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Cited by 206Pancreatic function and diabetesDiabetes, Cardiovascular Risks, and LipoproteinsDiabetes and associated disorders

Insulin secretion, insulin action, and hepatic glucose production in identical twins discordant for non-insulin-dependent diabetes mellitus.

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Vaag, A, Henriksen, J E, Madsbad, S, Holm, N, Beck-Nielsen, H·1995·Journal of Clinical Investigation
DOI 10.1172/jci117715PMC PMC295536
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Abstract

12 identical twin pairs discordant for non-insulin-dependent diabetes mellitus (NIDDM) were studied for insulin sensitivity (euglycemic insulin clamp, 40 mU/m2 per min), hepatic glucose production (HGP, [3-3H]glucose infusion), and insulin secretion (oral glucose tolerance test and hyperglycemic [12 mM] clamp, including glucagon administration). Five of the nondiabetic twins had normal and seven had impaired glucose tolerance. 13 matched, healthy subjects without a family history of diabetes were included as control subjects. The NIDDM twins were more obese compared with their non-diabetic co-twins. The nondiabetic twins were insulin resistant and had a delayed insulin and C-peptide response during oral glucose tolerance tests compared with controls. Furthermore, the nondiabetic twins had a decreased first-phase insulin response and a decreased maximal insulin secretion capacity during hyperglycemic clamping and intravenous glucagon administration. Nondiabetic twins and controls had similar rates of HGP. Compared with both nondiabetic twins and controls, the NIDDM twins had an elevated basal rate of HGP, a further decreased insulin sensitivity, and a further impaired insulin secretion pattern as determined by all tests. In conclusion, defects of both in vivo insulin secretion and insulin action are present in non- and possibly prediabetic twins who possess the necessary NIDDM susceptibility genes. However, all defects of both insulin secretion and glucose metabolism are expressed quantitatively more severely in their identical co-twins with overt NIDDM.

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  • Impaired glycogen synthesis has been documented in normal-glucose-tolerant offspring of two diabetic parents, first-degree relatives of type 2 diabetic individuals, and the normoglycemic twin of a monozygotic twin pair in which the other twin has type 2 diabetes.

    “Impaired glycogen synthesis also has been documented in the normal-glucose tolerant offspring of two diabetic parents, in the first-degree relatives of type 2 diabetic individuals, and in the normoglycemic twin of a monozygotic twin pair in which the other twin has type 2 diabetes [206, 210, 211].”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [211]

  • Obese, IGT, and diabetic subjects have severe impairment in insulin-stimulated glycogen synthase that accounts for most of the defect in insulin-mediated whole-body glucose disposal.

    “Obese, IGT, and diabetic subjects have severe impairment in insulin-stimulated glycogen synthase that accounts for the majority of the defect in insulin-mediated whole-body glucose disposal [1, 2, 21, 195, 206–218].”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [211]

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Authors
Vaag, A., Henriksen, J. E., Madsbad, S., Holm, N., & Beck-Nielsen, H.
Affiliations
Odense University Hospital (DK)
ORCID
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
1995-02-01
Volume
95
Issue
2
Pages
690-698
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci117715
PMC
PMC295536
OpenAlex
W2155904812
Cited by
206
References
41
Citations by year
2024: 1 · 2023: 4 · 2022: 6 · 2021: 3 · 2020: 1 · 2019: 6 · 2018: 3 · 2017: 4 · 2016: 2 · 2015: 3 · 2014: 12 · 2013: 2 · 2012: 2
FWCI
14.66
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
Funders
  • Velux Stiftung
  • Odense Universitetshospital
  • Diabetesforeningen
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Keywords
type 2 diabetes, insulin secretion, insulin sensitivity, hepatic glucose production, monozygotic twins, discordant twins, impaired glucose tolerance, prediabetes, obesity, first-phase insulin response, C-peptide, glucagon, genetic susceptibility
MeSH terms
Insulin Secretion, Aged, Blood Glucose, C-Peptide, Cholesterol, Diabetes Mellitus, Diabetes Mellitus, Type 2, Glucagon, Gluconeogenesis, Glucose Tolerance Test, Glycated Hemoglobin, Humans, Insulin, Cholesterol, HDL, Cholesterol, LDL, Liver, Middle Aged, Obesity, Reference Values, Triglycerides, Tritium, Twins, Monozygotic, Glucose Clamp Technique, Age of Onset

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