Ethanol causes acute inhibition of carbohydrate, fat, and protein oxidation and insulin resistance.
Open accessAbstract
To study the mechanism of the diabetogenic action of ethanol, ethanol (0.75 g/kg over 30 min) and then glucose (0.5 g/kg over 5 min) were infused intravenously into six normal males. During the 4-h study, 21.8 +/- 2.1 g of ethanol was metabolized and oxidized to CO2 and H2O. Ethanol decreased total body fat oxidation by 79% and protein oxidation by 39%, and almost completely abolished the 249% rise in carbohydrate (CHO) oxidation seen in controls after glucose infusion. Ethanol decreased the basal rate of glucose appearance (GRa) by 30% and the basal rate of glucose disappearance (GRd) by 38%, potentiated glucose-stimulated insulin release by 54%, and had no effect on glucose tolerance. In hyperinsulinemic-euglycemic clamp studies, ethanol caused a 36% decrease in glucose disposal. We conclude that ethanol was a preferred fuel preventing fat, and to lesser degrees, CHO and protein, from being oxidized. It also caused acute insulin resistance which was compensated for by hypersecretion of insulin.
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Alcohol consumption may have profound effects on glucose homeostasis, especially in the fasting state, but its effects on metabolism the following day do not appear to have been tested.
“Alcohol consumption may have profound effects on glucose homeostasis (Shelmet et al. 1988;Siler et al. 1998), especially in the fasting state, although the effects of alcohol consumption on metabolism the following day do not appear to have been tested.”
From Glycaemic index methodology (2005) · cites this paper as Shelmet et al. 1988
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- Authors
- Shelmet, J. J., Reichard, G. A., Skutches, C. L., Hoeldtke, R. D., Owen, O. E., & Boden, G.
- Affiliations
- Temple University Hospital (US)
- Lankenau Medical Center (US)
- ORCID
- Reichard, G A
- Venue
- Journal of Clinical Investigation
- Published
- 1988-04-01
- Volume
- 81
- Issue
- 4
- Pages
- 1137-1145
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC329642
- OpenAlex
- W1987392704
- Cited by
- 199
- References
- 43
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 1 · 2023: 4 · 2021: 7 · 2020: 4 · 2018: 4 · 2017: 2 · 2016: 4 · 2015: 5 · 2014: 8 · 2013: 2 · 2012: 4
- FWCI
- 3.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Temple University
- National Institutes of Health (AM-36192, 5t32am007162-09, 5r01am034548-03)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- ethanol, insulin resistance, carbohydrate oxidation, fat oxidation, protein oxidation, glucose infusion, glucose appearance, glucose disappearance, glucose-stimulated insulin secretion, hyperinsulinemic-euglycemic clamp, alcohol metabolism, diabetogenic effect, glucose tolerance
- MeSH terms
- Acetates, Adult, Ethanol, Blood Glucose, Calorimetry, Fatty Acids, Nonesterified, Humans, Insulin, Insulin Resistance, Liver, Male, Oxidation-Reduction, Proteins, Receptor, Insulin, Carbohydrate Metabolism, Lipid Metabolism
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