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)

The authors compared the effect of glucagon on the post-heparinic lipolytic activity in normal and alloxan induced diabetic rats. Within their experimental conditions, it was considered that an injury of the cell stimulates a decrease of the glucagon-stimulating activity on the lipoprotein lipase: this hormone does not seem to have a direct action on the PHLA but an indirect one by the way of the insulin secretion it induces.
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PMID:[The influence of glucagon on post-heparin plasma lipolytic activity in normal rats and in rats with diabetes induced by alloxan injection]. 127 70

The study was undertaken to examine the effects of l-carnitine and acetyl-l-carnitine in rats and mice with experimental alloxan diabetes. The findings suggest that acetyl-l-carnitine is more effective against diabetes in increasing glucose tolerance, restoring the impaired response of glucagon to glucose, showing glycogen-sparing action than is l-carnitine.
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PMID:[The action of carnitine-series preparations in experimental alloxan diabetes mellitus]. 145 84

Outbred Wistar rats were randomly assigned to three experimental groups: GI, 10 nondiabetic control rats; GII, 10 alloxan-diabetic control rats; GIII, 25 alloxan-diabetic rats that received pancreaticoduodenal transplantation (PDT) from normal donor Wistar rats and were immunosuppressed with cyclosporin A. For 7 prior and 4, 7, 14, 21, and 30 days posttransplantation (during which the animals were housed in metabolic cages for periods of 24 hours) body weight, water and food intake, urine output, blood and urinary glucose, plasma insulin, and glucagon were recorded. These parameters were also concurrently recorded for diabetic and nondiabetic control rats. Animals were sacrificed after 30 days and histological and immunohistochemical studies of the pancreas were performed. Pancreatic transplants consistently and significantly improved the metabolic abnormalities of the diabetic rat (P less than 0.01) by restoring body weight gain, and by immediate relief of hyperglycemia, glucosuria, polyuria, polydipsia, and also the low levels of plasma insulin. The plasma glucagon, elevated in diabetic control rats, did not change after transplant.
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PMID:Metabolic effect of pancreaticoduodenal transplantation in diabetic rats. 159 82

Changes of concentration of serum glucose, insulin and glucagon induced by preadministration of indomethacin were observed in normal rats and diabetic rats induced by alloxan. The results demonstrated that the level of serum glucose in diabetic rats was lowered significantly after preadministration of indomethacin (10 mg/kg) dose-dependently. After preadministration of 5, 10, 15 mg/kg of indomethacin the level of serum glucose 48 h after injecting alloxan was decreased from the control value of 591.5 +/- 38.2 mg% to 559.1 +/- 53.2, 436 +/- 16.6 and 266.6 +/- 29.9 mg% respectively. The concentration of serum insulin was increased from the control 10.5 +/- 2.7 microU/ml to 31.9 +/- 7.0 microU/ml and glucagon from 550.0 +/- 27.0 pg/ml to 303.1 +/- 22.9 pg/ml after preadministration of 10 mg/kg indomethacin. Histologic observation showed that alloxan induced beta cell lesion in pancreatic islet could indeed be prevented by indomethacin to a significant extent.
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PMID:[Protective effect of indomethacin on alloxan-induced diabetes in rat]. 162 Nov 11

Colenol, a diterpenoid isolated from the roots of Coleus forskohlii stimulates the release of insulin and glucagon from the islets both in vitro and in vivo. Colenol-stimulated release of glucagon from islets in vitro is much more pronounced as compared to that of insulin. Glucose concentration of 5.6 mM in the medium is required for the colenol stimulation of insulin release. Feeding of coleonol to alloxan diabetic rats cause 36.5% increase in blood glucose level as compared to alloxan diabetic control. Oral feeding of coleonol for 7 days to normal rats causes increase in blood glucose, serum insulin, glucagon and free fatty acid levels with corresponding increase in glucose-6-phosphatase activity and depletion of liver glycogen. Predominant stimulation of A-cells by coleonol is suggested for the above effects.
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PMID:Insulin and glucagon releasing activity of coleonol (forskolin) and its effect on blood glucose level in normal and alloxan diabetic rats. 165 May 16

