels in the subjects randomized to leptin (r = -0.76, P = 0.03) but not placebo (r = -0.18, P = 0.70) at the end of the study. Diminished hunger was seen among subjects achieving the highest leptin levels. Our data provide new evidence of the important role of physiologic leptin regulation in the neuroendocrine response to acute caloric deprivation.
...
PMID:Endocrine and metabolic effects of physiologic r-metHuLeptin administration during acute caloric deprivation in normal-weight women. 1553 89

Obesity is strongly associated with hypertension and cardiovascular disease. Several central and peripheral abnormalities that can explain the development or maintenance of high arterial pressure in obesity have been identified. These include activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Obesity is also associated with endothelial dysfunction and renal functional abnormalities that may play a role in the development of hypertension. The continuing discovery of mechanisms regulating appetite and metabolism is likely to lead to new therapies for obesity-induced hypertension. Better understanding of leptin signaling in the hypothalamus and the mechanisms of leptin resistance should facilitate therapeutic approaches to reverse the phenomenon of selective leptin resistance. Other hunger and satiety signals such as ghrelin and peptide YY are potentially attractive therapeutic strategies for treatment of obesity and its complications. These recent discoveries should lead to novel strategies for treatment of obesity and hypertension.
...
PMID:Obesity-associated hypertension: new insights into mechanisms. 1558 75

Ghrelin is a peptidic hormone composed of 28 aminoacid residues. It is produced by enteroendocrine cells of stomach and intestine. It is also produced in pancreas, kidney, placental tissue, thyroid gland, hypothalamus, and hypophysis. Gastrectomy leads to 65-80% decrease of plasma levels of ghrelin. In human organism, ghrelin stimulates secretion of growth hormone, prolactin, and ACTH. Ghrelin also has orexigenic activity (increases food intake), influences the sleep/wake cycle, gastric motility and secretion, cardiovascular functions, regulates endocrine function of pancreas and metabolism of glucose and shows an antiproliferative effect. Ghrelin is an important regulatory part of the homeostasis of the organism, and iterconnects neuroendocrine and metabolic response of the organism to starvation, and it is considered as a counterpart to leptin. Ghrelin was discovered by Japanese scientists in 1999 as a natural ligand of an "orphan" receptor GHS1a, which is specific for a group of synthetic peptides (growth hormone secretagogues--GHS) stimulating secretion of growth hormone. Plasma levels of ghrelin reflect short-time changes of food intake, as well as long-time changes of the nutritional state of the organism. Plasma levels of ghrelin are decreased after food intake and in obese humans, and they are increased during starvation and in patients with mental anorexia. Plasma levels of ghrelin in humans correlate negatively with body mass index, amount of body fat, size of adipocytes, and plasma levels of insulin, glucose, and leptin. Thus, ghrelin probably plays a role as a metabolic signal of hunger.
...
PMID:[Ghrelin--structure, function and clinical applications]. 1570 43

<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>