Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diazepam doses of 0.2, 0.4, and 0.8 mg/kg induced feeding in sated gray wolves in a dose-dependent manner (p less than 0.001). Neither 0.8 mg/kg of the benzodiazepine antagonist, beta-CCP (p = 0.36), nor 0.8 mg/kg of the benzodiazepine inverse agonist, beta-CCE (p = 0.85), decreased the diazepam-induced hyperphagia. Five of 6 naive wolves (p = 0.003) ate dry dog food within 15.4 +/- 1.9 min of being given 0.4 mg/kg diazepam and freely chose dog food after the single diazepam administration.
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PMID:Diazepam-induced feeding in captive gray wolves (Canis lupus). 178 84

Diazepam and pentobarbital administered intravenously increased food intake in a dose-dependent manner in nondeprived rats. Low doses of naloxone inhibited diazepam-induced feeding, but did not inhibit pentobarbital-induced feeding. On the other hand, picrotoxin inhibited feeding induced by both drugs. These findings suggest that diazepam-induced hyperphagia is related to endogenous opioid mechanisms, but pentobarbital-induced hyperphagia is not. Hyperphagia induced by both drugs may be related to GABAergic neurons.
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PMID:Effects of naloxone and picrotoxin on diazepam- or pentobarbital-induced hyperphagia in nondeprived rats. 325 Dec 54

Effects of repeated intravenous (i.v.) administration of diazepam on food intake were investigated in freely moving rats implanted with a chronic i.v. cannula. Diazepam (0.2 and 2 mg/kg) was automatically injected i.v. at 3-h intervals for 3 consecutive days. Food intake was measured twice daily, ie for the light phase (7 00-19 00) and dark phase (19 00-7 00). Food intake during the light phase was increased in a dose-dependent manner following diazepam. Each injection of diazepam provoked hyperphagia, followed by a compensatory hypophagia until the next diazepam injection. Body weight, however, was increased significantly in rats treated with diazepam. When diazepam (2 mg/kg) was automatically injected at 3-h intervals for 10 consecutive days, tolerance did not develop to the hyperphagia and body weight was increased significantly following diazepam injection. After cessation of diazepam injection, both food intake and body weight decreased. These findings suggest that such excessive i.v. treatment with diazepam induces hyperphagia showing no tolerance accompanied by an increase in body weight, thus resulting in a trend toward obesity in rats.
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PMID:Effects of repeated intravenous administration of diazepam on food intake in rats. 785 44

The hypothesis that benzodiazepine-induced hyperphagia is due to a specific enhancement of the palatability of foods has been supported by previous 'taste reactivity' studies of affective (hedonic and aversive) reactions to taste palatability. Diazepam and chlordiazepoxide enhance hedonic reactions of rats (rhythmic tongue protrusions, etc.) to sweet tastes in a receptor-specific fashion. A role for brainstem circuits has been indicated by a previous demonstration of the persistence of the taste reactivity enhancement by diazepam after midbrain decerebration. The present study examined whether benzodiazepine brainstem receptors are the chief substrates for palatability enhancement even in intact brains. We compared the effectiveness of benzodiazepine microinjections to elicit feeding and enhance hedonic reactions when delivered into either the lateral ventricle (forebrain) or the fourth ventricle (brainstem) of rats. The results show diazepam is reliably more effective at eliciting feeding and enhancing positive hedonic reactions to oral sucrose when microinjections are made in the fourth ventricle than in the lateral ventricle. We conclude that brainstem neural systems containing benzodiazepine-GABA receptors are likely to be the chief substrates for benzodiazepine-induced palatability enhancement.
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PMID:Brainstem mediates diazepam enhancement of palatability and feeding: microinjections into fourth ventricle versus lateral ventricle. 884 79

Food, Mood, and Attitude (FMA) is a CD-ROM prevention program developed to decrease risk for eating disorders in college women. Female 1st-year students (N = 240) were randomly assigned to the intervention (FMA) or control group. Equal numbers of students at risk and of low risk for developing an eating disorder were assigned to each condition. Participants in the FMA condition improved on all measures relative to controls. Significant 3-way interactions (Time x Condition x Risk Status) were found on measures of internalization of sociocultural attitudes about thinness, shape concerns, and weight concerns, indicating that at-risk participants in the intervention group improved to a greater extent than did low-risk participants. At follow-up, significantly fewer women in the FMA group reported overeating and excessive exercise relative to controls.
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PMID:Food, mood, and attitude: reducing risk for eating disorders in college women. 1628 2

Previous research has related impulsivity to overeating and obesity. However, the precise nature of this relation has not been examined yet. One possibility is that impulsivity causes overeating and hence contributes to overweight. To test this possibility we induced impulsivity versus inhibition to see whether this would affect food intake. In the first study participants were cognitively primed with the concepts "impulsivity" or "inhibition". Caloric intake was significantly higher in the Impulsivity Condition compared to the Inhibition Condition. This effect was even stronger for highly restrained participants. In the second study impulsivity was manipulated via behavioural instructions. Restrained and unrestrained nondieters acted as expected: their caloric intake was significantly higher when impulsivity was induced compared to inhibition. Current dieters sharply reduced their caloric intake following the impulsivity induction. These results are in accordance with Lowe's model that, contrary to restraint theory, states that restraint and current dieting are different constructs that affect eating regulation differently. At least for nondieters it can be concluded that heightened impulsivity versus inhibition leads to a higher food intake in the lab.
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PMID:Inducing impulsivity leads high and low restrained eaters into overeating, whereas current dieters stick to their diet. 1946 78

Early weight loss is associated with greater weight loss following treatment cessation and years later. The present study aimed to identify pretreatment correlates associated with early weight loss in adults participating in weight-loss treatment in primary care. Participants (N = 89) were in the overweight/obesity range seeking weight-loss treatment in primary-care settings and randomized to one of three treatments: Motivational Interviewing and Internet Condition (MIC), Nutrition Psychoeducation and Internet Condition (NPC), or Usual Care (UC). At baseline, participants were assessed with the Eating Disorder Examination (EDE) interview and completed self-report measures of emotional overeating, exercise, exercise self-efficacy, and depression. Percent weight loss at week six was used as the Early Weight Loss variable. MIC/NPC groups had significantly greater Early Weight Loss than UC. Among MIC/NPC participants only, greater Early Weight Loss was associated with significantly lower pretreatment disordered eating and depressive symptoms. Participants in MIC/NPC who achieved clinically meaningful weight loss (>2.5%) by week six compared with those who did not (<2.5%) reported lower pretreatment disordered eating. Demographic factors and binge-eating disorder diagnosis were unrelated to Early Weight Loss. Our findings suggest that greater early weight loss may be associated with less pretreatment disordered eating and depressive symptoms.
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PMID:Getting a head start: identifying pretreatment correlates associated with early weight loss for individuals participating in weight loss treatment. 3181 53