Inhibition of pancreatic glucagon secretion during hyperglycemia could be mediated by (a) glucose, (b) insulin, (c) somatostatin, or (d) glucose in conjunction with insulin. To determine the role of these factors in the mediation of glucagon suppression, we injected alloxan while clamping the arterial supply of the pancreatic splenic lobe of dogs, thus inducing insulin deficiency localized to the ventral lobe and avoiding hyperglycemia. Ventral lobe insulin, glucagon, and somatostatin outputs were then measured in response to a stepped IV glucose infusion. In control dogs glucagon suppression occurred at a glucose level of 150 mg/dl and somatostatin output increased at glucose greater than 250 mg/dl. In alloxan-treated dogs glucagon output was not suppressed nor did somatostatin output increase. We concluded that insulin was required in the mediation of glucagon suppression and somatostatin stimulation. Subsequently, we infused insulin at high rates directly into the artery that supplied the beta cell-deficient lobe in six alloxan-treated dogs. Insulin infusion alone did not cause suppression of glucagon or stimulation of somatostatin; however, insulin repletion during glucose infusions did restore the ability of hyperglycemia to suppress glucagon and stimulate somatostatin. We conclude that intra-islet insulin permits glucose to suppress glucagon secretion and stimulate somatostatin during hyperglycemia.
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PMID:Intra-islet insulin permits glucose to directly suppress pancreatic A cell function. 167 40

The effect of bombesin against injury on rat islet B cells was studied in three kinds of experiments: (1). In vivo experiment, it was found that preinjection of bombesin (50 micrograms/kg, sublingual v.) could effectively prevent an increase of plasma glucose and decrease of plasma insulin in diabetic rat induced by alloxan (200 mg/kg, s.c.) (2). In vitro experiment, isolated pancreas perfusion showed that alloxan-induced (14 mmol/L) perfusion fluid inhibition of insulin secretion could be reversed by pretreatment of bombesin (10(-3) mmol/L). (3). Investigation on isolated and incubated islets demonstrated that alloxan induced decrease of insulin and somatostatin secretion and increase of glucagon secretion could be prevented by bombesin. The above-mentioned results suggest that bombesin may play an important role in the regulation of plasma glucose in diabetic rat and have a potent preventive effect against the development of diabetes.
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PMID:[Preventive effect of bombesin on alloxan-induced diabetes in rat]. 179 6

Hepatic regeneration in alloxan-induced diabetic rats that underwent a 70% hepatectomy was compared to that of a series of non-treated rats. In diabetic rats, hepatic regeneration is lower and the liver reaches only 70% of the original weight ten days after hepatectomy. Analytical studies in these rats show a diminution of insulin and glucagon. Hepatic microcirculation as shown by measurements of CLV-CLV and CLV area undergoes changes which evolve at a different rate in the central and peripheral zones of the liver. These findings as well as the diminished hepatic regeneration may be attributed to the diminution of the insulin and glucagon values. Insulin and glucagon may be responsible for hepatic regeneration.
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PMID:[Effect of alloxan-induced diabetes on hepatic regeneration]. 186 18

