Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown that central injection of bombesin produces hypothermia in food-deprived, but not food satiated rats at normal ambient temperatures. The present study evaluated the effects of bombesin on core body temperature (Tb) and feeding behavior in rats pretreated with insulin. Administration of bombesin (0.25, 0.5, and 1.0 microgram) into the lateral cerebral ventricle produced hypothermia in rats injected with insulin (10 U/kg; i.m.). No significant change in core temperature was observed in control rats following bombesin. Insulin treatments significantly stimulated feeding behavior and the highest dose of bombesin significantly reduced feeding behavior. The results demonstrate bombesin-induced hypothermia under metabolic conditions similar to acute starvation. These findings are consistent with the hypothesis that bombesin-induced hypothermia in food-deprived rats is directly related to the fasting state.
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PMID:Bombesin produces hypothermia in insulin treated rats. 266 43

The influence of food deprivation on the release of somatostatin and gastrin from the rat stomach was investigated using an isolated, vascularly perfused rat stomach preparation. Basal and acetylcholine-stimulated gastrin release were significantly lower after a 3 day starvation, whereas the inhibitory effect of acetylcholine and the stimulatory effect of glucagon on somatostatin secretion were not influenced by fasting. In dose-response studies, isoproterenol dose-dependently stimulated somatostatin secretion. The increases were similar in both groups fasted for 12 and 72 h. Gastrin release remained at basal levels. Bombesin dose-dependently increased gastrin secretion; this stimulatory effect on the G cell was significantly reduced after a 72-h starvation. Somatostatin secretion was only weakly stimulated by high concentration of bombesin revealing no effect of fasting. Somatostatin content of the nonperfused stomach declined from 57 +/- 4 pmol/stomach in fed controls to 36 +/- 3 pmol/stomach after a 72-h fast. Antral gastrin concentration decreased by 42% in a 3-day fasting period. It is concluded that rat gastric somatostatin release in vitro is--in contrast to gastrin--not altered by food deprivation while the somatostatin content in gastric tissue declined during fasting.
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PMID:Effect of food deprivation on rat gastric somatostatin and gastrin release. 612 Aug 79

Modulation of feeding by opiates, putative satiety peptides, and dopamine was explored in the Chinese hamster, an animal that develops diabetes mellitus in certain inbred strains. Diabetic hamsters were hyperphagic relative to their nondiabetic controls, but both groups exhibited natural circadian variation in feeding. Starvation provoked hyperphagia of about 1-h duration in both groups. Naloxone and butorphanol had no effects on Chinese hamster feeding. Opiate receptor binding on Chinese hamster brains demonstrated no specific binding of naloxone or ethylketocyclazocine, but IR-dynorphin concentrations were comparable with that in rats. N-allylnormetazocine, a sigma-opiate receptor agonist, appeared to stimulate diabetic hamster feeding. Peptides reputed to have satiety effects in rats were without effect in Chinese hamsters: cholecystokinin, bombesin, somatostatin, and pancreatic polypeptide. Calcitonin limited feeding in both groups but may be nonspecific. Dopaminergic blockade by haloperidol also limited feeding, and diabetic hamsters were more sensitive to this. Although Chinese hamsters clearly can modulate their food intake when diabetic, we conclude that the opiatergic and peptidergic influences on feeding are very different from those in rats and may be of little importance.
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PMID:Feeding systems in Chinese hamsters. 614 21

Endogenous opioid peptides appear to play a role in the initiation of feeding. Butorphanol, an exogenous opiate which preferentially generalizes to the kappa-sigma opiate receptors, is a potent initiator of feeding. In these studies, we examined the effect of peripherally administered putative satiety substances, cholecystokininoctapeptide, somatostatin, bombesin, gastrin-releasing peptide, thyrotropin-releasing hormone, calcitonin and glucagon on butorphanol induced feeding. With the exception of bombesin, all the other putative satiety factors required 2 to 32 times as high a dose to significantly suppress feeding following butorphanol compared to the dosages required to suppress starvation or tail pinch induced feeding. Bombesin appeared to be approximately equipotent in all systems tested. Haloperidol and atropine both suppressed butorphanol induced feeding supporting our previous hypothesis of an integral relationship between acetylcholinergic-dopaminergic and opioid mechanisms in the initiation of feeding. The findings reported here are compatible with an important role for opioid mechanisms in the initiation of feeding.
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PMID:The effect of peripherally administered satiety substances on feeding induced by butorphanol tartrate. 631 70

