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Insulin secretion, insulin action, and hepatic glucose production in identical twins discordant for non-insulin-dependent diabetes mellitus.
Open accessAbstract
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 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]
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“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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Huang, X., Vaag, A. A., Carlsson, E., Hansson, M., Åhrén, B., & Groop, L. (2003) · Diabetes · doi:10.2337/diabetes.52.9.2411 · Cited by 31
Self-citationRedefining the clinical management of type 2 diabetes: matching therapy to pathophysiology
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Metadata
- Authors
- Vaag, A., Henriksen, J. E., Madsbad, S., Holm, N., & Beck-Nielsen, H.
- Affiliations
- Odense University Hospital (DK)
- Venue
- Journal of Clinical Investigation
- Published
- 1995-02-01
- Volume
- 95
- Issue
- 2
- Pages
- 690-698
- ISSN
- 0021-9738 (ISSN-L)
- 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
- bronze
- doi.org
- 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 › Endocrinology, Diabetes and Metabolism › 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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