Cited by 299Metabolism, Diabetes, and CancerDiabetes, Cardiovascular Risks, and LipoproteinsGlycogen Storage Diseases and Myoclonus

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Decreased insulin activation of glycogen synthase in skeletal muscles in young nonobese Caucasian first-degree relatives of patients with non-insulin-dependent diabetes mellitus

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Vaag, A, Henriksen, J E, Beck-Nielsen, H·1992·Journal of Clinical Investigation

DOI 10.1172/jci115656PMC PMC442922

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Abstract

Insulin resistance in non-insulin-dependent diabetes is associated with a defective insulin activation of the enzyme glycogen synthase in skeletal muscles. To investigate whether this may be a primary defect, we studied 20 young (25 +/- 1 yr) Caucasian first-degree relatives (children) of patients with non-insulin-dependent diabetes, and 20 matched controls without a family history of diabetes. Relatives and controls had a normal oral glucose tolerance, and were studied by means of the euglycemic hyperinsulinemic clamp technique, which included performance of indirect calorimetry and muscle biopsies. Insulin-stimulated glucose disposal was decreased in the relatives (9.2 +/- 0.6 vs 11.5 +/- 0.5 mg/kg fat-free mass per (FFM) min, P less than 0.02), and was due to a decreased rate of insulin-stimulated nonoxidative glucose metabolism (5.0 +/- 0.5 vs 7.5 +/- 0.4 mg/kg fat-free mass per min, P less than 0.001). The insulin-stimulated, fractional glycogen synthase activity (0.1/10 mmol liter glucose-6-phosphate) was decreased in the relatives (46.9 +/- 2.3 vs 56.4 +/- 3.2%, P less than 0.01), and there was a significant correlation between insulin-stimulated, fractional glycogen synthase activity and nonoxidative glucose metabolism in relatives (r = 0.76, P less than 0.001) and controls (r = 0.63, P less than 0.01). Furthermore, the insulin-stimulated increase in muscle glycogen content over basal values was lower in the relatives (13 +/- 25 vs 46 +/- 9 mmol/kg dry wt, P = 0.05). We conclude that the defect in insulin activation of muscle glycogen synthase may be a primary, possibly genetically determined, defect that contributes to the development of non-insulin-dependent diabetes.

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“The key feature in the development of type 2 diabetes (T2D), insulin resistance, has been repeatedly shown to characterize first-degree relatives (FDRs) ( 3-6 ).”
Background
Gene expression in human skeletal muscle : Effects of activity, fibre type and inheritance for diabetes
Ahlsén, M. (2006) · Figshare
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The relationship between birth weight, insulin resistance and glucose intolerance in 7-year old black children
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Role of Adipose-to-Muscle Communication in PCB126-induced Metabolic Defects
Caron, A. (2018) · uO Research (University of Ottawa) · doi:10.20381/ruor-22048
“Interestingly, it has been shown that individuals with a family history of T2D have an increased phosphorylation of IRS-1 on serine/threonine residues, a reduced activity of PI3K [76], and have normal glucose tolerance but moderate to severe insulin resistance in skeletal muscle [77]–[79].”
Background
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Insulin Resistance and Glycogen Synthesis
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Résistance à l’Insuline du Système Sérotoninergique : Implication dans les Troubles de l’Humeur Comorbides au Diabete De Type 2
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The ortholog of the Human T2D Risk Gene STEAP2 is Required for Glucose Stimulated Insulin Secretion in MicePreprint
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Authors: Vaag, A., Henriksen, J. E., & Beck-Nielsen, H.
Affiliations: Odense University Hospital (DK)
ORCID: Vaag, A
Henriksen, J E
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1992-03-01
Volume: 89
Issue: 3
Pages: 782-788
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci115656
PMC: PMC442922
OpenAlex: W2041249629
Cited by: 299
References: 58
Citations by year: 2026: 2 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 3 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 7 · 2017: 2 · 2016: 5 · 2015: 6 · 2014: 3 · 2013: 5 · 2012: 3
FWCI: 6.62
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Diabetesforeningen
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Glycogen Storage Diseases and Myoclonus
Keywords: insulin resistance, type 2 diabetes, glycogen synthase, skeletal muscle, first-degree relatives, genetic susceptibility, insulin-stimulated glucose disposal, nonoxidative glucose metabolism, muscle glycogen, hyperinsulinemic-euglycemic clamp
MeSH terms: Adult, Blood Glucose, Diabetes Mellitus, Type 2, Enzyme Activation, Glycogen Synthase, Humans, Insulin, Insulin Resistance, Muscles, White People

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Decreased insulin activation of glycogen synthase in skeletal muscles in young nonobese Caucasian first-degree relatives of patients with non-insulin-dependent diabetes mellitus

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