Glucagon Response to Arginine after Treatment of Diabetes Mellitus

Ohneda, Akira; Ishii, Soh; Horigome, Ken; Yamagata, Shoichi

doi:10.2337/diab.24.9.811

Cited by 53 publications

(11 citation statements)

References 6 publications

(6 reference statements)

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“…Insulin treatment for 4weeks reduced plasma glucagon, which was still higher than that of the control group. These changes in plasma glucagon after treatment with insulin are already recognized in human diabetes [12]. From clinical observation, the elevated response of plasma glucagon has been attributed to insulin deficiency [21] or diabetic metabolic derangement [12].…”

Section: Discussionmentioning

confidence: 93%

Insulin and glucagon in spontaneously diabetic non-obese mice

et al. 1984

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To investigate the role of glucagon in the development of diabetes mellitus, spontaneously diabetic non-obese mice were studied before (group 1) and after the onset of diabetes mellitus (group 2). In group 1, fasting blood glucose and insulin in plasma and pancreas did not differ significantly, while plasma glucagon was elevated (48.9 +/- 10.4 versus control 18.6 +/- 6.0 pmol/l). In group 2, the insulin content of plasma and the pancreas were markedly reduced, whereas plasma glucagon was elevated (180.9 +/- 59.1 pmol/l). When diabetic mice were treated with insulin for 4 weeks (group 3), plasma glucagon was markedly reduced compared with that of group 2 (30.3 +/- 9.0 pmol/l). In group 1, glucagon and glucagon-like immunoreactivity of the intestine were reduced. The glucagon content of the intestine was elevated in group 2. Group 3 elicited increased contents of gastric glucagon as well as intestinal glucagon-like immunoreactivity. We conclude that, in addition to insulin deficiency, hypersecretion of glucagon might contribute to the development and clinical course of diabetes mellitus in the non-obese diabetic mouse.

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Section: Discussionmentioning

confidence: 93%

Insulin and glucagon in spontaneously diabetic non-obese mice

et al. 1984

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“…In this context, it seems possible that the rise in glucagon in the pancreatic vein foIlowing the infusion of VIP derives from a cross-reactivity of VIP infused, within the radioimmunoassay of glucagon. However, the possibility may be excluded by the fact that the antiserum, G 21, used for glucagon assay in the present study, does not react with VIP (Ohneda et al 1975). Therefore, it is reasonable to suppose that VIP, in the doses used in the experiments, stimulates glucagon secretion from the pancreas.…”

Section: Minutes After Start Of Vip Infusionmentioning

confidence: 83%

Effect of Intrapancreatic Administration of Vasoactive Intestinal Peptide upon the Release of Insulin and Glucagon in Dogs

Ohneda¹,

Ishii²,

Horigome³

et al. 1977

Horm Metab Res

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To investigate the effect of vasoactive intestinal peptide (VIP) on the endocrine function ofthe pancreatic islet, experiments with a local circulation of the pancreas were performed in anesthetized dogs. VIP was infused into the pancreatic artery in doscs of 20, 100,200 and 400 ng for 10 min. Blood glucose level in the femoral artery did not change during and after the infusion of VIP. Since VIP is known to increase blood !low, a circuit was made in the pancreatic vein and blood !low rate of the pancreatic vein was calculatcd from the time necessary to obtain a volume of blood. Blood !low rate of the pancreatic vein did not change throughout the experiment with graded doses of VIP. Plasma insulin in the pancreatic vein increased transiently following the infusion of 20 ng VIP but a constant and significant rise of plasma insulin was observed in the experiment with 400 ng of VIP. To the contrary, plasma glucagon in the pancreatic vein increased significantly after the infusion of VIP in doses of 20 to 400 ng for 10 min. The changes in the secretion of these hormones were similar to those in the plasma levels of these hormones in the pancreatic vein. From the present experiment it is concluded that VIP even in a sm all dose, wh ich does not induce hyperglycemia or increase in blood flow, stimulates the secretion of insulin and glucagon from the pancreas.

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“…In 1969, Samols and co-workers reported a significant decrease in glucagon when hypoglycemia was induced by a tolbutamide injection whereas glucagon increased after iv insulin in ducks (28), but others argued that this was a species-dependent result, as glucagon is a hormone essential to life in the fowl (29), and a species difference was later confirmed in a Japanese study (30). However, in patients with type 2 diabetes starting treatment with either SU or insulin, the glucagon response to an arginine infusion after 1-2 months of treatment was markedly reduced in patients treated with SU compared to that in the patients taking insulin (33). However, in patients with type 2 diabetes starting treatment with either SU or insulin, the glucagon response to an arginine infusion after 1-2 months of treatment was markedly reduced in patients treated with SU compared to that in the patients taking insulin (33).…”

Section: Discussionmentioning

confidence: 99%

Oral Glibenclamide Suppresses Glucagon Secretion during Insulin-Induced Hypoglycemia in Patients with Type 2 Diabetes1

Landstedt-Hallin

Adamson

Lins

1999

The Journal of Clinical Endocrinology &Amp; Metabolism

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Intensifying pharmacological therapy in patients with type 2 diabetes increases the risk of hypoglycemia and often requires the simultaneous use of more than one agent. Combining insulin and sulfonylurea is an effective and frequently used therapy in such patients. However, sulfonylurea derivatives have been shown to affect the release of glucagon, indicating a possible effect of such therapy on hormonal counterregulation to hypoglycemia. Thirteen patients receiving combined therapy were studied on two occasions: 1) after a wash-out period of glibenclamide (-GLIB), and 2) after resuming combined treatment for 6 months (+GLIB). We performed nonstep-wise, hyperinsulinemic hypoglycemic clamps using a constant i.v. insulin infusion and clamping blood glucose at 2.7 mmol/L (48 mg/dL) for 60 min. C Peptide levels were significantly higher during + GLIB, but no significant differences were seen in peripheral plasma insulin levels (+GLIB mean +/- SD, 70 +/- 17 mU/L vs. -GLIB, 75 +/- 14; P = 0.26). Epinephrine responses were similar in the two tests, but when glibenclamide was present the glucagon response was smaller, both the peak value (P = 0.016) and the incremental area under the curve (P = 0.011) as well as the total area under the curve (P = 0.016). These results suggest that intraislet insulin secretion is of importance for the alpha-cell responsiveness to hypoglycemia in these patients.

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Glucagon Response to Arginine after Treatment of Diabetes Mellitus

Cited by 53 publications

References 6 publications

Insulin and glucagon in spontaneously diabetic non-obese mice

Insulin and glucagon in spontaneously diabetic non-obese mice

Effect of Intrapancreatic Administration of Vasoactive Intestinal Peptide upon the Release of Insulin and Glucagon in Dogs

Oral Glibenclamide Suppresses Glucagon Secretion during Insulin-Induced Hypoglycemia in Patients with Type 2 Diabetes1

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