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

Evidence is growing that appetite regulating peptides such as leptin and ghrelin, but also other hormones including prolactin are altered in alcoholism. The brain pro-opiomelanocortin (POMC) system which has important mediating roles in alcohol intake also has important functions in prolactin regulation and energy homeostasis. Furthermore, it has been demonstrated to be functionally integrated with leptin regulation. The satiety factor leptin seems to be counteracted by the gut-derived peptide ghrelin which increases hunger and food intake. Consequently, the POMC system may have a role in integrating regulation of alcohol effects and these seemingly disparate regulatory systems. The goal of this mini-review is to discuss the results of some recent investigations of the potential interactions of these systems with acute and chronic alcohol responses.
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PMID:Alcoholism, craving, and hormones: the role of leptin, ghrelin, prolactin, and the pro-opiomelanocortin system in modulating ethanol intake. 1803 91

Bariatric surgery is one of the most effective treatments for achieving long-term weight loss in morbidly obese patients. Bariatric surgery causes weight loss through substantial decline of hunger and increased satiety. Recently our understanding of neuroendocrine regulation of food intake and weight gain, especially regarding the role of gut hormones, has significantly increased. The changes in these hormones following bariatric surgery can partly explain the mechanism behind weight loss achieved through these procedures. In this paper, we review the effect bariatric procedures have on different gut hormone levels and how they in turn can alter the complex neuroendocrine regulation of energy homeostasis.
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PMID:Changes in gut hormones after bariatric surgery. 1816 36

Terms as treatment failure or ineffective treatment after bariatric surgery are not clearly defined and difficult to handle. About one third of all persons who were formerly treated with a Lapband have either mechanical problems or do not lose enough weight. The current review argues in favor of adequate nutrition to suppress hunger and optimize satiety together with effective but least malabsorptive revisional surgery. This approach aims at switching the gut-brain axis, thereby facilitating homeostatic eating control.
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PMID:Adequate nutrition followed by revisional bariatric surgery to optimize homeostatic eating control. 1817 33

Following the discovery of secretin in 1902, a host of further peptide hormones that are synthesised and released from the gastrointestinal tract have been identified. While their roles in the regulation of gastrointestinal function have been known for some time, it is now evident that many of these hormones also physiologically regulate energy balance. Our understanding of how gut hormones signal to the brain has advanced significantly in recent years. Several hormones, including peptide YY, pancreatic polypeptide, oxyntomodulin, glucagon-like peptide 1 and cholecystokinin function as satiety signals. In contrast, only ghrelin, produced by the stomach, has emerged as a putative hunger signal, appearing to act both as a meal initiator and a long-term body weight regulator. Recent research suggests that gut hormones can be manipulated to regulate energy balance in man and that obese subjects retain sensitivity to the actions of gut hormones. The worldwide obesity pandemic continues unabated, despite public health initiatives and current best therapy. Future gut hormone-based therapies may provide an effective and well-tolerated treatment for obesity.
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PMID:Gut and hormones and obesity. 1823 Sep 2

During the first few days after weaning, pigs often experience BW loss as they adapt to eating solid food. During this time period, they are also known to drink excessively and develop abnormal oral behavior such as belly nosing. The excessive drinking may stem from the piglets' attempt to satiate hunger through gut fill from a familiar ingestive source. Gut fill through water intake may affect the establishment of feeding behavior. Using drinker devices other than the standard nipple drinker may ease the piglets' transition at weaning by facilitating the initiation of feeding and preventing the development of behavioral problems such as excessive drinking and belly nosing. In this experiment, we examined the effect of drinker type on water and food intake, growth rates, and belly nosing in newly weaned piglets. Eighteen pens of 15 piglets each (270 piglets total) were weaned at 18.1 +/- 0.1 d of age and housed in pens containing 1 of 3 drinker devices (standard nipple, push-lever bowl, and float bowl). Piglets' water and feed intake, water use, BW, and behavior were examined on a pen basis through 2 wk after weaning. Piglets with nipple drinkers wasted more water than the other piglets (P < 0.001; float, 295 +/- 70 mL x pig(-1) . d(-1); nipple, 1,114 +/- 63 mL x pig(-1) . d(-1); and push-lever, 186 +/- 63 mL x pig(-1) . d(-1)), whereas piglets with float bowls consumed less water than the other piglets (P < 0.001; float, 475 +/- 81 mL . pig(-1) x d(-1); nipple, 870 +/- 76 mL x pig(-1) . d(-1); push-lever, 774 +/- 76 mL x pig(-1) . d(-1)). Drinker type affected feeding behavior (P = 0.02); piglets with push-lever bowls spent less time at the feeder than the other piglets, although no difference was detected for feed intake (P = 0.64) or overall ADG (P = 0.16). Piglets with push-lever bowls also tended to perform less piglet-directed nosing behavior than piglets with the float bowl (P = 0.04). Piglets appear to use more water during the first 2 d after weaning with certain drinker devices. However, piglets do not appear to attain satiety through water consumption because most of the water used during the first few days after weaning is wasted. This excessive drinking and water wastage can be abated through the use of push-lever drinkers without negative implications for feed intake or growth rates.
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PMID:Effect of drinker type on water intake and waste in newly weaned piglets. 1827 51

