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)

A 30% body surface area, open-flame, full-thickness burn of adult rats induced a 4-day period of anorexia that was followed by hyperphagia beginning on postburn day 10. The hyperphagic burned rats also exhibited increased resting energy expenditure and no gain in body weight, suggesting hypermetabolism. Plasma levels of immunoreactive insulin and albumin were decreased in both groups of burned rats; immunoreactive pancreatic glucagon concentrations were elevated only in the anorectic burned rats. Plasma levels of epinephrine were elevated in the hyperphagic burned rats. In the brain, dopamine metabolism appeared to be increased in the corpus striatum, nucleus accumbens, and amygdala of anorectic burned rats; norepinephrine levels were elevated in the hypothalamus and nucleus accumbens of the hyperphagic-hypermetabolic rats. These data indicate that this animal model of major burn trauma exhibits anorexia, hyperphagia, catabolism, and hypermetabolism. Furthermore, elevated dopamine metabolism appears to be associated with the anorexia, while the hyperphagia-hypermetabolism may be mediated by norepinephrine.
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PMID:Burn-induced alterations in feeding, energy expenditure, and brain amine neurotransmitters in rats. 357 6

The hypothesis that epinephrine (EPI) and pancreatic glucagon (PG) inhibit feeding by activating a common physiological satiety mechanism was tested by comparing the two agents' behavioral effects. In several tests of specificity, EPI and PG had functionally different inhibitory actions. Intraperitoneal injection of 6.25-50 micrograms/kg EPI and 100-400 micrograms/kg PG elicited overlapping dose-related inhibitions of intake of milk diet in rats maintained ad lib on pelleted chow. Twenty-five to 50 micrograms/kg EPI also elicited anomalous behaviors that are not normally associated with feeding, including supine postures with limbs extended and crawling with trunk dorsoflexed and abdomen pressed against cage floor. EPI elicited similar anomalous behaviors in rats that either sham fed with open gastric cannulas, drank after water deprivation, or were presented neither food nor water. Fifty to 200 micrograms/kg EPI also inhibited water intake in the thirsty rats, and 25-50 micrograms/kg EPI inhibited sham feeding. PG, in contrast, neither elicited anomalous behaviors nor inhibited water intake nor inhibited sham feeding. These data demonstrate that the inhibitory actions of exogenous EPI and PG are functionally dissociable. We conclude that 25-200 micrograms/kg EPI acts nonspecifically to produce anorexia and adipsia, while PG elicits postprandial satiety.
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PMID:Epinephrine inhibits feeding nonspecifically in the rat. 361 47

A 29-year-old nullipara was admitted at 31 weeks' gestation because of toxemia. She noted gradually polyuria, severe thirst, malaise, nausea and anorexia. A water-deprivation test and administration of aqueous vasopressin confirmed the diagnosis of nephrogenic diabetes insipidus. At 33 weeks' gestation, blood chemistry studies revealed moderately elevated transaminase levels and hyperuricemia. Male twins were delivered by vacuum extraction at 35 weeks' gestation. After delivery, she became drousy and icterus appeared. Acute hepatic failure with marked hyperuricemia was diagnosed. She was treated with glucose solution with glucagon and soluble insulin, branched chain amino acids, gabexate mesilate, lactulose and famotidine. Her consciousness cleared rapidly and all laboratory data became normal by 15 days postpartum. The urine volume was about 5 liters per day from the first to sixth postpartum day. The diuresis decreased after the eighth postpartum day. Rare pregnancy complicated by transient nephrogenic diabetes insipidus and acute hepatic failure is discussed.
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PMID:Transient nephrogenic diabetes insipidus associated with acute hepatic failure in pregnancy. 365 42

Three experiments were conducted to assess the effects of magnesium deficiency on the activities of hepatic glucose-6-phosphatase (G6Pase), fructose 1,6-bisphosphatase (FDPase) and phosphoenolpyruvate carboxykinase (PEPCK). Experiment 1 was designed to determine if magnesium deficiency interfered with the gluconeogenic response to fasting. Rats were fed either a control (C) or magnesium-deficient (MD) diet for 12 days. One-half of each group of rats was fasted for 24 hours prior to death. Hepatic enzyme activities, plasma and liver magnesium, and whole blood glucose were measured. Activities of G6Pase and PEPCK were higher in fasted group C rats compared to fed group C rats. Activity of FDPase was lower. The response was similar in the MD groups. Comparison of C and MD groups indicated that magnesium deficiency was accompanied by an increase in PEPCK activity. To verify this result and to investigate the role of anorexia in producing increased PEPCK activity, experiment 2 included a pair-fed group (PF). The results indicated that anorexia was not responsible for increased PEPCK activity in MD rats. The relation of circulating insulin and glucagon concentrations to effects of magnesium deficiency was explored in experiment 3. A decreased insulin:glucagon ratio was observed in MD rats. The results of these experiments suggest that magnesium deficiency alters PEPCK activity by affecting secretion of pancreatic hormones.
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PMID:Hepatic gluconeogenic enzymes, plasma insulin and glucagon response to magnesium deficiency and fasting. 627 7

