Analysis of the gene sequences of the insulin receptor and the insulin-sensitive glucose transporter (GLUT-4) in patients with common-type non-insulin-dependent diabetes mellitus.
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Insulin resistance is a common feature of non-insulin-dependent diabetes mellitus (NIDDM) and "diabetes susceptibility genes" may be involved in this abnormality. Two potential candidate genes are the insulin receptor (IR) and the insulin-sensitive glucose transporter (GLUT-4). To elucidate whether structural defects in the IR and/or GLUT-4 could be a primary cause of insulin resistance in NIDDM, we have sequenced the entire coding region of the GLUT-4 gene from DNA of six NIDDM patients. Since binding properties of the IRs from NIDDM subjects are normal, we also analyzed the sequence of exons 16-22 (encoding the entire cytoplasmic domain of the IR) of the IR gene from the same six patients. When compared with the normal IR sequence, no difference was found in the predicted amino acid sequence of the IR cytoplasmic domain derived from the NIDDM patients. Sequence analysis of the GLUT-4 gene revealed that one patient was heterozygous for a mutation in which isoleucine (ATC) was substituted for valine (GTC) at position 383. Consequently, the GLUT-4 sequence at position 383 was determined in 24 additional NIDDM patients and 30 nondiabetic controls and all showed only the normal sequence. From these studies, we conclude that the insulin resistance seen in the great majority of subjects with the common form of NIDDM is not due to genetic variation in the coding sequence of the IR beta subunit, nor to any single mutation in the GLUT-4 gene. Possibly, a subpopulation of NIDDM patients exists displaying variation in the GLUT-4 gene.
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With very rare exceptions, physiologically significant mutations in the insulin receptor gene have not been observed in type 2 diabetic patients from diverse ethnic populations.
“The insulin receptor gene, however, has been sequenced in a large number of type 2 diabetic patients from diverse ethnic populations and, with very rare exceptions, physiologically significant mutations in the insulin receptor gene have not been observed [159, 160].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [160]
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- Authors
- Kusari, J., Verma, U. S., Buse, J. B., Henry, R. R., & Olefsky, J. M.
- Affiliations
- University of California San Diego (US)
- University of Chicago (US)
- United States Department of Veterans Affairs (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1991-10-01
- Volume
- 88
- Issue
- 4
- Pages
- 1323-1330
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W1986731021
- Cited by
- 90
- References
- 38
- Citations by year
- 2026: 1 · 2021: 1 · 2018: 3 · 2015: 3 · 2014: 2 · 2013: 2 · 2012: 2
- FWCI
- 3.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed (publishedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-33649)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- insulin receptor, GLUT4, type 2 diabetes, insulin resistance, diabetes susceptibility genes, gene sequencing, insulin receptor beta-subunit, cytoplasmic domain, glucose transporters
- MeSH terms
- Aged, Base Sequence, Diabetes Mellitus, Type 2, Female, Humans, Insulin Resistance, Male, Middle Aged, Molecular Sequence Data, Monosaccharide Transport Proteins, Receptor, Insulin, Polymerase Chain Reaction
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