Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020175 (hunger)
 5,670 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Resistance (muscle strengthening) exercise is a key component of exercise recommendations for weight control, yet very little is known about the effects of resistance exercise on appetite. We investigated the effects of resistance and aerobic exercise on hunger and circulating levels of the gut hormones acylated ghrelin and peptide YY (PYY). Eleven healthy male students: age 21.1 +/- 0.3 yr, body mass index 23.1 +/- 0.4 kg/m(2), maximum oxygen uptake 62.1 +/- 1.8 ml.kg(-1).min(-1) (means +/- SE) undertook three, 8-h trials, 1) resistance exercise: a 90-min free weight lifting session followed by a 6.5-h rest period, 2) aerobic exercise: a 60-min run followed by a 7-h rest period, 3) control: an 8-h rest, in a randomized crossover design. Meals were provided 2 and 5 h into each trial. Hunger ratings and plasma concentrations of acylated ghrelin and PYY were measured throughout. Two-way ANOVA revealed significant (P < 0.05) interaction effects for hunger, acylated ghrelin, and PYY, indicating suppressed hunger and acylated ghrelin during aerobic and resistance exercise and increased PYY during aerobic exercise. A significant trial effect was observed for PYY, indicating higher concentrations on the aerobic exercise trial than the other trials (8 h area under the curve: control 1,411 +/- 110, resistance 1,381 +/- 97, aerobic 1,750 +/- 170 pg/ml 8 h). These findings suggest ghrelin and PYY may regulate appetite during and after exercise, but further research is required to establish whether exercise-induced changes in ghrelin and PYY influence subsequent food intake.
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PMID:Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males. 1898 87

In this issue of Neurogastroenterology and Motility we find three new articles on different aspects of ghrelin, dealing with physiological and pathophysiological actions of the peptide. For the reader this is food for thoughts: Does this peptide do everything? Ghrelin is a gut peptide hormone well established to stimulate motility throughout most parts of the gastrointestinal (GI) tract and appetite. Ghrelin has been linked to various GI regulatory mechanisms, the most evident being hunger, over-eating and obesity. In this setting ghrelin has been studied under physiological conditions converging on obesity as a pathophysiological process where the peptide has been employed as an interesting tool for studying the development of obesity. With a widespread distribution of ghrelin receptors on various immune cells, it has been assumed that ghrelin also possesses immunoregulatory properties, thus also being of interest in intestinal inflammation research. Anti-inflammatory effects of exogenous ghrelin have been claimed in experimental colitis in mice. Further studies on this concept using ghrelin gene knock-out mice, however, show an increased inflammatory activity in experimental colitis in wild-type mice pointing to ghrelin as an enhancer of the inflammatory course of the disease. Taken together, recent studies on ghrelin indicate that the peptide is not only a regulatory agent in pathophysiological processes, but also participates in pathological disease conditions with actions that seem to even involve genetic mechanisms.
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PMID:Faces of ghrelin--research for the 21st century. 1914 Sep 53

Malnutrition is a common complication in patients on dialysis and is strongly associated with poor prognosis. Effective therapy could substantially improve morbidity and mortality, but neither enteral nor parenteral supplementation provide long-term benefit because of the strong appetite suppression seen in such patients. We performed a double-blinded randomized crossover study of a week-long treatment with daily subcutaneous ghrelin, a gut hormone that regulates hunger through the hypothalamus, in a group of 12 malnourished dialysis patients. Ghrelin administration increased ghrelin levels in circulation, modestly reduced blood pressure for up to 2 h, and immediately and significantly increased appetite, with an increase in energy intake noted at the first study meal. Persistence of this effect throughout the week was confirmed with food diaries and final study meals. Energy expenditure, measured with free-living pulse and motion monitors, was unchanged by ghrelin. Our study shows that daily treatment with ghrelin achieves a sustained positive change in energy balance in malnourished dialysis patients. Direct manipulation of appetite with ghrelin or its analogs represents an attractive and promising therapeutic strategy for this difficult clinical problem.
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PMID:Sustained appetite improvement in malnourished dialysis patients by daily ghrelin treatment. 1956 55

