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)

Repetitive intermittent immobilization stress has been shown to induce an improved cold tolerance through an enhanced capacity of nonshivering thermogenesis (NST). In the present study, effects of immobilization (3 hrs daily for 4-5 weeks), exercise training (running with treadmill 30 min daily, 30 m/min under 8 degrees inclination for 4-5 weeks) and chronic corticosterone treatment (subcutaneous injection at a dose of 0.3 mg/100 g for 4-5 weeks) were investigated on in vitro and/or in vivo thermogenesis of rat interscapular brown adipose tissue (BAT). BAT thermogenesis in vitro was measured in the minced tissue blocks in Krebs-Ringer phosphate buffer using a Clark type oxygen electrode. DNA content per whole BAT pad was greater in the stressed rats, while it was not affected by exercise training and corticosterone. Noradrenaline-and glucagon-stimulated oxygen consumptions were significantly greater in the stressed rats, while significantly smaller in the trained rats as compared with respective controls. Corticosterone treatment failed to affect those values in terms with both per mg tissue and per whole tissue pad, except the less noradrenaline-stimulated oxygen consumption in terms with per mg tissue and DNA. In vivo thermogenesis was assessed by the changes of temperatures in colon (Tcol), BAT (TBAT) and tail skin (Tsk) induced by noradrenaline or glucagon infusion under anesthesia Noradrenaline and glucagon increased the TBAT and the extent of increase was greater in the stressed rats. These results indicated: 1. Repetitive immobilization stress induces the tissue hyperplasia and enhances thermogenic activity of BAT. 2. Exercise training suppresses BAT thermogenesis. 3. Chronic corticosterone administration does not affect BAT thermogenesis. It may be concluded that the enhancing or suppressing effect of nonthermal stress on BAT thermogenesis is due to other factor(s) than corticosterone.
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PMID:[Effects of nonthermal stresses on brown adipose tissue thermogenesis]. 151 57

Pancreastatin, a novel peptide recently isolated from porcine pancreas, significantly inhibits insulin and somatostatin release and augments glucagon release from the isolated perfused rat pancreas. This implies a role for endogenous pancreatic pancreastatin in the regulation of blood glucose and free fatty acids, the two major metabolic fuels. Since many peptides have similar biological effects when administered centrally and peripherally, the effects of centrally administered pancreastatin on blood glucose and free fatty acids were examined in 3 studies. Corticosterone was also measured in two of these studies. Intraventricular microinfusion of pancreastatin significantly elevated blood glucose, free fatty acid, and corticosterone concentrations in a dose-related manner. None of these effects was seen after subcutaneous injection of the same doses. Centrally administered pancreastatin appears to produce its effects on glucose and free fatty acids through actions in the brain, and either the brain, the median eminence, and/or pituitary for corticosterone.
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PMID:Intracranial microinfusion of pancreastatin elevates blood glucose, free fatty acids, and corticosterone in rats. 272 Apr 11

Hyperglycemia-inducing hyperosmolality has recently been proven beneficial in the maintenance of blood volume and extracellular fluid volume during early hemorrhagic hypotension. Fed animals benefitted from better plasma refill compared with starved ones when subjected to equal blood loss. Using lightly sedated fed and 24-30 h starved rats, hormones with relevance to glucose homeostasis were studied during 90 min of hemorrhagic hypotension of 70 mmHg (1 mmHg = 133.32 Pa). Marked differences in the overall hormonal developments were found between the two groups. In fed rats, insulin and glucagon responses were initially attenuated, while somatostatin increased to an early peak level at 30 min, returning to basal at 90 min. In starved rats, somatostatin increased gradually during the 90 min. Adrenaline release was massive in both groups. Corticosterone showed no increase from basal levels in the fed group during hemorrhage, while starved rats increased their basal level fourfold already at 30 min. These data are presented as evidence that changing nutritional status alters hormonal response to hypovolemic stress.
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PMID:Nutritional status and endocrine response to hemorrhage. 287 24

Fetal pancreatic islets were cultured using a recently described technique (1). After 1 day in culture, half of the plates were continued in control medium and half were grown in identical medium supplemented with corticosterone (0.1 microgram/ml). Media were renewed daily, and culture was continued for a total of 8 days. Insulin, glucagon, and somatostatin contents in the media were determined daily. These hormones were also estimated in the tissue at the time of plating, and after 1 and 8 days in culture. Islets were fixed on day 8, and the cells containing each of these hormones were identified by immunocytochemical staining. Corticosterone supplementation of the medium resulted in a 3-fold increase in the somatostatin concentration of the medium. The insulin and glucagon contents of the supplemented medium were slightly reduced. On day 8, there was no difference in the insulin content of the cultured tissue regardless of medium. The glucagon and somatostatin contents of the tissue grown in the steroid-supplemented medium were greater (1.8- and 3.1-fold, respectively) than those of the tissue grown in control medium. D cells were rare in the islets grown in control medium volume density, 0.4%, but were more numerous in the islets maintained in supplemented medium (2.2%). Islets grown in corticosterone-supplemented medium lacked an insulin secretory response to 22 mM glucose. These findings indicate that the volume densities of the cells within the islets can be altered during an 8-day period in culture, suggesting that nutritional and other requirements of the individual subpopulations of islet cells may be different. In addition, corticosterone may prevent the maturation of the secretory responsiveness of cultured B cells to glucose.
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PMID:Tissue culture of fetal rat islets: corticosterone promotes D cell maintenance and function. 611 36

