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PubMed2000

Pharmacological characterization of the nociceptin receptor mediating hyperphagia: identification of a selective antagonist.

RATIONALE: Central injections of nociceptin (NC) stimulate feeding in rats. OBJECTIVE: The present study evaluated the effect of N-terminal partial sequences or analogues of NC on food intake in male Wistar rats, to characterize pharmacologically the NC receptor mediating the hyperphagic effect. METHODS: NC and related peptides were injected into the lateral (LV) or third (3V) cerebroventricle in freely feeding rats. RESULTS: In the LV, NC stimulated feeding. The N-terminal fragment NC(1-13)NH2 proved to be the least active sequence with hyperphagic activity; NC(1-12)NH2 and NC(1-9)NH2 were inactive. [Phe(1)psi(CH2-NH)Gly(2)]NC(1-13)NH2 ([F/G)]NC(1-13)NH2), an analogue of NC(1-13)NH2, markedly stimulated feeding and, coadministered in the LV with NC, never reduced the hyperphagic effect of the natural sequence. These findings suggest that [F/G)]NC(1-13)NH2, which has been reported to act as a NC receptor antagonist in peripheral tissues, behaves as a full agonist at the central NC receptors controlling feeding. The hyperphagic potencies of NC and [F/G)]NC(1-13)NH2 were much higher following injection into the 3V than in the LV. Another analogue of NC(1-13)NH2, namely [Nphe(1)]NC(1-13)NH2, injected into the 3V did not stimulate feeding, but reduced the effect of NC. [Nphe(1)]NC(1-13)NH2 at a dose of 16.8 nmol/rat significantly reduced, and at 168 nmol/rat almost completely abolished the effect of NC (1.68 nmol/rat). The latter dose of [Nphe(1)]NC(1-13)NH2 significantly reduced also feeding induced by food deprivation, but did not modify the hyperphagic effect of neuropeptide Y (0.3 nmol/rat). CONCLUSIONS: The present results confirm the orexigenic effect of NC in freely feeding rats and indicate that [Nphe(1)]NC(1-13)NH2 may represent a selective NC receptor antagonist to study the physiological and pathophysiological role of NC in feeding behaviour.

Animals↗
PubMed1996

Palatability-induced hyperphagia increases hypothalamic Dynorphin peptide and mRNA levels.

Opioid involvement in regulating the intake of highly palatable diets was studied by examining the effect of feeding either a cornstarch-based diet (CHO) or a high fat diet containing sucrose (Fat/Sucrose) on hypothalamic opioid levels. Rats received either CHO ad libitum, Fat/Sucrose ad libitum, Fat/Sucrose pair-fed to the caloric intake of CHO, or Fat/Sucrose at 60% of ad libitum Fat/Sucrose intake. Animals receiving Fat/Sucrose ad libitum consumed more calories and gained more weight than animals receiving CHO (P < 0.001). Relative to CHO, ad libitum intake of Fat/Sucrose elevated proDynorphin mRNA levels in the arcuate and Dynorphin A1-17 levels in the paraventricular nucleus (PVN) (P < 0.05), but did not affect arcuate mRNA levels of proEnkephalin or proOpiomelanocortin (POMC), or PVN levels of Met-Enkephalin or beta-Endorphin. Pair-feeding the Fat/Sucrose diet to the level of intake of the CHO diet resulted in levels of proDynorphin and Dynorphin A1-17 that were similar in the two diet groups. Pair-feeding Fat/Sucrose reduced mRNA levels of proDynorpin, proEnkephalin and POMC, and Dynorphin A1-17 levels, relative to ad libitum feeding of Fat/Sucrose. Met-Enkephalin and beta-Endorphin were not affected by dietary treatment. Feeding Fat/Sucrose at 60% of ad libitum intake resulted in mRNA levels of proDynorphin, proEnkephalin and POMC, and Dynorphin A1-17 levels that were similar to those observed in CHO group. Hypothalamic Dynorphin A1-17 and proDynorphin mRNA levels are stimulated by feeding a highly palatable diet rich in fat and sucrose. The increased synthesis may be due in part to a palatability-induced overconsumption of calories. Caloric restriction of the same diet decreases mRNA levels of proDynorphin, proEnkephalin and POMC, as well as levels of Dynorphin A1-17.