In order to ascertain direct central anorectic actions of mazindol (MZD), subtle changes in meal patterns and endogenous feeding related chemical substances were examined in rats following intra-third ventricle injection of 0.03 mumole MZD. In ad lib feeding, MZD decreased meal size and prolonged postprandial intermeal interval during a 4 hr period starting 2 hr after injection. The magnitude of anorectic actions of MZD was depressed by hunger. Although the action of MZD is short in duration, long duration anorexia was achieved by chronic infusion for 8 days. Infusion of MZD starting at 5:50 p.m. decreased plasma insulin, leaving glucose and glucagon unaffected, although no change in plasma glucose or insulin was observed following injection at 11:30 a.m. These findings, together with other reports, can be explained by MZD's direct effects on the hypothalamic hunger and satiation centers.
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PMID:Changes in meal pattern and endogenous feeding related substances following mazindol administration. 638 20

cis-Dichlorodiammineplatinum (cis-Pt) is a heavy metal complex used in cancer chemotherapy. Since this drug has been shown to induce hyperglycemia in rats, these studies were initiated to elucidate the effects of cis-Pt on carbohydrate tolerance and insulin and glucagon secretion. Two days following i.v. cis-Pt (2.5 or 7.5 mg/kg, 5 ml/kg) or vehicle administration to male F-344 rats, plasma glucose, immunoreactive insulin (IRI) and glucagon (IRG) concentrations were determined in the basal state and serially following a glucose load (2 g/kg, i.p.). Since cis-Pt induces a dose-related anorexia, a pair-fed control group was also studied. Administration of 7.5 mg/kg cis-Pt was associated with plasma glucose concentrations 2.5-5 times greater than ad-libitum and pair-fed controls at every time point during the 2-h glucose tolerance test. Although basal plasma IRI concentrations of the 7.5-mg/kg group were comparable to ad-libitum fed controls, they were significantly greater than those of pair-fed partners. Furthermore, the appropriate IRI response to a glucose stimulus observed in both controls and the 2.5-mg/kg group was absent in the 7.5-mg/kg group. Basal plasma IRG concentrations of the 7.5-mg/kg group were approximately 3-4 times greater than ad-libitum and pair-fed controls and were not suppressed following a glucose load. These results suggest that cis-Pt induces marked glucose intolerance in association with an impaired IRI response and abnormal glucagon response to a glucose stimulus.
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PMID:Glucose intolerance following cis-platinum treatment in rats. 676 98

We studied a patient with lung cancer, who exhibited severe systemic derangements of metabolism causing cachexia preceding the appearance of a large bulky tumor. The data described herein left no doubt that lung cancer growing in the patient acted as a powerful hypoglycemic factor, setting in motion widespread metabolic disorders. Inappropriate secretion of insulin may be involved in the manifestation of hypoglycemia. However, no ectopic secretion of insulin, glucagon, ACTH and aldosterone appeared to be associated with the carcinoma in the patient. From the present and previous observations, it is stressed that progressive energy loss from the patient occurs by virtue of a combination of severe anorexia and the establishment of a systemic energy-losing cycle dependent on an interplay of glycolysis in the cancer cells and stimulated gluconeogenesis in the host tissues, which in turn results in derangements of protein, lipid and electrolyte metabolism. Attempts to ameliorate the patient's distress and counterbalance the effect of the tumor by parenteral hyperalimentation were not satisfactory and resulted in only a temporary improvement. This study also demonstrated that marked granulocytosis was the result of production of an excess granulopoietic colony stimulating activity by the cancer cells.
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PMID:Hypoglycemia, hypopotassemia and hyperleukocytosis associated with squamous cell carcinoma of the lung. 697 22