Because controversy exists as to the interpretation of the known feeding-suppressive effects of various neuropeptides, we attempted to construct a model that could differentiate satiety from other nonspecific effects. Reasoning that a satiety factor should be less inhibiting of feeding in a hungrier animal, whereas aversive agents should be unaffected by hunger, we studied the neuropharmacologic dose responses of five substances administered peripherally to rats at two different degrees of starvation. Included were four neuropeptides with putative satiety effects: cholecystokinin, calcitonin, bombesin, and pancreatic polypeptide, as well as the known aversive agent lithium chloride. In the study, cholecystokinin behaved as we postulated a satiety factor would, showing significant effect of starvation at every dose and in the ANOVA. The aversive agent lithium showed overlapping among the starvation groups and no starvation effect by ANOVA. Calcitonin failed to show differences attributable to starvation. Bombesin produced some overlapping of starvation groups and a barely significant starvation effect by ANOVA. Pancreatic polypeptide produced no feeding suppression in the rat. We conclude that cholecystokinin is a short-term satiety signal and that calcitonin acts peripherally by some nonspecific nonsatiating means. Bombesin's effects are unclear but may be nonspecific.
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PMID:Are peptides truly satiety agents? A method of testing for neurohumoral satiety effects. 666 Mar 34

Subcutaneous administration of insulin(10 U/kg) produced hypoglycemia in rats with a concomitant induction of feeding. The opiate antagonist naloxone failed to alter food ingestion following insulin administration when quantitated over a 3-hour period; however, naloxone (20 mg/kg) significantly suppressed eating during the first hour of the study. Starvation-induced feeding was markedly suppressed by relatively low doses of naloxone (1 mg/kg). The dopamine antagonist haloperidol, the cholinergic antagonist atropine, and the putative satiety factors CCK-8, bombesin, histidyl-proline diketopiperazine and calcitonin suppressed insulin-induced feeding. Naloxone, CCK-8 and bombesin significantly raised blood glucose levels following insulin induced hypoglycemia.
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PMID:Peptidergic control of insulin-induced feeding. 702 93

Mild tail pinch (TP) in rats resulted in 72% of animals displaying ingestive behavior with 20% demonstrating gnawing behavior without food ingestion and 8% demonstrating licking behavior only. The animals ate steadily over 5 min with a maximum rate occurring at 1 min (0.5 +/- 0.2 g). There was a circadian rhythm of TP-induced behavior with the peak food ingestion occurring at 24 h. A mild increase in blood glucose occurred 120 s after commencement of TP (115 +/- 4 mg/dl). Common satiety signals such as stomach distension and glucose decreased food ingestion. Parenteral administration of glucagon, cholecystokinin-octapeptide, bombesin, and thyrotropin-releasing hormone resulted in suppression of TP-induced food ingestion. Chronic TP (12 5-min TP periods/day) resulted in a fall in spontaneous food intake with the total intake remaining similar to food intake prior to the chronic TP period. We suggest that TP serves as an excellent model for eating behavior because 1) it correlates well with starvation-induced eating; 2) it precludes the necessary deprivation of food and water to adrenalectomized animals; and 3) animals subjected to TP continue chewing in the face of decreased food intake allowing one to exclude the possibility that the effects of an anorectic are secondary to nausea.
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PMID:Stress-induced eating in rats. 719 55

G-protein coupled receptor (GPCR) agonists such as neuropeptides activate the insulin-like growth factor-1 receptor (IGF-IR) or the serine-threonine protein kinase Akt, suggesting that neuropeptides-GPCR signaling can cross-communicate with IGF-IR-Akt signaling pathways. Neutral endopeptidase 24.11 (NEP) is a cell-surface peptidase that cleaves and inactivates the neuropeptides endothelin-1 (ET-1) and bombesin, which are implicated in progression to androgen-independent prostate cancer (PC). We investigated the mechanisms of NEP regulation of neuropeptide-mediated cell survival in PC cells, including whether neuropeptide substrates of NEP induce phosphorylations of IGF-IR and Akt in PC cells. Western analyses revealed ET-1 and bombesin treatment induced phosphorylation of IGF-IRbeta and Akt independent of IGF-I in TSU-Pr1, DU145, and PC-3 PC cells, which lack NEP expression, but not in NEP-expressing LNCaP cells. Recombinant NEP and induced NEP expression in TSU-Pr1 cells using a tetracycline-repressive expression system inhibited ET-1-mediated phosphorylation of IGF-IRbeta and Akt, and blocked the protective effects of ET-1 against apoptosis induced by serum starvation. Incubation of TSU-Pr1 cells with specific kinase inhibitors together with ET-1 or bombesin showed that IGF-IR activation is required for neuropeptide-induced Akt phosphorylation, and that neuropeptide-induced Akt activation is predominantly mediated by Src and phosphatidylinositol 3-kinase but not by mitogen-activated protein kinase or protein kinase C. These data show that the neuropeptides ET-1 and bombesin stimulate ligand-independent activation of the IGF-IR, which results in Akt activation, and that this cross-communication between GPCR and IGF-IR signaling is inhibited by NEP.
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PMID:Neutral endopeptidase inhibits neuropeptide-mediated transactivation of the insulin-like growth factor receptor-Akt cell survival pathway. 1130 83