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Results for “Feeding Behavior”

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At least 397 records · Page 22Linked to original sources
PubMed2003

[Roles of biologically active peptide in regulation of feeding behavior and energy homeostasis].

The mechanisms for regulating food intake involve a complicated interplay between peripheral systems (including gastrointestinal peptide secretion, leptin, and vagal afferent nerve responses) and central nervous system (CNS) neuropeptides and/or monoamines. Many hypothalamic neuropeptides are involved in the regulation of energy homeostasis and feeding behavior, including melanocortins, Agouti-related peptide, neuropeptide-Y, cocaine, and amphetamine-regulated transcript, orexin, and melanine concentrating hormone (MCH) as well as monamines (serotonin, dopamine, norepinephrine). Many of these systems are regulated by peripheral metabolic cues including plasma leptin levels. This review summarizes roles of neuropeptides in the regulatory mechanism of feeding and energy homeostasis.

Animals↗
PubMed1986

Vasopressin and glucoprivic-feeding behavior: a new perspective on an 'old' peptide.

The feeding responses induced by systemic administration of 2-deoxy-D-glucose (2-DG) and paraventricular hypothalamic injection of norepinephrine were assessed in Brattleboro rats deficient in vasopressin (VP). Controlling for the non-specific complications of diabetes insipidus, it was found that Brattleboro rats have a deficient 2-DG-feeding response, but an essentially normal noradrenergic-feeding response. Specific carbohydrate appetite abnormalities were also demonstrated. It is argued that VP influences 2-DG feeding by mobilizing endogenous energy stores following its acute release from the hypothalamoneurohypophysial system. A new function is thus ascribed for VP and the neural lobe of the pituitary. It is suggested that VP plays a role in stress-induced feeding and in specific aspects of carbohydrate appetite. The potential relevancy of vasopressin perturbations to bulimia nervosa and to the Prader-Willi obesity syndrome is also discussed.

Animals↗
PubMed2006

A neuropeptide ligand of the G protein-coupled receptor GPR103 regulates feeding, behavioral arousal, and blood pressure in mice.

Here, we report the isolation and characterization of an endogenous peptide ligand of GPR103 from rat brains. The purified peptide was found to be the 43-residue RF-amide peptide QRFP. We also describe two mouse homologues of human GPR103, termed mouse GPR103A and GPR103B. QRFP binds and activates the human GPR103, as well as mouse GPR103A and GPR103B, with nanomolar affinities in transfected cells. Systematic in situ hybridization analysis in mouse brains showed that QRFP is expressed exclusively in the periventricular and lateral hypothalamus, whereas the two receptor mRNAs are distinctly localized in various brain areas without an overlap to each other. When administered centrally in mice, QRFP induced feeding behavior, accompanied by increased general locomotor activity and metabolic rate. QRFP-induced food intake was abolished by preadministration of BIBP3226, a specific antagonist for the Y1 neuropeptide Y receptor. Hypothalamic prepro-QRFP mRNA expression was up-regulated upon fasting and in genetically obese ob/ob and db/db mice. Central QRFP administration also evoked highly sustained elevation of blood pressure and heart rate. Our findings suggest that QRFP and GPR103A/B may regulate diverse neuroendocrine and behavioral functions and implicate this neuropeptide system in metabolic syndrome.

Amino Acid Sequence↗
PubMed2004

Intra-amygdalar injection of DAMGO: effects on c-Fos levels in brain sites associated with feeding behavior.

