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Cited by 199Alcohol Consumption and Health EffectsDiet, Metabolism, and DiseaseDiabetes, Cardiovascular Risks, and Lipoproteins

The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.

Ethanol causes acute inhibition of carbohydrate, fat, and protein oxidation and insulin resistance.

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Shelmet, J J, Reichard, G A, Skutches, C L, Hoeldtke, R D, Owen, O E, Boden, G·1988·Journal of Clinical Investigation
DOI 10.1172/jci113428PMC PMC329642
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Abstract

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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Research works printed but not linked: 2

  1. Faloona, G. R., and R. H. Unger. 1974. Glucagon. In Methods of Hormone Radioimmunoassay. B. M. Jaffe, and H. R. Behrman, editors. Academic Press, Inc., New York. 317-330.
  2. Lieber, C. S. 1982. Ethanol and lipid disorders, including fatty liver, hyperlipemia and arterosclerosis. In Medical Disorders of Alco- holism: Pathogenesis and Treatment. L. H. Smith, editor. W. B. Saunders Co., Philadelphia. 14 1-177.

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Metadata

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
Publisher
American Society for Clinical Investigation
Published
1988-04-01
Volume
81
Issue
4
Pages
1137-1145
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci113428
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
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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