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)

Twelve rats with amygdala damage (CBM) and 20 sham-operated controls were tested in several food-related situations. The CBM rats showed a longer latency to eat than controls in a novel environment due to more pronounced exploration. In the competition for food, CBM rats lost 85% of encounters with controls. Immediately after the contest, when allowed to eat singly, CBM rats displayed a higher persistence of alimentary responses to an emptied cup than did controls, presumably because they experienced more losses in the food competition. Both groups were equally able to overcome obstacles on the way to food, which suggests similar alimentary motivation. The only direct indication of a lowered responsiveness to hunger in CBM rats was 24-hr-fasting-induced hypophagia. The results of this study indicate the involvement of the cortico-basomedial amygdaloid region in the control of relations between alimentary and other motivations. The contribution of eventual changes of food motivation in the postoperative alteration of this balance is discussed.
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PMID:Food-motivated behavior in rats with cortico-basomedial amygdala damage. 673 25

Three genotypes of mice were shown to increase their intake of 3% sodium chloride (NaCl) following administration of fludrocortisone acetate (25 mg/kg), a synthetic steroid having strong mineralocorticoid/glucocorticoid activity. However, treatment with deoxycorticosterone acetate (DOCA) (10 mg/kg), a corticosteroid with predominantly mineralocorticoid activity, did not increase 3% NaCl consumption by the stock tested. In contrast, both fludrocortisone and DOCA have been shown to be effective activators of sodium appetite in rats. The essential importance of glucocorticoids in potentiating mineralocorticoid activation of sodium hunger in mice is suggested.
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PMID:The effects of fludrocortisone acetate and deoxycorticosterone acetate on salt appetite in mice. 824 44

Research investigating sodium hunger in mice has failed to produce evidence that mineralocorticoids are involved in sodium appetite. In our own laboratory, doses of deoxycorticosterone acetate (DOCA) ranging from 1 mg/kg to 20 mg/kg have failed to induce a sodium appetite. In rats, glucocorticoids have been effective in potentiating mineralocorticoid-induced sodium appetite. Recent research has suggested that the mouse, like the rat, does possess mineralocorticoid sensitivity for sodium hunger but, unlike the rat, has a strong dependency on an accompanying glucocorticoid action. The present experiment was conducted to study the effects of DOCA on sodium appetite in mice under housing conditions that attempted to eliminate the reduction of corticosterone associated with social isolation. Therefore, male GHSC mice were group-housed and were tested within two counterbalanced treatment conditions. One condition consisted of an injection of 10 mg/kg DOCA on 2 consecutive days, and the other condition consisted of an injection of the vehicle on 2 consecutive days. Group-housed male GHSC mice showed a significantly larger amount of NaCl consumption after injections of DOCA than after injections of the vehicle.
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PMID:Deoxycorticosterone acetate (DOCA)-induced sodium appetite in group-housed mice. 891

This randomized, open-labeled, multicenter study was designed to assess safety and pharmacokinetics of dronabinol (Marinol) tablets and megestrol acetate (Megace) micronized tablets, alone and in combination, for treatment of HIV wasting syndrome. Weight and quality of life data were also collected. Fifty-two patients (mean CD4+ count, 59 cells/microliter) were randomized to one of four treatment arms: dronabinol 2.5 mg twice/day (D); megestrol acetate 750 mg/day (M750); megestrol acetate 750 mg/day+dronabinol 2.5 mg twice/day (M750+D); or megestrol acetate 250 mg/day+dronabinol 2.5 mg twice/day (M250+D). After therapy initiation, 47 patients returned for at least one visit, and 39 completed the planned 12 weeks of study visits. Occurrence of adverse events, drug discontinuation, new AIDS-defining conditions, or CD4+ T lymphocyte changes were not statistically significantly different among arms. Serious adverse events assessed as related to dronabinol included CNS events (e.g., confusion, anxiety, emotional lability, euphoria, hallucinations) and those assessed as related to megestrol acetate included dyspnea, liver enzyme changes, and hyperglycemia. The mean weight change +/- SE over 12 weeks was as follows: D, -2.0 +/- 1.3 kg; M750, +6.5 +/- 1.1 kg; M750+D, +6.0 +/- 1.0 kg; and M250+D, -0.3 +/- 1.0 kg (difference among treatment arms, p = 0.0001). Pharmacokinetic parameters measured after 2 weeks of therapy for M750 were Cmax = 985 ng/ml and AUC = 22,487 ng x hr/ml, and for dronabinol and its active metabolite (HO-THC), respectively, were Cmax = 2.01; 4.61 ng/ml and AUC = 5.3; 23.7 ng x hr/ml. For megestrol acetate, but not dronabinol, there was a positive correlation at week 2 between both Cmax and AUC with each of the following: (1) weight change, (2) breakfast visual analog scale for hunger (VASH) score, and (3) dinner VASH score.
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PMID:The safety and pharmacokinetics of single-agent and combination therapy with megestrol acetate and dronabinol for the treatment of HIV wasting syndrome. The DATRI 004 Study Group. Division of AIDS Treatment Research Initiative. 907 30

