Elsevier

Metabolism

Volume 53, Issue 11, November 2004, Pages 1454-1461
Metabolism

Adiponectin and C-reactive protein in obesity, type 2 diabetes, and monodrug therapy

https://doi.org/10.1016/j.metabol.2004.06.013Get rights and content

Abstract

To learn more about the factors that regulate adipokines in diabetes, we examined fasting plasma concentrations of adiponectin and C-reactive protein (CRP) in well-characterized groups of age-matched individuals classified as: (1) type 2 diabetes; (2) impaired fasting glucose or mild diabetes (IFG/mild DM); (3) obese, matched for body mass index (BMI); and (4) non-obese. Diabetic subjects were also studied on no phamacologic treatment, after 3 months randomization to metformin or glyburide, and after 3 months crossover to the opposite drug. CRP decreased and adiponectin increased progressively between subjects in groups 1 through 4. CRP was significantly associated with percent (r = 0.45) and total (r = 0.50) fat, insulin sensitivity as SI (r = −0.39) or homeostasis model assessment of insulin resistance [HOMA (IR)] (r = −0.36), and hemoglobin A1c (HbA1c) (r = 0.41). The relationship of CRP to percent fat appeared to be logarithmic and log CRP varied with percent fat independent of gender. Adiponectin concentration was significantly associated with insulin sensitivity as SI (r = 0.55) or HOMA (IR) (r = −0.46). Adiponectin concentrations were higher among women overall (all groups included) but not in women classified as type 2 diabetes. Although mean adiponectin was higher in subjects classified as non-obese compared to obese, adiponectin, in sharp contrast to leptin (previously reported data) and to CRP, varied markedly when expressed as a function of adiposity. Multiple regression models confirmed the strong relationship of adiponectin to insulin sensitivity, as well as the relationships of CRP to adiposity and insulin sensitivity. Glyburide treatment of diabetes decreased CRP and did so even though body weight increased. We conclude that both CRP and adiponectin correlate strongly to SI. CRP, in contrast to adiponectin, is far more dependent on adiposity. The relationship between CRP (like leptin) and gender depends on how CRP is expressed relative to adiposity. Our data raise the possibility that gender differences in adiponectin may be lost in diabetes. Finally, pharmacologic treatment of diabetes may modulate CRP independent of adiposity.

Section snippets

Design

The protocol was reviewed and approved by our institutional Human Subjects Committee. The study protocol and inclusion and exclusion criteria have been previously reported.21 No subjects had evidence of vascular disease.

In brief, 3 groups of subjects were initially recruited: (1) type 2 diabetes, defined for the purposes of this study as fasting plasma glucose (FPG) greater than 6.9 mmol/L; (2) obese controls with FPG less than 6.1 mmol/L matched to the diabetic subjects for BMI, age, and

Results

Table 1 lists characteristics of the study participants. Diabetic subjects had been advised in a weight maintenance diet and body weights were stable at the time of GCRC admission (92.3 ± 3.1 kg at the initial GCRC admission and 92.4 ± 3.1 when determined at SV2, 2 to 3 weeks before admission).

As shown in Fig 1, adiponectin concentrations were highest in non-obese controls and progressively decreased when compared to obese subjects, IFG/mild diabetes, and type 2 diabetes. CRP concentrations

Discussion

Previous studies show that adiponectin is reduced,9, 10 while CRP is elevated2, 13, 14, 15 in subjects with features of the metabolic syndrome. While confirming these general concepts, our current work examines both of these parameters concurrently over a spectrum of age-matched subjects with varying glucose tolerance and adiposity from normal, through IFG, to type 2 diabetes. We also report the effect of 2 forms of monotherapy on adiponectin and CRP in subjects off drug treatment at the onset

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    Supported by The Department of Veterans Affairs Office of Research and Development, the Juvenile Diabetes Foundation International, Grant No. DK25295 from the National Institutes of Health, and by Grant No. M01-RR00059 from the National Center for Research Resources, General Clinical Research Centers Program, National Institutes of Health.

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