The obesity epidemic is fast becoming one of the leading causes of mortality and morbidity worldwide. Over the past 30 years, gastrointestinal hormones have been increasingly understood to have an important role as regulators of appetite and energy balance in obese individuals. The levels of these hormones are modulated by bariatric surgery, and understanding how they are affected by such procedures can contribute to our comprehension of the underlying mechanisms by which these hormones affect obesity and its treatment. In this Review, we consider several gastrointestinal hormones that can contribute to obesity by modulating the activity of the gut-brain axis, and examine their specific effects on appetite, hunger and energy balance. Better understanding of the mechanisms by which these peptides exert their effects may enable the development of improved weight-loss medications and new treatments for obesity.
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PMID:Mechanisms of disease: the role of gastrointestinal hormones in appetite and obesity. 1838 32

The gastrointestinal tract plays a pivotal role in the regulation of food intake and energy balance. Signals from the gastrointestinal tract generally function to limit ingestion in the interest of efficient digestion. These signals may be released into the bloodstream or may activate afferent neurones that carry information to the brain and its cognitive centres, which regulates food intake. The rate at which nutrients become systemically available is also influenced by gastrointestinal motility: a delay in gastric emptying may evoke a satiety effect. Recent evidence suggests that the endocannabinoid anandamide and the related acylethanolamide oleoylethanolamide are produced in the intestine and might regulate feeding behaviour by engaging sensory afferent neurones that converge information to specific areas of the brain. The intestinal levels of these acylethanolamides are inversely correlated to feeding, as food deprivation increases intestinal levels of anandamide (which acts in the gut as a 'hunger signal'), while it decreases the levels of oleoylethanolamide (which acts in the gut as a 'satiety signal'). Additionally, these acylethanolamides, whose gastric levels change in response to diet-induced obesity, alter gastrointestinal motility, which might contribute to their effect on food intake and nutrient absorption.
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PMID:Gastrointestinal regulation of food intake: general aspects and focus on anandamide and oleoylethanolamide. 1842 98

Feeding behavior is often separated into homeostatic and hedonic components. Hedonic feeding, which can be triggered by visual or olfactory food cues, involves brain regions that play a role in reward and motivation, while homeostatic feeding is thought to be under the control of circulating hormones acting primarily on the hypothalamus. Ghrelin is a peptide hormone secreted by the gut that causes hunger and food consumption. Here, we show that ghrelin administered intravenously to healthy volunteers during functional magnetic resonance imaging increased the neural response to food pictures in regions of the brain, including the amygdala, orbitofrontal cortex, anterior insula, and striatum, implicated in encoding the incentive value of food cues. The effects of ghrelin on the amygdala and OFC response were correlated with self-rated hunger ratings. This demonstrates that metabolic signals such as ghrelin may favor food consumption by enhancing the hedonic and incentive responses to food-related cues.
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PMID:Ghrelin modulates brain activity in areas that control appetitive behavior. 1846 Mar 31

BED is characterized by overeating with a loss of control. The primary aim of the study was to measure plasma concentrations of three key gut peptides influencing hunger (ghrelin) and satiety (PYY, GLP-1) to ascertain potential abnormalities in BED. The participants were 10 obese BED and 9 obese nonBED premenopausal women. They did not differ in age, 30.1+/-8.1 SD, BMI, 36.2+/-5.9, or % body fat, 43.3+/-5.7. Following a13-h overnight fast, blood was drawn (-15, 0, 5, 15, 30, 60, 90, 120 min) for measurement of total plasma concentrations of ghrelin, PYY and GLP-1, pre and post ingestion of a nutritionally complete liquid meal (1256 kJ) at 9 am (0-5 min). Ratings of hunger and fullness preceded each blood draw. Ghrelin was significantly lower premeal at -15 min (P=.05) and postmeal at 90 min (P=.027) and 120 min (P=.025) in the BED group as compared to the nonBED group. Ghrelin also declined less postprandially in the BED group (P=.019) with a longer time to the nadir value (P=.004). However, fasting and meal-related changes in levels of PYY and GLP-1 did not differ between the groups nor did ratings of hunger and fullness. Following a randomized cognitive behavior and dietary intervention, the ghrelin values in BED normalized. Prior to treatment, the lower fasting ghrelin in BED may be a consequence of down regulation by overeating. The lack of differences in the satiety promoting hormones, PYY and GLP-1, makes them unlikely contributors to the binge eating in BED.
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PMID:Appetite-related gut peptides, ghrelin, PYY, and GLP-1 in obese women with and without binge eating disorder (BED). 1853 36

The objective of this study was to identify mechanisms through which valproic acid (VPA) causes weight gain. Healthy participants (N = 52) were randomized to VPA or placebo in a double-blind study. Energy intake (EI) was measured in the laboratory at lunch and dinner, and physical activity (PA) was measured with accelerometry. Glucose levels and hormones [Peptide YY(3-36), glucagon-like peptide-1 (GLP-1), leptin, ghrelin, insulin] that regulate EI were measured. Assessments occurred at baseline and week 3. Change from baseline was evaluated with mixed models (alpha = 0.05). Weight significantly increased in the VPA group (+0.49 kg), but not the placebo group. The VPA group increased fast food fats cravings and decreased glucose levels compared with placebo. Change in weight, EI and PA did not differ by group. Within group analyses indicated that the VPA group increased PA, hunger, binge eating, depression and GLP-1. VPA-associated weight gain is not likely due to changes in PA or the gut hormones studied. Although EI did not increase when measured after 3 weeks of treatment, VPA decreased glucose levels and increased motivation to eat; hence, EI might have increased in the short-term. Research testing VPA on short-term (1 week) EI, metabolism, and substrate partitioning is warranted.
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PMID:Effect of valproic acid on body weight, food intake, physical activity and hormones: results of a randomized controlled trial. 1858 34


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