The dose-response effects of intraruminal infusion of propionate on feeding behavior of lactating dairy cows were evaluated with eight ruminally cannulated Holstein cows past peak lactation. Treatments were mixtures of propionic acid and acetic acid containing propionic acid at eight different concentrations in Experiment 1, and mixtures of sodium propionate and sodium acetate containing sodium propionate at 4 different concentrations in Experiment 2. Experimental designs were an 8 x 8 and duplicated 4 x 4 Latin squares, respectively, for Experiments 1 and 2. Treatment solutions were infused into the rumen continuously for 14 h at a rate of 16.7 and 25 mmol/min, respectively, for Experiments 1 and 2. Infusion started 2 h before feeding and ended 12 h after feeding; feeding behavior was monitored for 12 h after feeding using a computerized data acquisition system. Total metabolizable energy (ME) intake was calculated by adding the energy of infusates to dietary energy intake. In both experiments, as the proportion of propionate of the infusates increased, total ME intake and dry matter intake decreased linearly. As infusion of propionate increased, meal size tended (P < 0.09) to decrease linearly and intermeal interval tended (P < 0.07) to increase linearly in Experiment 1; meal size decreased linearly and number of meal bouts tended (P < 0.08) to decrease linearly in Experiment 2. These observations indicate that the reduction in dietary energy intake from propionate infusion was greater than the energy supplied from infusates, and that propionate plays an important role in feed intake regulation by affecting both satiety and hunger.
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PMID:Intraruminal infusion of propionate alters feeding behavior and decreases energy intake of lactating dairy cows. 1267 25

The objective of this experiment was to determine interactions between hypophagic effects of propionate and ammonium in lactating dairy cows. Eight ruminally cannulated Holstein cows in mid-lactation were used in a duplicated 4 x 4 Latin square design experiment with a 2 x 2 factorial arrangement of treatments. Factors evaluated were type of volatile fatty acid (VFA; acetate vs. propionate) and type of salt (sodium vs. ammonium). Treatment solutions were infused continuously into the rumen at a rate of 16.7 mmol of VFA salts/min starting 2 h before feeding and ending 12 h after feeding. Hypophagic effects of ammonium were significantly greater for cows infused with propionate (4.3 vs. 12.1 kg/12 h; SEM = 1.3) compared with acetate (13.5 vs. 15.3 kg/12 h; SEM = 1.3; interaction P < 0.01). This interaction was attributed to a greater reduction in meal frequency for ammonium treatment compared with sodium treatment when infused with propionate (3.9 vs. 7.2/12 h; SEM = 0.8) compared with acetate (6.6 vs. 7.0/12 h; SEM = 0.8), indicating that infusion of ammonium propionate reduced hunger. Meal size was decreased by infusion of propionate compared with acetate, but was not affected by ammonium compared with sodium, indicating that ammonium did not affect satiety. Mechanisms to explain the interactions between ammonium and propionate on meal frequency and feed intake warrant further investigation.
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PMID:Hypophagic effects of ammonium are greater when infused with propionate compared with acetate in lactating dairy cows. 1267 26

America is experiencing a major obesity epidemic. The ramifications of this epidemic are immense since obesity is associated with chronic metabolic abnormalities such as insulin resistance, dyslipidemia, and heart disease. Reduced physical activity and/or increased energy intakes are important factors in this epidemic. Additionally, a genetic susceptibility to obesity is associated with gene polymorphisms affecting biochemical pathways that regulate fat oxidation, energy expenditure, or energy intake. However, these pathways are also impacted by specific foods and nutrients. Vitamin C status is inversely related to body mass. Individuals with adequate vitamin C status oxidize 30% more fat during a moderate exercise bout than individuals with low vitamin C status; thus, vitamin C depleted individuals may be more resistant to fat mass loss. Food choices can impact post-meal satiety and hunger. High-protein foods promote postprandial thermogenesis and greater satiety as compared to high-carbohydrate, low-fat foods; thus, diet regimens high in protein foods may improve diet compliance and diet effectiveness. Vinegar and peanut ingestion can reduce the glycemic effect of a meal, a phenomenon that has been related to satiety and reduced food consumption. Thus, the effectiveness of regular exercise and a prudent diet for weight loss may be enhanced by attention to specific diet details.
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PMID:Strategies for healthy weight loss: from vitamin C to the glycemic response. 1703 Oct 14

