C‐reactive protein is more strongly related to post‐glucose load glucose than to fasting glucose in non‐diabetic subjects; the Insulin Resistance Atherosclerosis Study
- 6 November 2002
- journal article
- research article
- Published by Wiley in Diabetic Medicine
- Vol. 19 (11) , 939-943
- https://doi.org/10.1046/j.1464-5491.2002.00824.x
Abstract
Aims It has been suggested that cardiovascular disease may be more strongly related to post‐challenge glycaemia than to fasting glucose concentrations. We hypothesized that subclinical inflammation, as indicated by elevated serum levels of C‐reactive protein (CRP), may partially explain the association of cardiovascular disease with post‐challenge glycaemia.Methods We studied the relationship of CRP (measured with a highly sensitive immunoassay) with fasting glucose and 2‐h glucose concentrations during an oral glucose tolerance test in non‐diabetic subjects from the Insulin Resistance Atherosclerosis Study.Results Spearman correlation analyses and multiple linear regression analyses showed a significant association of both fasting glucose and 2‐h glucose concentrations with CRP levels, after adjusting for demographic covariates (age, sex, ethnicity, clinical centre; Spearman correlation coefficients: r = 0.18 for fasting glucose, r = 0.27 for 2‐h glucose, both P < 0.0001). However, after additional adjustment for body mass index and waist–hip ratio only 2‐h glucose (and not fasting glucose) was significantly related to CRP (r = 0.03 for fasting glucose, P = NS; r = 0.14 for 2‐h glucose, P < 0.0001). Adding insulin sensitivity to the multivariate models further weakened the relationship of CRP to 2‐h glucose (r = 0.07, P < 0.05). CRP mean values increased by 2‐h glucose category (normal vs. impaired glucose tolerance vs. isolated post‐challenge hyperglycaemia).Conclusions Chronic, subclinical inflammation, as indicated by elevated circulating CRP levels, is more strongly associated with post‐challenge glycaemia than with fasting glucose levels in non‐diabetic subjects. This association is partially independent of body fat and insulin resistance.Diabet. Med. 19, 939–943 (2002)Keywords
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