Ethanol-induced alterations of glucose tolerance, postglucose hypoglycemia, and insulin secretion in normal, obese, and diabetic subjects
- PMID: 1100461
- DOI: 10.2337/diab.24.10.933
Ethanol-induced alterations of glucose tolerance, postglucose hypoglycemia, and insulin secretion in normal, obese, and diabetic subjects
Abstract
Ethanol at an average blood concentration of 1 mg. per milliliter enhanced the immediate (first-phase) and prolonged (second-phase) insulin response to an intravenous glucose load in nonfasting normal human subjects. Simultaneously, the glucose disposal rate was increased and the postglucose hypoglycemia was accentuated, resulting in definite hypoglycemic symptoms in some individuals. Oral glucose tolerance was not changed by ethanol administration, but the thirty-minute blood glucose and plasma insulin values were increased, suggesting that alcohol might accelerate the absorption of glucose from the gut. Ethanol given orally during evening hours (1.5 gm. per kilogram) caused a nocturnal hyperinsulinemia and a decrease of blood glucose, but not an actual hypoglycemia. Oral glucose tolerance and plasma insulin response tested the next morning, when ethanol had disappeared from the blood, were not influenced by drinking the previous evening. The K-value of intravenous glucose was increased at this time, however. When alcohol was administered for one week at a dose corresponding to 25 per cent of daily calories and substituting for fat, both the oral and intravenous glucose tolerances were impaired in each subject but the insulin response remained unchaged. In obese nondiabetic subjects, ethanol did not potentiate the early insulin response to intravenous glucose but it increased the second phase of insulin secretion in response to sustained hyperglycemia. In contrast to conditions in nonobese subjects, the glucose disposal rate was not incresed and postglucose hypoglycemia was not accentuated by ethanol in overweight subjects. In insulin-deficient diabetic patients the absent early insulin response could not be restored by ethanol, and the late component of insulin release was little increased by alcohol infusion. Ethanol did not improve the glucose utilization of diabetic patients.
Similar articles
-
Ethanol acutely stimulates islet blood flow, amplifies insulin secretion, and induces hypoglycemia via nitric oxide and vagally mediated mechanisms.Endocrinology. 2008 Jan;149(1):232-6. doi: 10.1210/en.2007-0632. Epub 2007 Oct 4. Endocrinology. 2008. PMID: 17916634
-
Effects of ethanol ingestion on glucose tolerance and insulin secretion in normal and diabetic subjects.Metabolism. 1975 May;24(5):625-32. doi: 10.1016/0026-0495(75)90142-0. Metabolism. 1975. PMID: 1128232
-
Counter-regulation of basal insulin secretion during alcohol hypoglycemia in diabetic and normal subjects.Diabetes. 1972 Feb;21(2):65-70. doi: 10.2337/diab.21.2.65. Diabetes. 1972. PMID: 5060106 No abstract available.
-
[Insulin secretion in the clinical stages of diabetes (with glucose tolerance test abnormalities)].Journ Annu Diabetol Hotel Dieu. 1972;13(0):55-65. Journ Annu Diabetol Hotel Dieu. 1972. PMID: 4605752 Review. French. No abstract available.
-
The pathogenesis of non-insulin-dependent diabetes: an update.Medicine (Baltimore). 1982 May;61(3):125-40. doi: 10.1097/00005792-198205000-00001. Medicine (Baltimore). 1982. PMID: 7043155 Review. No abstract available.
Cited by
-
Two-hour glucose and insulin responses after a standardized oral glucose load in relation to serum gamma-glutamyl transferase and alcohol consumption.Acta Diabetol Lat. 1981 Oct-Dec;18(4):311-7. doi: 10.1007/BF02042814. Acta Diabetol Lat. 1981. PMID: 6120606
-
Combination of alcohol and glucose consumption as a risk to induce reactive hypoglycemia.J Diabetes Investig. 2021 Apr;12(4):651-657. doi: 10.1111/jdi.13375. Epub 2020 Sep 7. J Diabetes Investig. 2021. PMID: 33448697 Free PMC article.
-
Alcohol consumption and impaired glycoregulation results in a population of 6665 salaried employees.Eur J Epidemiol. 1988 Sep;4(3):371-6. doi: 10.1007/BF00148927. Eur J Epidemiol. 1988. PMID: 3181390
-
Clinically and pharmacologically relevant interactions of antidiabetic drugs.Ther Adv Endocrinol Metab. 2016 Apr;7(2):69-83. doi: 10.1177/2042018816638050. Epub 2016 Mar 31. Ther Adv Endocrinol Metab. 2016. PMID: 27092232 Free PMC article. Review.
-
Risk factors for type 2 (non-insulin-dependent) diabetes mellitus. Thirteen and one-half years of follow-up of the participants in a study of Swedish men born in 1913.Diabetologia. 1988 Nov;31(11):798-805. doi: 10.1007/BF00277480. Diabetologia. 1988. PMID: 3234634
MeSH terms
Substances
LinkOut - more resources
Full Text Sources