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

• Published in: Metabolism, clinical and experimental clinical and experimental, 2004-11, Vol.53 (11), p.1454-1461
• Main Authors: PUTZ, Darcy M, GOLDNER, Whitney S, BAR, Robert S, HAYNES, William G, SIVITZ, William I
• Format: Article
• Language: English
• Subjects: Adiponectin; Biological and medical sciences; Blood Glucose - drug effects; Blood Glucose - metabolism; Body Composition; C-Reactive Protein - metabolism; Cross-Over Studies; Diabetes Mellitus, Type 2 - blood; Diabetes Mellitus, Type 2 - drug therapy; Female; Glyburide - therapeutic use; Glycated Hemoglobin A - metabolism; Humans; Hypoglycemic Agents - therapeutic use; Insulin - blood; Insulin Resistance; Intercellular Signaling Peptides and Proteins - blood; Leptin - blood; Linear Models; Lipids - blood; Male; Medical sciences; Metabolic diseases; Metformin - therapeutic use; Middle Aged; Obesity; Obesity - blood; Sex Factors
• ISSN: 0026-0495; 1532-8600
• DOI: 10.1016/j.metabol.2004.06.013

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 S(I) (r = -0.39) or homeostasis model assessment of insulin resistance [HOMA (IR)] (r = -0.36), and hemoglobin A(1c) (HbA(1c)) (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 S(I) (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 S(I). 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.