Animals↗
PubMed1996

Hyperphagia induced by direct administration of midazolam into the parabrachial nucleus of the rat.

Benzodiazepine receptor agonists increase food intake in many different species, yet there has been little investigation of the central site of actions of these drugs on ingestive behaviour. In the present experiments, direct administration of the benzodiazepine receptor agonist midazolam (3-30 micrograms/microliter) into the parabrachial nucleus of the pons significantly increased the consumption of a wet mash diet and a 3% sucrose solution in adult non-deprived rats. The hyperphagic response was blocked by pre-treatment with the selective benzodiazepine receptor antagonist flumazenil. Injection of midazolam into the parabrachial nucleus had no effect on locomotor activity, despite the fact that in the same animals an increase in mash intake was observed following intra-parabrachial midazolam. These data suggest that benzodiazepine receptors located in the parabrachial nucleus may be an important site of action for the effects of benzodiazepines specifically on ingestive behaviour.

Analysis of Variance↗
PubMed1990

Adaptive hyperphagia in patients with postsurgical malabsorption.

The specific nutritional consequences of malabsorption after small-bowel surgery were studied in a consecutive series of 48 ambulatory patients who had had small-bowel resection (n = 43) or bypass (n = 5) and in 10 patients who had an ileal pouch (n = 10). The patients received a 3-day standardized oral regimen providing daily 30 kcal/kg of ideal body weight (IBW). Throughout the study, 41 patients had malabsorption (fecal fat greater than 5%); 17 had fecal fat less than 5% and served as controls. The malabsorption patients absorbed 70% of protein and 71% of fat. Twenty-one were normonourished and 20 had features of mild energy malnutrition, vs. 15 and 2 controls, respectively. Compared with controls, malabsorption patients had decreased body weight and triceps skin-fold but no features of protein malnutrition. their mean daily food intake at home was significantly enhanced (39.6 +/- 13.1 kcal/IBW kg) vs. controls (28.8 +/- 5.8 kcal/IBW kg, P less than 0.001). In the malabsorption group, caloric intake was higher in the normonourished patients than in those with mild malnutrition. This study shows that a chronic malabsorption has limited nutritional consequences. The patients compensate for their absorptive handicap by increasing their oral intake.

Absorption↗
PubMed1984

Influence of diet form on the hyperphagia-promoting effect of polysaccharide in rats.

Adult female rats were fed chow only, or chow plus the polysaccharide Polycose presented as a solution (32% w/v), as a powder, or as a powder mixed into the chow diet. The rats fed the Polycose solution overate and gained three times as much weight as did the control rats in the 30-day test period. The rats fed the Polycose powder or mixed diet, on the other hand, did not differ from controls in food intake or weight gain. The solution-fed rats consumed more Polycose than did the powder-fed rats, but the two groups were equivalent in their chow intake. The absolute and percent body fat of the solution-fed rats exceeded that of control rats, as well as that of powder and mixed-diet animals. The percent body fat of the powder and mixed-diet groups exceeded that of the control animals. The findings demonstrate that the form of diet presentation has a major impact on the rat's feeding and body weight responses to polysaccharide diets.

Adipose Tissue↗
PubMed1984

Food intake during tumor growth: anorexia in genetically obese ob/ob mice and hyperphagia in lean mice.

Recent findings indicate that obese (ob/ob) mice suffer a low incidence of lung metastasis and survive longer than lean (+/?) littermates following injection with B16 melanoma cells [34]. The present study examined the food intake of obese and lean mice during the growth of this tumor. Mice from both groups increased their food intake by small and approximately equal amounts during the first three quarters of the survival period following injection with 10(6) cells, and body weights remained fairly stable. During the final quarter, however, obese mice became anorexic whereas lean mice became intensely hyperphagic; body weights changed accordingly. Thus, food intake is differentially affected by tumor growth in this form of genetic obesity.

Animals↗
PubMed1986

Medial hypothalamic lesions in Syrian hamsters: characterization of hyperphagia and weight gain.