It is well known that the mu opioid agonist, Tyr-D-Ala-Gly-(me) Phe-Gly-ol (DAMGO), increases food intake in rats when injected into a variety of brain sites including the central nucleus of the amygdala (CeA). Immunohistochemical studies measuring c-Fos immunoreactivity (IR) suggest that the CeA contributes to opioid-related feeding. In the current study, we injected 2 nmol of DAMGO and measured food intake, c-Fos IR levels in various brain sites involved in feeding behavior, and mu opioid receptor internalization. We also studied the effect of CeA-injected DAMGO on LiCl-induced increases in c-Fos IR in the amygdala. As was expected, intra-CeA injection of DAMGO increased food intake of rats over a 4-h period. DAMGO injection into the CeA also resulted in mu opioid receptor internalization in the CeA, indicating activation of mu opioid receptor expressing neurons in this site. Administration of DAMGO into the CeA increased c-Fos IR levels in the shell of the nucleus accumbens (NAcc), but not in 17 other brain sites that were studied. We also found that intra-CeA injection of DAMGO, prior to LiCl injection, decreased c-Fos IR levels in the CeA compared to vehicle-injected rats. Thus, intra-CeA administration of DAMGO may increase feeding, in part, by activating neurons in the shell of the nucleus accumbens and by inhibiting activity of selected neurons in the CeA.

Amygdala↗
PubMed1969

The control of feeding behavior by an imprinted stimulus.

Imprinted ducklings were trained to peck a pole using brief presentations of the imprinted stimulus as the response-contingent (reinforcing) event. Subjects were then permitted to spend extended periods with continuous access to food and the imprinted stimulus (via a pole peck). For other (control) subjects the experimental situation was restricted to either responding for the stimulus, or feeding in the absence of the stimulus. For subjects in the control conditions, both activities occurred in cyclic fashion. When, however, there was continuous opportunity to respond for the stimulus and food was available, the tendency to respond was related to the tendency to feed. Other experiments showed that independent presentations of the stimulus could initiate feeding in imprinted ducklings with no prior pairing of the stimulus with food and with no prior pole-peck training. The most consistent control over feeding, however, was exhibited by ducklings that were imprinted and also accustomed to periodic removals of the stimulus. It is concluded that in ducklings, imprinting procedures are sufficient to endow an arbitrary stimulus with the capacity to release feeding behavior.

Journal Article↗
PubMed1992

Feeding behavior and brain acetylcholinesterase activity in bream (Abramis brama L.) as affected by DDVP, an organophosphorus insecticide.

1. Bream (Abramis brama) were exposed to sublethal concentration of organophosphorus insecticide DDVP and the amount of food consumed and brain acetylcholinesterase (AChE) examined in exposed fish. 2. Exposure to DDVP resulted in decreased amount of food consumed and inhibited brain AChE activity. 3. Intraperitoneal injection of the fish with cholinergic drugs, atropine and TMB-4 recovered the feeding efficiency in exposed fish. TMB-4 recovered brain AChE activity as well. 4. The results revealed that cholinergic system in fish brain constitutes biochemical mechanism controlling feeding behavior in fish.

Acetylcholinesterase↗
PubMed1994

Nitric oxide controls feeding behavior in the chicken.

To investigate the effect of nitric oxide (NO) on food intake in the chicken, L-NG-nitro-arginine methyl ester HCl (L-NNA), an inhibitor of NO synthase, was applied. When i.p. administered, L-NNA significantly inhibited the food intake of broiler chickens in a dose response manner. Food ingestion was also depressed by the i.c.v. injection of L-NNA in a dose response fashion. The effect of L-NNA was attenuated by i.c.v. administration of L-arginine. These results suggest that central NO may control feeding behavior in the chicken.

Animals↗
PubMed2001

[Physiology of appetite and feeding behavior: introduction].

Food intake is regulated by the central nervous system depending on macronutrients and environmental changes. The hypothalamus is the target of hunger and satiety signals arising from the peripheral organs and the brain. Noradrenaline-neuropeptide Y and opioid-galanine are involved in carbohydrate and fat intake, respectively, while serotonin-CCK-insulin and dopamine-cyclic dipeptides systems inhibit them. Histamine and proinflammatory cytokines are involved in stress- and sickness-induced anorexia. Leptin accelerated intrahypothalamic anorexic mechanisms executed by POMC/CART and CRH but suppresses orexigenic mechanisms promoted by NPY and orexin. Although these mechanisms elegantly regulate appetite and feeding behavior, disruption of weight control has been accelerated and the incidence of obesity and eating disorder are dramatically increasing recent years in our modern society. New approach may be necessary to solve the problems of weight control.

Appetite↗