We investigated 1) the effect of immobilization stress on glucose metabolism in rats after sham operation (SHAM), adrenomedullectomy (ADMX), and adrenalectomy (ADX); and 2) the effect of glucoregulatory hormone infusion on plasma glucose using untreated normal fasted and fed rats under unanesthetized conditions. In immobilization stress, the plasma glucose concentration increased only in the SHAM group during fasting, while under fed conditions, all three groups showed significant increases (SHAM > ADMX > ADX). Plasma glucagon and norepinephrine significantly increased in all groups; plasma epinephrine increased only in the SHAM group, and plasma corticosterone increased in SHAM and ADMX groups under both conditions. The hepatic glycogen content in all fed groups significantly decreased after immobilization stress, while a very low content before stress and an undetectable level after stress were observed in all fasted groups. Only epinephrine infusion increased plasma glucose during fasting, while epinephrine and glucagon infusion increased it under fed conditions. Corticosterone infusion did not change it under either condition. These results suggest that in the fasted condition, only epinephrine plays an essential role, while under fed conditions, glucagon and corticosterone as well as epinephrine also act as synergistic factors in stress-induced hyperglycemia.
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PMID:Glucoregulatory hormones in the immobilization stress-induced increase of plasma glucose in fasted and fed rats. 847 65

Acute administration of neuropeptide Y(NPY) into the hypothalamus and cerebral ventricles can stimulate insulin secretion in the absence of available food. However, the relationship of this effect to blood glucose and other hormones which regulate glucose metabolism remains unclear. The purpose of this study was to compare the effects of NPY injected into the third ventricle (ICV) on serum insulin, glucose, glucagon, corticosterone and non-esterified fatty acids. Studies were performed on conscious, unrestrained female rats, not given access to food. ICV NPY, 2 and 5 micrograms produced an increase in serum insulin and glucagon, while the 5 micrograms dose only increased plasma glucose transiently and increased non-esterified fatty acids for a longer period. Corticosterone was not affected by ICV NPY. The insulinaemic response to i.v. glucose, 0.5 g/kg was doubled by ICV NPY, 4 micrograms. The maximal insulin levels were 113 +/- 18 for ICV NPY versus 67 +/- 8 microU/ml for ICV saline-treated animals. The glycaemic response was not altered. The hypoglycaemic response to i.v. insulin, 0.15 U/kg was significantly attenuated by ICV NPY, 5 micrograms. We concluded that ICV NPY promotes insulin secretion in the absence of available food and may potentiate the insulinaemic response to hyperglycaemia. Furthermore, possibly through its effects on glucagon and non-esterified fatty acids, ICV NPY may decrease the ability of insulin to control glucose metabolism.
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PMID:Some acute effects of intracerebroventricular neuropeptide Y on insulin secretion and glucose metabolism in the rat. 884 19

The circadian food entrainable oscillator (FEO) mediates an increase in activity preceding access to periodic meals. The FEO is anatomically independent of the suprachiasmatic nucleus (SCN), but its locus remains to be established. Whether the FEO is located in the central nervous system (CNS) or in the periphery, it seems reasonable to assume that there is a link of communication between the digestive system and the CNS because only nutritive meals entrain the FEO. Subdiaphragmatic vagotomy and visceral deafferentation with capsaicin do not eliminate food-anticipatory activity (FAA), indicating that a neural signal is not necessary. The present study investigates the hypothesis that humoral signals from the digestive system act upon the CNS to trigger or entrain FAA. Intact rats and rats with SCN lesions were entrained to daily meals and then sacrificed prior to FAA or during FAA, but before meal access. Average plasma concentrations of glucose and insulin were nearly identical in both groups. Plasma and duodenal mucosal motilin concentrations also were not different between the two times. Corticosterone was elevated during anticipation, but the difference was not statistically reliable. Glucagon concentration was decreased during FAA compared to concentration prior to FAA in both intact and SCN-lesioned subjects. This difference was not observed in control rats fasted for the same number of hours, but not previously entrained to a daily meal. Although the decrease in glucagon could be a signal that initiates FAA, a causal role remains to be established.
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PMID:Plasma glucagon, glucose, insulin, and motilin in rats anticipating daily meals. 1033 59

