The DOI matches its Crossref record.
Relationship of Generalized and Regional Adiposity to Insulin Sensitivity in Men With NIDDM
Abstract
Abdominal obesity, particularly excess intraperitoneal fat, is considered to play a major role in causing insulin resistance and NIDDM. To determine if NIDDM patients accumulate excess intraperitoneal fat, and whether this contributes significantly to their insulin resistance, 31 men with mild NIDDM with a wide range of adiposity were compared with 39 nondiabetic, control subjects for insulin sensitivity (measured using euglycemic-hyperinsulinemic clamp technique with [3-3H]glucose turnover) and total and regional adiposity (assessed by hydrodensitometry and by measuring subcutaneous abdominal, intraperitoneal, and retroperitoneal fat masses using magnetic resonance imaging [MRI], and truncal and peripheral skinfold thicknesses using calipers). MRI analysis revealed that intraperitoneal fat was not increased in NIDDM patients compared with control subjects; in both groups it averaged 11% of total body fat. NIDDM patients, however, had increased truncal-to-peripheral skinfolds thickness ratios. In NIDDM patients, as in control subjects, amounts of truncal subcutaneous fat showed a stronger correlation with glucose disposal rate than intraperitoneal or retroperitoneal fat; however, NIDDM patients were more insulin resistant at every level of total or regional adiposity. Further, no particular influence of excess intraperitoneal fat on hepatic insulin sensitivity was noted. We conclude that NIDDM patients do not have excess intraperitoneal fat, but that their fat distribution favors more truncal and less peripheral subcutaneous fat. Moreover, for each level of total and regional adiposity, NIDDM patients have a heightened state of insulin resistance.
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Metadata
- Authors
- Abate, N., Garg, A., Peshock, R. M., Stray-Gundersen, J., Adams-Huet, B., & Grundy, S. M.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1996-12-01
- Volume
- 45
- Issue
- 12
- Pages
- 1684-1693
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2111968328
- Cited by
- 297
- References
- 0
- FWCI
- 6.75
- Type
- journal article
- Language
- en
- Open access
- closed
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