PMID- 9920095
OWN - NLM
STAT- MEDLINE
DCOM- 19990203
LR  - 20220331
IS  - 0021-972X (Print)
IS  - 0021-972X (Linking)
VI  - 84
IP  - 1
DP  - 1999 Jan
TI  - Circulating tumor necrosis factor-alpha concentrations in a native Canadian 
      population with high rates of type 2 diabetes mellitus.
PG  - 272-8
AB  - 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.
FAU - Zinman, B
AU  - Zinman B
AD  - Samuel Lunenfeld Research Institute, Mount Sinai Hospital, and Banting and Best 
      Diabetes Center, University of Toronto, Ontario, Canada. zinman@mshri.on.ca
FAU - Hanley, A J
AU  - Hanley AJ
FAU - Harris, S B
AU  - Harris SB
FAU - Kwan, J
AU  - Kwan J
FAU - Fantus, I G
AU  - Fantus IG
LA  - eng
GR  - 91-DK-01/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Blood Pressure
MH  - Canada
MH  - Child
MH  - Diabetes Mellitus, Type 2/blood/*etiology
MH  - Female
MH  - Humans
MH  - *Insulin Resistance
MH  - Male
MH  - Middle Aged
MH  - Obesity/metabolism
MH  - Regression Analysis
MH  - Tumor Necrosis Factor-alpha/analysis/*physiology
EDAT- 1999/01/27 00:00
MHDA- 1999/01/27 00:01
CRDT- 1999/01/27 00:00
PHST- 1999/01/27 00:00 [pubmed]
PHST- 1999/01/27 00:01 [medline]
PHST- 1999/01/27 00:00 [entrez]
AID - 10.1210/jcem.84.1.5405 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 1999 Jan;84(1):272-8. doi: 10.1210/jcem.84.1.5405.