Syrian golden hamsters (Mesocricetus auratus) received bilateral lesions aimed at the ventromedial hypothalamus (VMH) or a sham lesion. In the first study, some of the animals in each surgical group were housed in standard sedentary conditions while others had free access to running wheels. The lesions produced a 30% increase in the daily intake of chow, and this was accomplished exclusively by increased meal sizes. As a result, lesioned hamsters gained body weight relative to controls both on the chow diet and in a subsequent high fat diet phase. The effects were comparable in both sedentary and exercising groups. The lesions produced increases in body length and fat content. In the second study, lesions were made in the VMH or in adjacent nuclei and, after an initial period on chow, the hamsters were then given a choice between chow and high fat diet. The lesioned hamsters showed no unusual preference for the high fat diet but, as before, those with damage to the VMH or paraventricular nucleus (PVN) showed exaggerated body weight gain. Hamsters with these lesions were hyperinsulinemic in both fed and fasted conditions at the end of the study.

Animals↗
PubMed1988

Sucrose-induced hyperphagia and obesity in rats fed a macronutrient self-selection diet.

Adult female rats were allowed to self-select their diet from separate sources of fat, protein, and carbohydrate (starch). Other rats were fed a composite diet that matched the nutrient composition chosen by the self-selecting rats (50% fat, 28% protein, 22% carbohydrate) or a low-fat, high-carbohydrate chow diet. Half of the rats in each diet condition were given access to a 32% sucrose solution for 30 days. Sucrose availability increased total caloric intake (approximately 20%) and body weight gain in all three groups compared to control groups not fed the sucrose solution. The selection animals compensated for their sucrose intake by reducing their fat intake, and to a lesser degree, their starch intake; protein intake was the least affected by sucrose availability. The selection rats consumed less sucrose than the chow-fed rats and displayed a smaller increase in weight, relative to controls, than the chow-fed rats. These differences were attributed to the high-fat intake of the selection animals since similar results were obtained with the rats fed the composite diet. In particular, both the selection and composite diets produced mild obesity in the absence of sucrose. The results demonstrate that sucrose-induced overeating and overweight is not an artifact of restraining the diet choices of rats to a pure sugar and a nutritionally complete diet.

Animal Nutritional Physiological Phenomena↗
PubMed1993

Suppression of peptide YY-induced hyperphagia by terbutaline.

Central administrations of neuropeptide Y and peptide YY (PYY) produce robust increases in food intake, and this response may be contingent upon the availability of insulin. In contrast, beta 2-adrenergic agonists decrease food intake, and this effect also appears to be dependent on circulating insulin. To investigate a possible interaction between PYY and beta 2-adrenergic function, rats were given systemic injections of terbutaline, a beta 2 agonist, at doses of 0, 5, 10, and 50 mg/kg prior to injections of 0.57 nmol PYY in the paraventricular nucleus of the hypothalamus. Terbutaline pretreatment significantly decreased feeding elicited by PYY in a dose-dependent fashion. This suggests that beta 2-adrenoreceptor activity is involved in PYY-induced feeding.

Adrenergic beta-Agonists↗
PubMed1992

Resistance to insulin-induced hyperphagia in fat-preferring rats.

Outbred male Sprague-Dawley rats were screened for their macronutrient (fat, carbohydrate and protein) preference profile and divided into two groups, the low- and high fat-preferring groups each deriving 23% and 72% of its total caloric intake from fat respectively. Subcutaneous administration of bovine insulin (6U/kg) resulted in an increase in total caloric intake in the low, but not the high fat-preferring group. Furthermore, the increased caloric intake in the low fat-preferring group was entirely due to increased carbohydrate consumption. These data suggest a defect in the action of insulin in fat-preferring rats.

Animals↗
PubMedDate not supplied

Intracerebroventricular injection of ostrich beta-endorphin to satiated pigeons induces hyperphagia but not hyperdipsia.

Satiated pigeons received intracerebroventricular injections of either ostrich (0.06, 0.3 and 1.5 nmoles) or human (0.06 and 1.5 nmoles) beta-endorphin, or a control solution, and their consumption of food and water was monitored during the half hour after these treatments. At each administered dose, ostrich beta-endorphin enhanced food without altering water intake. By contrast, human beta-endorphin did not induce any reliable alteration either of feeding or drinking. Together with previous studies performed in pigeons with opiate antagonists, these results suggest that the feeding system of pigeons is modulated by an endorphinergic mechanism. By contrast, no evidence exists so far that such a mechanism operates for controlling drinking, as appears to be the case in mammals.

Animals↗