The 'anorexia of aging' refers to reduced appetite and energy intakes observed in some older adults. Satiation (the process that leads to the termination of eating, which may be accompanied by a feeling of satisfaction) and satiety (the feeling of fullness that persists after eating, potentially suppressing further energy intake until hunger returns) are important factors in the control of appetite and energy intake, and there is evidence that some aspects of satiation and satiety are altered in older adults. Factors affected include gastric emptying, which could affect satiation, and levels of gut hormones which could affect satiety. Sensory specific satiety also appears to be reduced in older subjects. This might be important in the anorexia of aging and dietary strategies could be used to reduce satiety and encourage an increased energy intake. However, many other factors may affect the anorexia of aging and it is important to understand these in order to help those at risk of malnutrition.
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PMID:Satiety and the anorexia of ageing. 1968 53

Insensitivity to the bitter-tasting compound 6-n-propylthiouracil (PROP) has been proposed as a marker for individual differences in taste perception that influence food preference and intake. The principal genetic determinants of phenotypic variation in PROP taste sensitivity are alleles of the TAS2R38 gene, which encodes a chemosensory receptor sensitive to thiourea compounds including PROP and phenylthiocarbamide. Members of the TAS2R family are expressed in the gustatory system, where they function as bitter taste receptors, and throughout the gut, where their physiological roles in prandial, gut-derived hormone release are beginning to be elucidated. To better understand the relationship between TAS2R function and ingestive behaviors, we asked if TAS2R38 variants are associated with one or more of three eating behaviors: restraint, disinhibition, and hunger. We genotyped a single nucleotide polymorphism (SNP) located within the TAS2R38 gene, rs1726866 (T785C, Val262Ala) in 729 nondiabetic individuals (381 females, 348 males) within the Amish Family Diabetes Study. Eating behaviors were assessed using the Three-Factor Eating Questionnaire. An association analysis between rs1726866 and these three traits revealed a significant association of the PROP-insensitive "T" allele with increased disinhibition (p=0.03). Because eating behaviors differ substantially between males and females, we subsequently performed sex-stratified analyses, which revealed a strong association in females (p=0.0002) but not in males. Analyses with other SNPs in close proximity to rs1726866 suggest that this locus is principally responsible for the association. Therefore, our results indicate that a polymorphism in TAS2R38 is associated with differences in ingestive behavior.
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PMID:Variation in the gene TAS2R38 is associated with the eating behavior disinhibition in Old Order Amish women. 1978 9

It is important to investigate the effect of anesthesia on blood oxygenation level-dependent (BOLD) signals in an animal model. Many researchers have investigated the BOLD response to visual, sensory, and chemical stimuli in anesthetized rats. There are no reports, however, comparing the differences in the BOLD signal change between anesthetized and conscious rats when a visceral nutrient signal arises. Here, using functional magnetic resonance imaging (fMRI), we investigated the differences in the BOLD signal changes after intragastric administration of l-glutamate (Glu) under three anesthesia conditions: conscious, alpha-chloralose-anesthetized, and isoflurane-anesthetized condition. Under the conscious and alpha-chloralose condition, we observed the significant BOLD signal increase in the medial prefrontal cortex (mPFC), insular cortex (IC), hippocampus, and several hypothalamic regions including the lateral and ventromedial nucleus. In chloralose group, however, gut Glu stimulation induced BOLD signal increase in the prelimbic cortex and orbital cortex, which did not activate in conscious condition. Meanwhile, under isoflurane-anesthetized condition, we did not observe the BOLD signal increase in these areas. BOLD signal intensity in the nucleus of the solitary tract (NTS), to which vagus nerve transmits the visceral information from the gastrointestinal tract, increased in all conditions. Importantly, under conscious condition, we observed increased BOLD signal intensity in several regions related to the metabolic state (i.e. hunger or satiety), such as the mPFC, ventromedial and lateral hypothalamus (LH). Our results suggest that alpha-chloralose and isoflurane anesthesia caused distinct effects on BOLD response to the gut l-Glu stimulation in several brain regions.
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PMID:Effects of isoflurane and alpha-chloralose anesthesia on BOLD fMRI responses to ingested L-glutamate in rats. 1981 7

