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)

It has been easy to demonstrate, both in humans and animals, that the stresses which disturbed either the physiological homeostasis, the behavioural homeostasis or both simultaneously, induced the modifications of the food intake; these disorders often found expression in the inappropriate eating or, less frequently, in temporary anorectic phases. The most relevant hypotheses localized, in the anterior and median hypothalamus (paraventricular nuclei, ventral median nuclei, lateral hypothalamic area), the neurobiological mechanisms which were involved in this stress/eating behaviour relationship. In the brain, both aminergic and peptidergic systems were concerned; the stress-induced hyperphagia required the functionality of the dopamine, dorsal noradrenergic bundle and endogenous opioids of the central nervous system. The dramatic stress-induced anorexia was based upon the reciprocal actions of serotonin, norepinephrine and CRF systems. Other peptides, which some of them belonged to the brain-gut peptide group, could interfere with these mechanisms. The neuropeptides being common in the stress and eating physiological systems, the regulatory mechanisms were most coherent; nevertheless, the precise nervous structures and neurochemical circuits that produced the stress-induced hyperphagia or stress-induced anorexia, remain unknown.
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PMID:[Stress and feeding behavior]. 342 63

Infections of the gastrointestinal nematode, Nippostrongylus brasiliensis, in the laboratory rat result in a characteristic biphasic anorexia which is followed by hyperphagia once the worm burden has been cleared. Despite the importance of parasite-induced anorexia, relatively little is known of the underlying mechanisms. We have investigated the involvement of the central appetite drive in this anorexia by studying the gene expression of two neuropeptides with opposing actions on energy balance, NPY and CRF. Gene expression was assessed by in situ hybridization at 2, 8 and 16 days post-infection (p.i.) in infected rats, in uninfected controls, and in a group with food intake restricted to match that taken voluntarily by the parasitize animals. The sampling intervals corresponded to each of the two phases of maximum anorexia and the period of compensatory hyperphagia. Surprisingly, we found that increases in NPY gene expression in the hypothalamic arcuate nucleus (ARC) accompany anorexia in rats infected with N. brasiliensis; there was a significant relationship between degree of anorexia and induction of NPY mRNA after 8 days of infection. Furthermore, ARC NPY mRNA levels in parasitized animals were similar to those in pair-fed individuals with food intake restricted to match the infected rats. The number of larvae used to establish the infection affected both the degree of anorexia and the level of NPY mRNA at 8 days p.i. in a dose-dependent manner. NPY gene expression remained elevated in infected rats during at least the initial stages of compensatory hyperphagia. This suggests that animals detect a state of energy deficit during the early stages of the infection, yet do not feed, but become hyperphagic coincident with worm loss. The failure of anorectic parasitized animals to feed in response to activation of the NPYergic system makes this a novel system in which to study the regulation of hypothalamic NPY by physiological challenge. There were no significant differences in CRF gene expression between the groups at any of the sampling intervals.
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PMID:Anorexia induced by the parasitic nematode, Nippostrongylus brasiliensis: effects on NPY and CRF gene expression in the rat hypothalamus. 874 24

We investigated the role of corticotropin-releasing factor type 2 (CRF(2)) receptors in acute, chronic and withdrawal effects of nicotine on feeding behavior in rats. Nicotine was injected intraperitoneally, whereas CRF, CRF(2) receptors agonist urocortin-1 or selective antagonist astressin2-B were administered directly into the hypothalamic paraventricular nucleus (PVN). In acute studies, nicotine, CRF or urocortin-1 produced dose dependent anorexia at 2 and 4h post-injection time-points, however, astressin2-B did not alter the food intake. Prior treatment of CRF or urocortin-1 potentiated the anorectic effect of nicotine, while astressin2-B showed opposite response. Chronic administration of nicotine produced tolerance to anorexia and caused persistent weight loss. However, concomitant treatment with CRF or urocortin-1 resulted in early tolerance to nicotine-induced anorexia. In the same set of animals, while CRF pre-treatment potentiated the weight reducing effect of nicotine, urocortin-1 failed to do so. Although abrupt termination of chronic nicotine treatment caused hyperphagia and weight gain, administration of CRF or urocortin-1 prevented these effects. These results suggest that CRF(2) receptors, within the framework of PVN, may contribute to the acute, chronic and withdrawal responses of nicotine on feeding and body weight.
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PMID:Participation of corticotropin-releasing factor type 2 receptors in the acute, chronic and withdrawal actions of nicotine associated with feeding behavior in rats. 1963 11

Dieting to control body weight involves cycles of deprivation from palatable food that can promote compulsive eating. The present study shows that rats withdrawn from intermittent access to palatable food exhibit overeating of palatable food upon renewed access and an affective withdrawal-like state characterized by corticotropin-releasing factor-1 (CRF(1)) receptor antagonist-reversible behaviors, including hypophagia, motivational deficits to obtain less palatable food, and anxiogenic-like behavior. Withdrawal was accompanied by increased CRF expression and CRF(1) electrophysiological responsiveness in the central nucleus of the amygdala. We propose that recruitment of anti-reward extrahypothalamic CRF-CRF(1) systems during withdrawal from palatable food, analogous to abstinence from abused drugs, may promote compulsive selection of palatable food, undereating of healthier alternatives, and a negative emotional state when intake of palatable food is prevented.
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PMID:CRF system recruitment mediates dark side of compulsive eating. 1990 33

The "lethal yellow" mutation at the mouse agouti locus (A(y)) results in hyperphagia, obesity, and type 2 diabetes at rest, but helps to reduce food intake under stress. The aim of this work was to investigate mechanisms of exaggerated anorectic response to stress in A(y) mice. All parameters were measured in C57BL/6J male mice of a/a (control) and A(y)/a genotypes before, 0, 1, and 3h after a 1-h restraint. Baseline food intake and plasma insulin concentrations were higher in A(y)/a mice compared to a/a mice. Restraint reduced food intake and plasma insulin concentrations only in A(y)/a mice. Stress-induced anorexia in A(y)/a mice was independent of pathways involving hypothalamic-pituitary-adrenal axis activity and hypothalamic orexigenic neuropeptide (agouti-related peptide and neuropeptide Y) gene expressions and corticotrophin-releasing factor type 1 receptor (CRFR1). Gene expression of CRFR2 was elevated in A(y)/a mice with genotype differences particularly manifested immediately after the restraint. Hypothalamic CRFR2 is known to mediate anorectic signals from CRF-related peptides. Thus, our data suggest that stress-induced anorexia in A(y)/a mice may be associated with increased anorectic signals mediated by CRFR2 in the hypothalamus.
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PMID:Exaggerated anorexigenic response to restraint stress in A(y) mice is associated with elevated CRFR2 mRNA expression in the hypothalamus. 2383 94