In alloxan-diabetic (A-D) dogs, plasma glucagon does not increase when glycemia is decreased by insulin. Therefore, as in insulin-dependent diabetes mellitus (IDDM), increased glucose utilization is not matched by an increase in hepatic production. To explore further the abnormal effects of insulin on regulation of pancreatic glucagon, we studied content and morphology of pancreatic hormones in six normal (N) dogs, five hyperglycemic A-D (HD) dogs, and in four A-D dogs where normoglycemia was maintained by insulin (ND). Morphometric measurement of islets and of immunocytochemically localized A cells (glucagon) were performed by an image analysis system. In normal pancreas, islets of tail and body were bigger in size (tail = 4850 +/- 376 microns 2, body = 3256 +/- 198 microns 2), than the head (2009 +/- 207 microns 2). Glucagon content was 331 +/- 50 micrograms with a mean concentration of 8.5 +/- 0.9 micrograms/g in N dogs, and did not change in HD dogs (422 +/- 34 micrograms, 9.3 +/- 0.4 micrograms/g). With normoglycemia, glucagon content decreased by 5-fold (p less than 0.001). Morphometry indicated that, although A cell area per islet increased (2.7-fold), islet number decreased (70%), explaining the unchanged glucagon content in HD dogs. This decrease in islet number can also justify the dramatic glucagon decrease in ND dogs. Despite the 70% decrease in islet numbers in HD dogs, pancreatic somatostatin increased 3-fold (9.93 +/- 3.3 to 30.6 +/- 7.2 micrograms), indicating that its islet content was augmented 10-fold. Somatostatin content returned to normal with normoglycemia. Pancreatic insulin content in HD dogs was negligible (55 +/- 23 micrograms) when compared with that in N dogs (5500 micrograms) and it did not increase with normoglycemia. The distinct but markedly diminished insulin and proinsulin peaks in HD dogs nearly disappeared in ND dogs. Thus, in alloxan-diabetic HD dogs, 70% of islets are destroyed. A marked increase in glucagon in residual islets can explain the unchanged islet size despite the absence of B cells; however, the percent increase of somatostatin is larger than that of glucagon. Normoglycemia 1) normalizes somatostatin content, 2) further diminishes insulin and proinsulin synthesis presumably due to lack of hyperglycemic stimulus, and 3) paradoxically decreases pancreatic glucagon content 5-fold below its normal level. We hypothesize that with normalization of plasma insulin, glucagon content in each islet normalizes, but because of destruction of most islets, pancreatic glucagon content becomes extremely low.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Paradoxical reduction in pancreatic glucagon with normalization of somatostatin and decrease in insulin in normoglycemic alloxan-diabetic dogs: a putative mechanism of glucagon irresponsiveness to hypoglycemia. 196 77

During exercise, increased energy demands are met by increased glucose production that occurs simultaneously with the increased glucose uptake. We had previously observed that, during exercise, metabolic clearance rate of glucose (MCR) increases markedly in normal, but only marginally in poorly controlled diabetic dogs. We wished to determine (i) whether in a more general model of stress matched increases in rate of appearance of glucose and MCR also occur, or if MCR is suppressed, as during catecholamine infusion; and (ii) whether diabetes affects stress-induced changes in rate of glucose appearance and MCR. Therefore, we injected carbachol (27 nmol/50 microliters), an analog of acetylcholine, intracerebroventricularly in seven conscious dogs before and after induction of alloxan diabetes. In normal dogs, plasma epinephrine and cortisol increased 4- to 5-fold, whereas norepinephrine and glucagon doubled. Plasma insulin, however, remained unchanged. Tracer-determined hepatic glucose production increased rapidly, but transiently, by 2.5-fold. This increment can be fully explained by the observed increments in the counterregulatory hormones. Surprisingly, however, MCR also promptly increased, and therefore, plasma glucose changed only marginally. After induction of diabetes, the animals were given intracerebroventricular carbachol while plasma glucose was maintained at moderate hyperglycemia (9.0 +/- 0.4 mM). Increments in counterregulatory hormones were similar to those seen in normal dogs, except for exaggerated norepinephrine release. Peripheral insulin levels were higher in diabetic than in normal dogs; however, MCR was markedly reduced and the lipolytic response to stress increased, indicating insulin resistance. Interestingly, the hyperglycemic response to stress was 6-fold greater in diabetic than normal animals, relating mainly to the failure of MCR to rise. Plasma lactate increased equivalently in diabetic and normal animals despite suppression of MCR in the diabetics, indicating either greater muscle glycogenolysis and/or impairment in glucose oxidation. We conclude that in this stress model MCR increases as in exercise in normal but not in diabetic dogs. We speculate that glucose uptake in stress could be mediated through an insulin-dependent neural mechanism.
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PMID:Mechanism of glucoregulatory responses to stress and their deficiency in diabetes. 199 30


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