The obesity epidemic is a major health problem that is associated with increased morbidity and mortality. Gastrointestinal hormones have been increasingly understood to be an important element in appetite regulation. Several gastrointestinal hormones can contribute to obesity by modulating the activity of the gut-brain axis. Bariatric surgery is currently the most effective therapy for significant and sustained weight loss in morbidly obese patients. Understanding how gut hormones are altered by bariatric procedures has contributed to our understanding of the mechanisms of appetite. In this review, we address several gastrointestinal hormones that are associated with obesity and consider how their levels are altered after bariatric surgery. The review also addresses specific effects of different gut hormones on appetite, hunger, and energy balance.
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PMID:Mechanisms of weight loss after gastric bypass and gastric banding. 2005

Bariatric surgery is the only effective treatment for morbid obesity in the long term. Gut hormones are key players in the metabolic mechanisms causing obesity. Furthermore gut hormones are involved in the signalling process of hunger and satiety which leads to the control of nutrient intake. In this review, the role of these hormones as facilitators of appetite control after bariatric and metabolic surgery will be explored.
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PMID:The effect of bariatric surgery on gut hormones that alter appetite. 2015 35

There exists a substantial need to identify new neuropharmacological targets to treat alcohol-dependent individuals. Ghrelin represents a gut-brain peptide, initially discovered as the endogenous ligand for the growth hormone secretagogue receptor (GHS-R). The existing literature clearly demonstrates that ghrelin affects appetite and food intake. Both animal and human studies provide evidence that ghrelin not only influences hunger but also has a role in the search for rewarding substances, such as alcohol. Animal studies provide evidence that ghrelin stimulates the reward system, acting on specific brain reward nodes, and that ghrelin signaling is required for stimulation of the reward system by alcohol. Human studies show that ethanol acutely affects ghrelin levels. Interestingly, human studies with alcohol-dependent individuals suggest that higher ghrelin levels are associated with higher self-reported measurements of alcohol craving. Altogether, these findings suggest that the ghrelin system plays a role in alcohol dependence. Ghrelin antagonists (i.e., GHS-R1a antagonists and/or inverse agonists) might affect alcohol-seeking behavior, thus having therapeutic potential in alcohol use disorders. Future laboratory and clinical studies testing this hypothesis are warranted.
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PMID:Role of the ghrelin system in alcoholism: Acting on the growth hormone secretagogue receptor to treat alcohol-related diseases. 2044 Apr 17

Glycolysis is an essential metabolic function that lies at the core of any cellular life. Glucose homoeostasis is, thus, a crucial physiological function of living organisms. A system of plasma glucose-sensing in the portal vein plays a key role in this homoeostasis. Connected to the hypothalamus via the peripheral nervous system, the system allows the body to adapt its response to any variation of portal glycaemia. The hypothalamus controls food intake (exogenous glucose supply) and hepatic glycogenolysis (endogenous glucose supply). Intestinal gluconeogenesis, via the release of glucose into the portal vein, plays a key role in the control of hunger and satiety, and of endogenous glucose production through the modulation of liver insulin sensitivity. The induction of intestinal gluconeogenesis provides a physiological explanation for the satiety effects induced by protein-enriched diets. In particular, the influence of protein-enriched diets on the hypothalamus is comparable to the activation observed after glucose infusion into the portal vein. The induction of intestinal gluconeogenesis also offers an explanation for the early improvement in glycaemia control observed in obese diabetic patients treated by gastric-bypass surgery. In addition to intestinal gluconeogenesis, a number of gastrointestinal hormones involved in the control of food intake exert their effects, at least in part, via the peripheral afferent nervous system. These data emphasize the importance of the gut-brain axis in the understanding and treatment of obesity and type 2 diabetes.
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PMID:Hypothalamic integration of portal glucose signals and control of food intake and insulin sensitivity. 2056 8


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