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Cited by 123Diabetes, Cardiovascular Risks, and LipoproteinsMetabolism, Diabetes, and CancerAdipose Tissue and Metabolism

The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.

Effect of the antilipolytic nicotinic acid analogue acipimox on whole-body and skeletal muscle glucose metabolism in patients with non-insulin-dependent diabetes mellitus.

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Vaag, A, Skött, P, Damsbo, P, Gall, M A, Richter, E A, Beck-Nielsen, H·1991·Journal of Clinical Investigation
DOI 10.1172/jci115432
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Abstract

Increased nonesterified fatty acid (NEFA) levels may be important in causing insulin resistance in skeletal muscles in patients with non-insulin-dependent diabetes mellitus (NIDDM). The acute effect of the antilipolytic nicotinic acid analogue Acipimox (2 X 250 mg) on basal and insulin-stimulated (3 h, 40 mU/m2 per min) glucose metabolism was therefore studied in 12 patients with NIDDM. Whole-body glucose metabolism was assessed using [3-3H]glucose and indirect calorimetry. Biopsies were taken from the vastus lateralis muscle during basal and insulin-stimulated steady-state periods. Acipimox reduced NEFA in the basal state and during insulin stimulation. Lipid oxidation was inhibited by Acipimox in all patients in the basal state (20 +/- 2 vs. 33 +/- 3 mg/m2 per min, P less than 0.01) and during insulin infusion (8 +/- 2 vs. 17 +/- 2 mg/m2 per min, P less than 0.01). Acipimox increased the insulin-stimulated glucose disposal rate (369 +/- 49 vs. 262 +/- 31 mg/m2 per min, P less than 0.01), whereas the glucose disposal rate was unaffected by Acipimox in the basal state. Acipimox increased glucose oxidation in the basal state (76 +/- 4 vs. 50 +/- 4 mg/m2 per min, P less than 0.01). During insulin infusion Acipimox increased both glucose oxidation (121 +/- 7 vs. 95 +/- 4 mg/m2 per min, P less than 0.01) and nonoxidative glucose disposal (248 +/- 47 vs. 167 +/- 29 mg/m2 per min, P less than 0.01). Acipimox enhanced basal and insulin-stimulated muscle fractional glycogen synthase activities (32 +/- 2 vs. 25 +/- 3%, P less than 0.05, and 50 +/- 5 vs. 41 +/- 4%, P less than 0.05). Activities of muscle pyruvate dehydrogenase and phosphofructokinase were unaffected by Acipimox. In conclusion, Acipimox acutely improved insulin action in patients with NIDDM by increasing both glucose oxidation and nonoxidative glucose disposal. This supports the hypothesis that elevated NEFA concentrations may be important for the insulin resistance in NIDDM. The mechanism responsible for the increased insulin-stimulated nonoxidative glucose disposal may be a stimulatory effect of Acipimox on glycogen synthase activity in skeletal muscles.

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  1. Passonneau, J. V. 1974. L-(+)-lactate: fluorometric method. In Methods ofEnzymatic Analysis. Volume 3. H. V. Bergmeyer, editor. Academic Press, Inc. New York. 1468-1472.

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Metadata

Authors
Vaag, A., Skött, P., Damsbo, P., Gall, M. A., Richter, E. A., & Beck-Nielsen, H.
Affiliations
  • Odense University Hospital (DK)
  • University of Copenhagen (DK)
ORCID
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1991-10-01
Volume
88
Issue
4
Pages
1282-1290
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci115432
OpenAlex
W1987680714
Cited by
123
References
64
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2019: 2 · 2018: 1 · 2017: 3 · 2015: 2 · 2014: 3 · 2013: 5 · 2012: 3
FWCI
6.89
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed (publishedVersion)
  • Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
Funders
Diabetesforeningen
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Keywords
acipimox, type 2 diabetes, skeletal muscle glucose metabolism, insulin-stimulated glucose disposal, free fatty acids, lipolysis inhibition, lipid oxidation, glucose oxidation, glycogen synthase, insulin resistance, vastus lateralis, nonoxidative glucose disposal, pyruvate dehydrogenase, phosphofructokinase, glucose-6-phosphate
MeSH terms
Hypolipidemic Agents, Biological Transport, Diabetes Mellitus, Type 2, Fatty Acids, Nonesterified, Glucose, Glycogen Synthase, Humans, Lactates, Middle Aged, Muscles, Oxidation-Reduction, Pyrazines, Pyruvate Dehydrogenase Complex, Lactic Acid, Lipid Metabolism

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