Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nondeprived male Sprague-Dawley rats that were given scheduled access to running wheels for 60 min daily ran immediately and energetically. Intraperitoneal injections of 400 micrograms/kg pancreatic glucagon and 0.15 microgram/kg cholecystokinin octapeptide had no effect on scheduled running, but significantly inhibited feeding when the rats were offered condensed milk instead of access to the running wheels. This is consistent with the hypothesized function of these peptides as postprandial satiety signals. In contrast, 0.5 mg/kg amphetamine and 75 microM/kg LiCl, which produced similar degrees of anorexia, inhibited running by about 50%. Amphetamine, but neither peptide, also inhibited water drinking and disrupted the behavioral sequence of postprandial satiety. The distance run during scheduled running tests was inversely related to body weight, but the patterns of the drugs' effects were not altered by baseline running differences. Scheduled wheel running is a robust consummatory behavior that appears to provide a relatively valid, simple, and sensitive test of the behavioral specificity of pharmacological anorexia.
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PMID:Scheduled running wheel activity indexes the specificity of pharmacological anorexia. 141 67

The effect of satietin and amphetamine on the carbohydrate metabolism of free fed and food deprived rats was studied. Rats deprived of food for 96 hours maintained normal glucose and glucagon blood levels but the blood concentration of insulin dropped from 232.02 +/- 23.93 to 12.48 +/- 0.71 pmol/l. Amphetamine (500 micrograms/animal, intracerebroventricularly) left in normally fed rats the blood concentration of glucose, insulin and glucagon unchanged. The same treatment, however, increased the insulin concentration in the blood of food deprived rats from 11.37 +/- 4.43 to 73.47 +/- 8.29 pmol/l. Glucose and glucagon, as well as insulin levels remained unchanged in both normally fed and food deprived rats when treated with satietin (20 micrograms/rat, intracerebroventricularly). It was concluded that the anorectic effect of satietin is unrelated to carbohydrate metabolism.
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PMID:The anorectic effect of satietin is unrelated to carbohydrate metabolism. 388 46

The discovery of the adiposity signal leptin a decade ago revolutionised our understanding of the hypothalamic mechanisms underpinning the central control of ingestive behaviour. Subsequently, the structure and function of various hypothalamic peptide systems (Neuropeptide Y (NPY), Orexins, Melanocortins, Cocaine and Amphetamine Regulating Transcript (CART), Galanin/Galanin Like Peptides (GALP) and endocannabinoids) have been characterised in detail in rodent models. The therapeutic benefit of targeting these systems remains to be discovered. More is becoming known about the pharmacological potential of peripheral, meal-induced, episodic endogenous peptides. Hormones such as Cholecystokinin (CCK), Gastrin Releasing Peptides (GRP), Glucagon-Like Peptide I (GLP-1) Enterostatin, Amylin, Peptide YY (PYY) and Ghrelin are released prior to, during and/or after a meal, controlling intake and subjective feelings of appetite (hunger and satiety). In addition, there is an expanding body of literature detailing the effects of a wide variety of drugs on human appetite and food intake. Some of these drugs act upon CNS monoamine systems such as Serotonin (5-HT). Dopamine (DA) and Noradrenaline (NA), have long been implicated in appetite regulation. Detailed examination of both the effect of agonising endogenous gut peptide systems and the effect of various monoaminergic drugs on the expression of human appetite can provide a greater understanding of mechanisms underpinning normal appetite regulation. However, such an understanding must be based on knowledge of the effect of the treatment on meal size, eating rate, meal pattern, food choice and the subjective experience of appetite flux (hunger and satiety), and notjust food intake.
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PMID:The pharmacology of human appetite expression. 1505 9

Medications for the treatment of obesity began to appear in the late 19th and early 20th century. Amphetamine-addiction led to the search for similar drugs without addictive properties. Four sympathomimetic drugs currently approved in the US arose from this search, but may not be approved elsewhere. When noradrenergic drugs were combined with serotonergic drugs, additional weight loss was induced. At present there are three drugs (orlistat, phentermine/topiramate and lorcaserin) approved for long-term use and four sympathomimetic drugs approved by the US FDA for short-term treatment of obesity. Leptin produced in fat cells and glucagon-like peptide-1, a gastrointestinal hormone, provide a new molecular basis for treatment of obesity. New classes of agents acting on the melanocortin system in the brain or mimicking GLP-1 have been tried with variable success. Combination therapy can substantially increase weight loss; a promising approach for the future.
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PMID:Medical treatment of obesity: the past, the present and the future. 2519 83