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*Diabetes
The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 1 272-278
Copyright © 1999 by The Endocrine Society

Original Studies

Circulating Tumor Necrosis Factor-{alpha} Concentrations in a Native Canadian Population with High Rates of Type 2 Diabetes Mellitus1

Bernard Zinman, Anthony J. G. Hanley, Stewart B. Harris, Jeremy Kwan and I. George Fantus

Samuel Lunenfeld Research Institute, Mount Sinai Hospital (B.Z., A.J.G.H., I.G.F.); and the Banting and Best Diabetes Center (B.Z., J.K., I.G.F.) and the Department of Public Health Sciences (A.J.G.H.), University of Toronto, Toronto, Canada M5G 1X5; and the Thames Valley Family Practice Research Unit, University of Western Ontario (S.B.H.), London, Ontario, Canada N6G 4X8

Address all correspondence and requests for reprints to: Dr. Bernard Zinman, Division of Endocrinology and Metabolism, Mount Sinai Hospital, 600 University Avenue, Suite 782, Toronto, Ontario, Canada M5G 1X5. E-mail: zinman{at}mshri.on.ca

Recent research suggests that tumor necrosis factor-{alpha} (TNF{alpha}) may play an important role in obesity-associated insulin resistance and diabetes. We studied the relationship between TNF{alpha} and the anthropometric and physiological variables associated with insulin resistance and diabetes in an isolated Native Canadian population with very high rates of type 2 diabetes mellitus (DM).

A stratified random sample (n = 80) of participants was selected from a population-based survey designed to determine the prevalence of type 2 DM and its associated risk factors. Fasting blood samples for glucose, insulin, triglyceride, leptin, and TNF{alpha} were collected; a 75-g oral glucose tolerance test was administered, and a second blood sample was drawn after 120 min. Insulin resistance was estimated using the homeostasis assessment (HOMA) model. Systolic and diastolic blood pressure (BP), height, weight, and waist and hip circumferences were determined, and percent body fat was estimated using biological impedance analysis. The relationship between circulating concentrations of TNF{alpha} and the other variables was assessed using Spearman correlation coefficients, analysis of covariance, and multiple linear regression.

The mean TNF{alpha} concentration was 5.6 pg/mL (SD = 2.18) and ranged from 2.0–12.9 pg/mL, with no difference between men and women (P = 0.67). There were moderate, but statistically significant, correlations between TNF{alpha} and fasting insulin, HOMA insulin resistance (HOMA IR) waist circumference, fasting triglyceride, and systolic BP (r = 0.23–0.34; all P < 0.05); in all cases, coefficients for females were stronger than those for males. Individuals with normal glucose tolerance had lower log TNF{alpha} concentrations than those with impaired glucose tolerance or type 2 DM (both P = 0.03, adjusted for age and sex), although differences were not significant after adjustment for HOMA IR (both P > 0.25). Regression analysis indicated that log HOMA IR and log systolic BP were significant independent contributors to variations in log TNF{alpha} concentration (model r2 = 0.32). We conclude that in this homogeneous Native Canadian population, circulating TNF{alpha} concentrations are positively correlated with insulin resistance across a spectrum of glucose tolerance. The data suggest a possible role for TNF{alpha} in the pathophysiology of insulin resistance.




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