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)

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

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

The effect of a prolonged 5-day fast on the blood concentrations of vasoactive intestinal polypeptide (VIP), secretin, human pancreatic polypeptide (hPP), gastrin, and group I pepsinogens (PG I) was studied in 11 healthy subjects. During the fast there was a marked increase in the concentrations of VIP, secretin, and hPP, whereas the rise in the concentrations of gastrin and PG I was less pronounced. Refeeding suppressed the increased concentration of VIP and caused elevated postprandial concentrations of secretin and hPP, whereas starvation did not influence the postprandial release of gastrin and PG I. The study shows that prolonged starvation has a pronounced effect on gut endocrine responses.
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PMID:The fasting levels and the postprandial response of gastroenteropancreatic hormones before and after prolonged fasting. 666 32

The plasma concentrations of vasoactive intestinal polypeptide (VIP) and secretin and the serum concentration of human pancreatic polypeptide (hPP) were measured in nine healthy subjects during a 4-day fast. The fast induced a considerable increase in the concentrations of VIP and secretin but only a small increase in the concentration of hPP. The intravenous infusion of 50 g glucose and the oral ingestion of 50 g glucose temporarily suppressed the high concentrations of VIP and secretin. Conversely, hPP responded with a slight decrease in blood concentration after the intravenous infusion and with a modest increase after the oral ingestion. The study shows that glucose suppresses the high blood concentrations of VIP and secretin during starvation independent of the route of glucose administration. In addition, the results indicate that the blood concentration of hPP is not directly related to the blood glucose concentration during prolonged fasting.
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PMID:Responses of vasoactive intestinal polypeptide, secretin, and human pancreatic polypeptide to glucose during fasting. 671 78

1. Pancreatic endocrine function has been investigated in thyroidectomized calves given exogenous cortisol (2.0 mg.kg-1.day-1) in order to produce overt signs of diabetes. 2. Whenever this diabetic syndrome was induced it was associated with falling plasma insulin concentrations. A few days later, there was a significant rise in the post-absorptive concentration of both pancreatic glucagon and pancreatic polypeptide (PP) in the arterial plasma. Elevated levels of both hormones invariably persisted until the animals were given thyroxine. 3. Each of the pancreatic endocrine responses to cortisol was reversed by daily administration of thyroxine (25 microgram.kg-1. day-1) and the plasma glucose concentration was restored to normal within a few days. 4. Starvation was found to be an extremely effective way of reducing both the plasma glucose and glucagon concentration of diabetic calves without apparently affecting the concentration of either insulin of PP. 5. Neurally mediated release of insulin in response to 2-deoxyglucose, but not of either pancreatic glucagon or PP, was found to be defective in diabetic calves and recovered in response to thyroxine. 6. These results suggest that the primary defect that leads to the development of this diabetic syndrome in cortisol-treated thyroidectomized calves is failure of insulin release but that this is associated with consequential changes in the rates at which both glucagon and PP are released from the pancreas.
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PMID:Pancreatic endocrine function in cortisol-treated thyroidectomized calves. 703 2

Starvation inhibits and refeeding stimulates transcription of the malic enzyme gene in chick liver. DNA between -320 and +72 base pairs (bp) is DNase I-hypersensitive in hepatic nuclei from fed but not starved chicks (Ma, X. J., and Goodridge, A. G. (1992) Nucleic Acids Res. 20, 4997-5002). A polypyrimidine/polypurine (PPY/PPU) tract lies within the DNase I-hypersensitive region. In hepatocytes transiently transfected with plasmids containing triiodothyronine response elements and a minimal promoter from the malic enzyme gene linked to the chloramphenicol acetyltransferase gene, deletion of the PPY/PPU tract inhibited chloramphenicol acetyltransferase activity by about 90% with or without triiodothyronine. Fine mapping of S1 nuclease-sensitive sites suggests that the PPY/PPU tract can assume different isoforms of non-B-DNA, some of which may be triplex structures. The PPY/PPU tract contains specific binding sites for single- and double-stranded DNA binding proteins and, with 8 bp 3' of the tract, can function as a promoter. A (CT)7 repeat binds single-stranded DNA-binding protein and is essential for promoter activity. Two C-rich elements bind single-stranded DNA-binding proteins and may mediate inhibition of promoter function. The single- and double-stranded DNA-binding proteins that interact with the PPY/PPU tract may regulate transcription of the malic enzyme gene.
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PMID:Characterization of a polypyrimidine/polypurine tract in the promoter of the gene for chicken malic enzyme. 866 63

In this study we investigated comparative morphology of the endocrine pancreas of several species belonging to the family Gekkonidae and apoptotic processes of the pancreas which may be correlated to the seasonal cycle. The following species of the family Gekkonidae were studied: Phelsuma lineata, P. madagascariensis, P. dubia, P. abotti, Gekko gecko, G. vittatus, and Geckonia chazaliae. In all these species the pancreas consisted of large and medium islets as well as endocrine cells which were scattered throughout the acinar cells. Exocrine parenchyma consisted of tubuli-acini. Four mayor cell types were identified in the endocrine pancreas, using immunocytochemistry: glucagon-immunoreactive (A) cells, insulin-immunoreactive (B) cells, somatostatin-immunoreactive (D) cells, and pancreatic polypeptide immunoreactive (PP) cells. In the endocrine pancreas the amount of A cells and B cells was either equal or a prevalence of A cells was observed. In the wet season the pancreatic morphology presented normal features with very rare apoptotic cells. The animals belonging to the genus Phelsuma taken in the dry season (July) showed numerous vacuolated, Caspase 3, 9 and 11-immunoreactive acinar and some endocrine cells containing picnotic nuclei which were positive to tunel reaction. The animals belonging to the genus Gekko taken at the end of the dry season (October) exhibited strongly vacuolated, Caspase 3, 9 and 11-immunoreactive endocrine and some acinar cells containing nuclei which were positive to tunel reaction. These apoptosis events could be a reaction in response to stress mechanisms, such as a starvation period during the dry season.
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PMID:Morphology of the pancreas of some species belonging to the genera Phelsuma and Gecko (family Gekkonidae): evidence of apoptotic process during the seasonal cycle. 1676 10

The current obesity epidemic is fuelled by the availability of highly palatable, calorie-dense food, and the low requirement for physical activity in our modern environment. If energy intake exceeds energy use, the excess calories are stored as body fat. Although the body has mechanisms that act to maintain body weight over time, they primarily defend against starvation and are less robust in preventing the development of obesity. Knowledge of this homeostatic system that controls body weight has increased exponentially over the last decade and has revealed new possibilities for the treatment of obesity and its associated comorbidities. One therapeutic target is the development of agents based on the gastrointestinal hormones that control appetite. This review discusses the hormones oxyntomodulin, peptide YY, glucagon-like peptide 1, pancreatic polypeptide, and ghrelin and their emerging potential as anti-obesity treatments.
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PMID:Can gut hormones control appetite and prevent obesity? 1822 98