Previous experiments suggest that experimental cancer-induced anorexia is associated with hyperammonemia and that daily injections of insulin may attenuate the anorexia for several days. In the present study, we determined whether similar daily insulin treatments would correct anorexia induced by the infusion of ammonium salts and compared this feeding response with that of insulin-treated tumor-bearing (TB) rats. Daily treatment of control and anorectic TB rats with systemically administered insulin for six days increased feeding in all control rats and 40% of the TB rats. All insulin-treated groups exhibited equal degrees of hypoglycemia irrespective of anorexia. Basal concentrations of lactate and glucagon were elevated in saline-treated TB rats. Plasma lactate levels were normalized by insulin treatment, whereas glucagon was normalized only in the TB rats that fed to insulin and increased further in TB rats that did not feed to insulin. Elevated hypothalamic tyrosine was reduced in insulin-treated TB rats that ate, and 5-hydroxy-indoleacetic acid was increased further when the rats did not eat. Insulin also blocked anorexia resulting from the intravenous infusion of ammonium salts. Hypothalamic concentrations of tyrosine and tryptophan were increased by the ammonia infusion and reduced significantly in insulin-treated infused rats. These results indicate that insulin treatment can reverse experimental cancer-induced anorexia and hyperammonemia-induced anorexia. Neurochemical changes associated with these treatments are also similar, but not identical.
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PMID:Insulin reverses ammonia-induced anorexia and experimental cancer anorexia. 752 Oct 32

Substantial in vitro evidence suggests that nitric oxide may be a major mediator of interleukin 1 (IL-1) induced pancreatic beta-cell inhibition and destruction in the initial events leading to insulin-dependent diabetes mellitus. Using NG-nitro-L-arginine methyl ester, an inhibitor of both the constitutive and the cytokine inducible forms of nitric oxide synthase, and aminoguanidine, a preferential inhibitor of the inducible form of nitric oxide synthase, we investigated the impact of inhibiting nitric oxide production on food-intake, body weight and temperature, blood glucose, plasma insulin, glucagon, corticosterone and leukocyte- and differential-counts in normal rats injected once daily for 5 days with interleukin 1 beta (IL-1 beta) (0.8 microgram/rat = 4.0 micrograms/kg). Inhibition of both the constitutive and the inducible forms of nitric oxide synthase prevented IL-1 beta-induced fever, hyperglycaemia, hypoinsulinemia, and hyperglucagonemia, and partially prevented lymphopenia and neutrophilia, but had no effect on IL-1 beta-induced anorexia and changes in plasma corticosterone. Preferential inhibition of the inducible form of nitric oxide synthase using two daily injections of 5 mg/rat of aminoguanidine prevented IL-1 beta-induced hyperglycaemia and hypoinsulinaemia, and slightly reduced the pyrogenicity of IL-1 on 3 out of 5 days. Higher doses of aminoguanidine (100 mg/rat) prevented lymphopenia and neutrophilia. We conclude that nitric oxide produced by the inducible form of nitric oxide synthase, mediates the IL-1 beta-induced inhibition of insulin release and that the effect of IL-1 beta on temperature, pancreatic alpha-cells, and leukocyte differential counts seems to be mediated by nitric oxide produced by the constitutive form of nitric oxide synthase.
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PMID:Interleukin 1 beta induces diabetes and fever in normal rats by nitric oxide via induction of different nitric oxide synthases. 753 59

We have previously shown that spontaneous physical exercise can delay onset of experimental anorexia and cachexia, and retard tumour growth; we now report the effects on insulin sensitivity, hormonal levels and skeletal muscle protein metabolism. Insulin sensitivity determined with a euglycaemic hyperinsulinaemic clamp revealed a normalised glucose disposal rate in tumour-bearing exercising (TBE) versus sedentary (TBS) animals (TBE 15.55 +/- 2.71 versus TBS 2.47 +/- 2.12 mg/kg/min; P < 0.05). Both TBE and TBS animals had decreased levels of corticosterone during the clamp. Serum levels of insulin during tumour progression were unaffected by exercise, but the insulin: glucagon ratio increased and the progressive decrease in rT3 was attenuated. The concentration of glucagon decreased in both tumour-bearing groups during the experiment, while TBE animals showed a relative reduction in corticosterone. Capacity for skeletal muscle protein synthesis, expressed as RNA: protein ratio, was normalised in TBE animals in two tumour protocols (TBE 5.9 +/- 0.6 versus TBS 4.7 +/- 0.3; TBE 2.9 +/- 0.4 versus TBS 1.8 +/- 0.2; P < 0.05, respectively). Incorporation rate of 14C-phenylalanine into skeletal muscle protein was increased in the TBE group in vitro and in vivo. In the postexercise period, protein degradation evaluated by tyrosine release in vitro was increased, but decreased over time. This study has confirmed a positive skeletal muscle protein balance in exercising tumour-bearing animals, partly explained by the increased insulin sensitivity. This conclusion was further supported by the less catabolic pattern indicated by hormonal levels.
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PMID:Insulin sensitivity, hormonal levels and skeletal muscle protein metabolism in tumour-bearing exercising rats. 753 77


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