Effect of pulse administration of glucose or glucagon on insulin secretion in vitro

Grodsky, Gerold M.; Bennett, Leslie L.; Smith, Dorothy B.; Schmid, Florence G.

doi:10.1016/0026-0495(67)90171-0

Cited by 112 publications

(43 citation statements)

References 23 publications

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“…Therefore, the present studies were undertaken using the perfused rat pancreas to characterize further the individual and combined effects of arginine and glucose on pancreatic alpha and beta cell function. (33), was below the sensitivity of our assay. Maximal IRI release occurred around 16.7 mM glucose (300 mg/100 ml) and half-maximal release occurred between 9 and 10 mM glucose (160-180 mg/100 ml).…”

mentioning

confidence: 57%

Characterization of the Effects of Arginine and Glucose on Glucagon and Insulin Release from the Perfused Rat Pancreas

Gerich¹,

Charles²,

Grodsky³

1974

J. Clin. Invest.

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230

115

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A B S T R A C T To characterize the mechanisms by which arginine and glucose affect pancreatic alpha and beta cell function, the effects of these agents over their full dose response, both alone and in various combinations, were studied using the perfused rat pancreas. Arginine (0-38 mM), in the absence of glucose, stimulated biphasic glucagon (IRG) secretion (Km 34 mM) at concentrations less than 1 mM and caused nonphasic insulin (IRI) release (Km. 12-13 mM) but only at concentrations greater than 6 mM. Glucose (0-27.5 mM) alone stimulated biphasic IRI release (Km ' 9-10 mM) at concentrations in excess of 5.5 mM and caused nonphasic inhibition of IRG secretion (Ki5 -6 mM) at concentrations as low as 4.1 mM. These results demonstrate fundamental differences in pancreatic alpha and beta cell secretory patterns in response to glucose and arginine and suggest that glucagon secretion is more sensitive to the effect of both glucose and arginine. Various concentrations of arginine in the presence of 5.5 mM glucose stimulated biphasic IRG and IRI release; IRG responses were diminished and IRI responses were enhanced compared with those seen with arginine in the absence of glucose. Glucose (0-27.5 mM)in the presence of 3.2 or 19.2 mM arginine caused similar inhibition of IRG secretion (Km v 5-6 mM) and stimulation of IRI release (Km --9-10 mM) as that seen with glucose alone, although greater IRG and IRI release occurred. This augmentation of IRI secretion was greater than that expected from mere additive effects of glucose and arginine. Classical Lineweaver-Burk analysis of these results indicates that glucose is a noncompetitive inhibitor arginine-stimulated glucagon secretion and suggests that glucose and arginine affect pancreatic alpha and beta cell function via different

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mentioning

confidence: 57%

Characterization of the Effects of Arginine and Glucose on Glucagon and Insulin Release from the Perfused Rat Pancreas

Gerich¹,

Charles²,

Grodsky³

1974

J. Clin. Invest.

Self Cite

230

115

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“…The intravenous injection of glucose in dogs immediately after total pancreateetomy increases the levels of serum insulin provided the pre-operative concentrations of insulin were kept high [3]. Finally, the initial peak of serum insulin observed after a glucose injection can be reproduced with the perfused rat pancreas preparation [7]; however, with pieces of pancreatic tissue incubated in vitro in the presence of glucose, a rapid insulin secretion is lacking [10]. It is therefore possible that the initial rise of circulating insulin is due, at least in part, to a direct effect of glucose upon capillaries.…”

Section: Discussionmentioning

confidence: 99%

The displacement of insulin from blood capillaries

Rasio¹

1969

Diabetologia

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Summary. Normal anaesthetized bull-dogs were perfused with constant amounts of 125I bovine insulin. During the control period, steady state arterio-venous gradients and lymph levels were achieved. Positive arterio-venous differences were observed across the bind limbs and the head. Lower levels of 12aI-insulin were found in cervical and leg lymph than in corresponding venous plasma. The rapid intravascular injection of unlabelled insulin resulted in an almost immediate reversal of the arterio-venous gradients of x~sI-insulin in the head and the hind limb. The injection of small amounts of glucose into the lower abdominal aorta induced a very rapid diminution of the arterio-venous gradient across the hind quarters ; the effect was not mediated by the release of endogenous insulin. In both experiments, the lymph levels of 12sT-insulin remained relatively constant.The data indicate that the vascular pole of the capillary endothelial cells can adsorb labelled insulin and either exchange it with unlabelled insulin or release it under the direct influence of glucose.

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“…In addition to the effects of pancreatic hormones on target tissues, an intraislet action of the hormones is possible. Thus, glucagon is known to stimulate the release of insulin (2)(3)(4) and pancreatic somatostatin (5,6), somatostatin to inhibit both insulin (7)(8)(9) and glucagon (10)(11)(12)(13) secretion, and insulin to suppress glucagon secretion (14,15). In these studies, higher concentrations of the hormones than those found in peripheral blood were employed.…”

mentioning

confidence: 99%

Effect of Insulin on Glucose- and Arginine-Stimulated Somatostatin Secretion from the Isolated Perfused Rat Pancreas*

et al. 1981

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Effect of pulse administration of glucose or glucagon on insulin secretion in vitro

Cited by 112 publications

References 23 publications

Characterization of the Effects of Arginine and Glucose on Glucagon and Insulin Release from the Perfused Rat Pancreas

Characterization of the Effects of Arginine and Glucose on Glucagon and Insulin Release from the Perfused Rat Pancreas

The displacement of insulin from blood capillaries

Effect of Insulin on Glucose- and Arginine-Stimulated Somatostatin Secretion from the Isolated Perfused Rat Pancreas*

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