Hypoglycemia provokes a multifaceted counterregulatory response involving the sympathoadrenal system, stimulation of glucagon secretion, and the hypothalamo-pituitary-adrenal axis that is commonly impaired in diabetes. We examined whether modulation of inhibitory input from gamma-aminobutyric acid (GABA) in the ventromedial hypothalamus (VMH), a major glucose-sensing region within the brain, plays a role in affecting counterregulatory responses to hypoglycemia. Normal Sprague-Dawley rats had carotid artery and jugular vein catheters chronically implanted, as well as bilateral steel microinjection guide cannulas inserted down to the level of the VMH. Seven to 10 days following surgery, the rats were microinjected with artificial extracellular fluid, the GABA(A) receptor agonist muscimol (1 nmol/side), or the GABA(A) receptor antagonist bicuculline methiodide (12.5 pmol/side) before being subjected to a hyperinsulinemic-hypoglycemic (2.5 mmol/l) glucose clamp for 90 min. Following VMH administration of bicuculline methiodide, glucose infusion rates were significantly suppressed, whereas muscimol raised glucose infusion rates significantly compared with controls. Glucagon and epinephrine responses were elevated with the antagonist and suppressed with the agonist compared with controls. Corticosterone responses, however, were unaffected by either administration of the agonist or antagonist into the VMH. These data demonstrate that modulation of the GABAergic system in the VMH alters both glucagon and sympathoadrenal, but not corticosterone, responses to hypoglycemia. Our findings are consistent with the hypothesis that GABAergic inhibitory tone within the VMH can modulate glucose counterregulatory responses.
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PMID:Blockade of GABA(A) receptors in the ventromedial hypothalamus further stimulates glucagon and sympathoadrenal but not the hypothalamo-pituitary-adrenal response to hypoglycemia. 1656 32

Hexose-6-phosphate dehydrogenase (EC 1.1.1.47) catalyzes the conversion of glucose 6-phosphate to 6-phosphogluconolactone within the lumen of the endoplasmic reticulum, thereby generating reduced nicotinamide adenine dinucleotide phosphate. Reduced nicotinamide adenine dinucleotide phosphate is a necessary cofactor for the reductase activity of 11beta-hydroxysteroid dehydrogenase type 1 (EC 1.1.1.146), which converts hormonally inactive cortisone to active cortisol (in rodents, 11-dehydrocorticosterone to corticosterone). Mice with targeted inactivation of hexose-6-phosphate dehydrogenase lack 11beta-hydroxysteroid dehydrogenase type 1 reductase activity, whereas dehydrogenase activity (corticosterone to 11-dehydrocorticosterone) is increased. We now report that both glucose output and glucose use are abnormal in these mice. Mutant mice have fasting hypoglycemia. In mutant primary hepatocytes, glucose output does not increase normally in response to glucagon. Mutant animals have lower hepatic glycogen content when fed and cannot mobilize it normally when fasting. As assessed by RT-PCR, responses of hepatic enzymes to fasting are blunted; enzymes involved in gluconeogenesis (phosphoenolpyruvate carboxykinase, tyrosine aminotransferase) are not appropriately up-regulated, and expression of glucokinase, an enzyme required for glycolysis, is not suppressed. Corticosterone has attenuated effects on expression of these enzymes in cultured mutant primary hepatocytes. Mutant mice have increased sensitivity to insulin, as assessed by homeostatic model assessment values and by increased glucose uptake by the muscle. The hypothalamic-pituitary-adrenal axis is also abnormal. Circulating ACTH, deoxycorticosterone, and corticosterone levels are increased in mutant animals, suggesting decreased negative feedback on the hypothalamic-pituitary-adrenal axis. Comparison with other animal models of adrenal insufficiency suggests that many of the observed abnormalities can be explained by blunted intracellular corticosterone actions, despite elevated circulating levels of this hormone.
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PMID:Abnormalities of glucose homeostasis and the hypothalamic-pituitary-adrenal axis in mice lacking hexose-6-phosphate dehydrogenase. 1765 60

Corticosterone and insulin play complex roles in the amount and composition of calories ingested, and the utilization and deposition of this energy. Understanding the interplay of these two hormones is complicated because increasing concentrations of corticosterone dose-dependently increase circulating insulin levels. We addressed individual contributions of each hormone by controlling, at steady-state levels, corticosterone (by adrenalectomy and exogenous replacement) and insulin (by streptozotocin-induced destruction of pancreatic beta-cells and exogenous replacement) across a spectrum of concentrations in rats, creating 8 hormonal combinations. For 5 days after surgery, all rats received chow. At day 5, they were subdivided into those that continued to receive chow and those that had a choice between chow, lard, and 32% sucrose for a further 5 days. During the choice/chow period, total calories ingested were stimulated by corticosterone and choice diet, and subject to a corticosterone-insulin interaction. Sucrose, but not lard, intake was stimulated by insulin. Body weight was increased by insulin, decreased by high corticosterone, and unaffected by diet. White adipose tissue depot weights were stimulated by insulin, corticosterone, and diet. Plasma triglycerides, free fatty acids, total ketone bodies, glucose, and glycerol were all significantly increased by corticosterone and the choice diet but inhibited by insulin. In contrast, plasma leptin was only increased by insulin and diet, plasma glucagon and liver glycogen was only affected by insulin and liver triglycerides, and arcuate nucleus proopiomelanocortin mRNA was only influenced by diet. Collectively, these data show that corticosterone and insulin determine the intake, form, and compartmentalization of energy both independently and interactively.
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PMID:Disengaging insulin from corticosterone: roles of each on energy intake and disposition. 1927 89


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