Traditionally, molting was initiated by withdrawing feed. However, public criticism of feed deprivation, based on the perception that it inhumanely increases hunger, has led the poultry industry to ban the practice. Thus far, alternatives have not been demonstrated to ameliorate the increase in hunger that led to the ban on inducing molting by feed deprivation. Incorporating melengestrol acetate (MGA), an orally active progestin, into a balanced layer diet induces molting and increases postmolt egg quality. Hy-Line W-98 hens (n = 60) were randomly assigned to a balanced layer ration (control), a balanced layer ration containing MGA, or a 94% wheat middlings diet (wheat) for 20 d, or were feed deprived for 8 d. Hens were trained to peck a switch to receive a feed reward based on a progressive ratio reinforcement schedule. Motivation of hens to acquire feed was measured as the total number of pecks recorded in 15 min on d 0, 4, 8, 12, 16, and 20. On d 20, abdominal fat pad and digesta-free gizzards were weighed. The number of pecks in the feed-deprived group was greater than controls by d 4 and remained greater at d 8, when these hens were removed from the experiment. Hens in the wheat group that were rewarded with a layer diet pecked more than controls from d 8 to 20. Hens in the MGA group pecked for a reward at the same rate as control hens throughout the experiment. Hens fed the wheat diet had heavier gizzards compared with control and MGA-fed hens. Hens fed MGA had greater abdominal fat pad compared with wheat and control hens. Hens molted using a diet containing MGA have a similar motivation to obtain feed as control hens; therefore, this alternative does not appear to increase hunger. However, hens molted with a wheat middling diet appear to be as motivated to obtain feed as did the feed-deprived hens.
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PMID:Motivation of hens to obtain feed during a molt induced by feed withdrawal, wheat middlings, or melengestrol acetate. 1736 30

The regulation of appetite relies on the integration of numerous episodic (meal) and tonic (energy storage) generated signals in energy regulatory centres within the central nervous system (CNS). These centers provide the pharmacological potential to modify human appetite (hunger and satiety) to increase or decrease caloric intake, or to normalize aberrant eating behavior. With regard to obesity, the satiety enhancing anti-obesity drug sibutramine has proved effective at reducing body weight. Additionally, the endocannabinoid CB(1) antagonist rimonabant has recently been approved for use in Europe (but not in the US). A 5-HT(2C) agonist lorcaserin is also currently undergoing large-scale clinical trials, but the effect of the drug on human appetite is unknown as yet. Appetite enhancing drugs such as magestrol acetate and dronabiol are currently used to promote weight gain. Finally, sibutramine, selective serotonergic reuptake inhibitors such as fluoxetine and some anti-epileptic drugs have all been used to normalise aberrant eating behaviour. All these drugs act by modifying the expression of human appetite. An assessment of a drug's effects on caloric intake and feelings of hunger and satiety is necessary before they can be considered for clinical use.
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PMID:Neuropharmacology of human appetite expression. 1864 16

In cell line and animal models, sweet and bitter tastants induce secretion of signaling peptides (e.g., glucagon-like peptide-1 and cholecystokinin) and slow gastric emptying (GE). Whether human GE and appetite responses are regulated by the sweetness or bitterness per se of ingested food is, however, unknown. We aimed to determine whether intragastric infusion of "equisweet" (Study A) or "equibitter" (Study B) solutions slow GE to the same extent, and whether a glucose solution made sweeter by the addition of saccharin will slow GE more potently than glucose alone. Healthy nonobese subjects were studied in a single-blind, randomized fashion. Subjects received 500-ml intragastric infusions of predetermined equisweet solutions of glucose (560 mosmol/kgH(2)O), fructose (290 mosmol/kgH(2)O), aspartame (200 mg), and saccharin (50 mg); twice as sweet glucose + saccharin, water (volumetric control) (Study A); or equibitter solutions of quinine (0.198 mM), naringin (1 mM), or water (Study B). GE was evaluated using a [(13)C]acetate breath test, and hunger and fullness were scored using visual analog scales. In Study A, equisweet solutions did not empty similarly. Fructose, aspartame, and saccharin did not slow GE compared with water, but glucose did (P < 0.05). There was no additional effect of the sweeter glucose + saccharin solution (P > 0.05, compared with glucose alone). In Study B, neither bitter tastant slowed GE compared with water. None of the solutions modulated perceptions of hunger or fullness. We conclude that, in humans, the presence of sweetness and bitterness taste per se in ingested solutions does not appear to signal to influence GE or appetite perceptions.
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PMID:Sweetness and bitterness taste of meals per se does not mediate gastric emptying in humans. 1953 79


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