Observations on the effect of a ganglion blocking agent on responses to intravenous glucose infusion

Burr, Ian M.; Hudson, William Henry; Page, Doris; Taft, H. P.

doi:10.1007/bf01211885

Cited by 7 publications

(5 citation statements)

References 33 publications

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“…Finally, the above studies provide support for the suggestion that the anomalies observed in insulin release in some diabetics (54)(55)(56) could be related to anomalous or absent autonomic modification of B-cell function (31,42,57). The anomalies include: a quantitative reduction in the amount of insulin released in response to glucose challenge (54) in some, but not all, (58) diabetics with retention of apparently normal responsiveness to theophyllin (59) and glucagon (60), and a "delay" in insulin release in response to glucose challenge (54)(55)(56)61).…”

Section: Discussionsupporting

confidence: 57%

Interactions of acetylcholine and epinephrine on the dynamics of insulin release in vitro.

Burr¹,

Slonim²,

Sharp³

1976

J. Clin. Invest.

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A B S T R A C T An in vitro system for perifusion of rat pancreatic islets has been utilized to define the effects of epinephrine on acetylcholine-induced insulin release over varying concentrations of the two agents. Perifusion of islets with epinephrine before challenge with acetylcholine produced marked enhancement of both phases of cholinergically induced insulin release; enhancement of the first phase being more marked with increase in acetylcholine concentration and the converse being observed with the second phase. Perifusion of islets with epinephrine during stimulation with acetylcholine produced inhibition of insulin release, an effect dependent upon the concentration of epinephrine and of acetylcholine. There was an order of difference in the acetylcholine concentration needed to overcome significant epinephrine-mediated inhibition of the first phase of insulin release (5 X 10' Ag/ml) and that needed to overcome inhibition of the second phase (5 X 10-' g/ ml). Comparison of the effects of various concentrations of epinephrine on glucose-and acetyl-choline-induced insulin release revealed that epinephrine was a less potent inhibitor of the first phase of acetylcholine-induced insulin release than of the first phase of glucose-induced insulin release. These data provide some insight into the potential interactions between cholinergic and adrenergic autonomic systems in modifying insulin release.

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Section: Discussionsupporting

confidence: 57%

Interactions of acetylcholine and epinephrine on the dynamics of insulin release in vitro.

Burr¹,

Slonim²,

Sharp³

1976

J. Clin. Invest.

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“…Our results are contradictory to those published by Rayis and Bethune (1970) showing a fall in plasma ACTH to undetectable levels 10-20 minutes after intravenous glucose load or 30 minutes after oral administration. In the same way Bllrr, Hudson, Page and Taft (1970) have observed in a few subjects a fall in plasma cortisol after intravenous glucose load. But owing to the half life of plasma cortisol their results are compatible with an abrupt stop in cortisol secretion therefore ACTH one, phenomen on we did not observe.…”

Section: Discussionsupporting

confidence: 68%

The Influence of Blood Glucose on ACTH Secretion in Man

Vague¹,

Oliver²,

Vague³

2009

Horm Metab Res

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In man cortisol is necessary for anormal neoglycogenesis and fasted patients with adrenocortical insufficiency develop hypoglycemia. ACTH, among other hormones, is released during the course of severe insulin-induced hypoglycemia.However, it is not proven that the ACTH secretion is implicated in the moment-to-moment maintenance of blood glucose.The variations in plasma ACTH levels detennined by radioimmunoassay have been studied: a) in response to oral -or intravenous -glucose administration. It was found, that neither orally nor intravenously administered glucose suppresses plasma ACTH levels in normal su bjects as weil as in those with elevated ACTH values after administration of Metyrapone. b) in 20 healthy subjects after administration of various doses of insulin. A significant rise in plasma ACTH levels is observed only if blood glucose falls below 45 mg(lOO ml, and is not correlated with the magnitude of this fall nor the degree of hypoglycemia but with the c1inical symptoms 01 stress.ACTH secretion does not appear to be involved in the instant maintenance of blood glucose level as HGH does. furthermore, in one patient with documented isolated HGH deficiency insulin-induced hypoglycemia is not corrected at 90 minutes in spite of a striking rise is plasma ACTH.

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“…Possible reasons for such an anomaly in our preparation might result from changes in the basal metabolic state and the reactivity of insulin release mechanisms of pancreatic P-cells obtained from animals fasted overnight and isolated from all other tonic or facilitating influences originating elsewhere in the organism, such as humoral regulators of gastrointestinal origin (33,34,(38)(39)(40)(41), hormones originating in other endocrine glands (15,42,43), and the autonomic nervous system (28, [44][45][46][47][48][49][50][51][52]. The absence of such factors may result in failure to maintain critical concentrations of cAMP or of other as yet hypothetical cofactors required for full effectiveness of substrate stimulation.…”

Section: Resultsmentioning

confidence: 99%

Perifusion of rat pancreatic tissue in vitro: substrate modification of theophylline-induced biphasic insulin release

Burr¹,

Balant²,

Stauffacher³

et al. 1970

J. Clin. Invest.

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A B S T R A C T The immunoreactive insulin (IRI) re-lease patterns produced by continuous theophylline stimulation of rat pancreas have been defined, using an in vitro perifusion system. In the presence of glucose, citrate, and pyruvate at concentrations which were nonstimulatory by themselves, continuous stimulation with theophylline produced a biphasic IRI release profile. In the absence of substrate, continuous theophylline stimulation produced only an abrupt and limited primary response. Of the substrates tested, only glucose significantly enhanced this primary response. With increasing theophylline concentrations, whether in the presence or absence of substrate, significant increases were noted in the primary response as estimated by either the maximum rate of IRI release attained or by the total amount of IRI released during this time. Similarly, the secondary responses to theophylline increased with theophylline concentration in the presence of either citrate or pyruvate. With glucose as substrate, however, increasing theophylline concentrations from 2.5 to 5, then 10 mM produced a progressive reduction in both indices of the secondary response, which was inversely related to the primary response. These findings suggest that cyclic AMP not only mediates IRI release in quantitative terms but is also implicated in the qualitative nature of the response pattern. They also indicate a possible metabolic basis for biphasic IRI release, the acute or primary response being dependent upon the basal state of the cell and the availability of endogenous energy sources, the secondary response upon the availability of exogenous substrate.

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Observations on the effect of a ganglion blocking agent on responses to intravenous glucose infusion

Cited by 7 publications

References 33 publications

Interactions of acetylcholine and epinephrine on the dynamics of insulin release in vitro.

Interactions of acetylcholine and epinephrine on the dynamics of insulin release in vitro.

The Influence of Blood Glucose on ACTH Secretion in Man

Perifusion of rat pancreatic tissue in vitro: substrate modification of theophylline-induced biphasic insulin release

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