Cited by 189Pancreatic function and diabetesDiabetes and associated disordersDiabetes, Cardiovascular Risks, and Lipoproteins

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Pancreatic Beta-Cell Dysfunction as the Primary Genetic Lesion in NIDDM: Evidence From Studies in Normal Glucose-Tolerant Individuals With a First-Degree NIDDM Relative

Pimenta, Walkyria·1995·JAMA

DOI 10.1001/jama.1995.03520470063033

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Abstract

Objective. —To test the hypothesis that insulin resistance precedes impaired insulin secretion in individuals genetically predisposed to non-insulin-dependent diabetes mellitus (NIDDM). Design. —Case-control study. Setting. —Outpatient facility of clinical research center. Participants. —One hundred volunteers of European ancestry having normal glucose tolerance, 50 with and 50 without a first-degree NIDDM relative, matched for age, sex, and degree of obesity. Main Outcome Measures. —Insulin secretion and insulin sensitivity assessed by hyperglycemic (N=100) and euglycemic-hyperinsulinemic (N=62) clamp experiments. Results. —The individuals with a first-degree NIDDM relative had reduced first-and second-phase insulin responses (mean±SEM, 939±68 vs 1209±82 pmol/L, and 322±19 vs 407±24 pmol/L, respectively,P=.001 and.01), but their insulin sensitivity (148±6 and 92±6 nmol·kg-1·min-1/pmol·L-1in hyperglycemic and euglycemic clamp studies) did not differ from that of the control group (126±5 and 81±7 nmol·kg-1·min-1/pmol·L-1, in hyperglycemic and euglycemic clamp studies,P=.07 and.24, respectively). In some individuals only first- or only second-phase insulin responses were reduced. Conclusion. —In this study population, heterogeneous defects in insulin secretion were demonstrated, while defects in insulin sensitivity were not evident. We therefore conclude that since the earliest defects identified in a group genetically at high risk to develop NIDDM are those related to insulin secretion, defects in insulin secretion rather than insulin sensitivity are likely the major genetic factor predisposing to development of NIDDM. (JAMA. 1995;273:1855-1861)

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Authors: Pimenta, W.
Corresponding author: Pimenta, Walkyria
Venue: JAMA
Publisher: American Medical Association (AMA)
Published: 1995-06-21
Volume: 273
Issue: 23
Pages: 1855
ISSN: 0002-9955 (ISSN-L)
0098-7484
DOI: 10.1001/jama.1995.03520470063033
OpenAlex: W4321059897
Cited by: 174
References: 0
Citations by year: 2024: 3 · 2023: 4 · 2022: 1 · 2021: 6 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 5 · 2016: 4 · 2015: 4 · 2014: 3 · 2013: 4 · 2012: 7
FWCI: 7.15
Type: journal article
Language: en
Open access: closed
Locations: JAMA (publishedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (DK-20411)
National Center for Research Resources (M501 RR00056, M501 RR00044)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords: type 2 diabetes, beta-cell dysfunction, insulin secretion, insulin resistance, genetic susceptibility, first-degree relatives, hyperglycemic clamp, hyperinsulinemic-euglycemic clamp, insulin sensitivity

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Pancreatic Beta-Cell Dysfunction as the Primary Genetic Lesion in NIDDM: Evidence From Studies in Normal Glucose-Tolerant Individuals With a First-Degree NIDDM Relative

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