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Ethanol Acutely Stimulates Islet Blood Flow, Amplifies Insulin Secretion, and Induces Hypoglycemia

Ethanol Acutely Stimulates Islet Blood Flow, Amplifies Insulin Secretion, and Induces Hypoglycemia

Hypoglycemia induced by alcohol ingestion is a well-known problem in diabetics. However, the mechanisms underlying this phenomenon have remained largely unknown.

Because insulin secretion can be rapidly adjusted in vivo by changes in pancreatic microcirculation, we investigated the effect of acute alcohol administration on pancreatic islet blood flow (IBF) and dynamic changes in insulin secretion and glycemia in the rat.

Wistar rats were injected intravenously with ethanol (10%) or saline as a bolus, resulting in serum ethanol concentrations of approximately 8 mmol/liter. Pancreatic blood flow (PBF) measurements were performed using a microsphere technique in combination with a freeze-thaw technique after 10 minutes of injection.

Alcohol preferentially and significantly increased pancreatic IBF by approximately 4-fold, whereas it did not affect total PBF. Alcohol also increased insulin secretion in the late phase and induced late hypoglycemia after ip glucose tolerance tests. The nitric oxide synthase inhibitor N-w-nitro-L-arginine methyl ester and atropine prevented the increased pancreatic IBF, increased insulin secretion, and ethanol-induced hypoglycemia.

Thus, our results show that ethanol acutely exerts substantial influences on the pancreatic microcirculation by inducing a massive redistribution of PBF from the exocrine to the endocrine part via mechanisms mediated by nitric oxide and vagal stimuli, which enhances insulin secretion in the late phase, thereby inducing hypoglycemia.

This effect may partly underlie the known hypoglycemic properties of alcohol in diabetics or in alcoholics with liver failure.


Endocrinology: Ethanol Acutely Stimulates Islet Blood Flow, Amplifies Insulin Secretion, and Induces Hypoglycemia via Nitric Oxide and Vagally Mediated Mechanisms

Found at Alkohol adé (german)

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