Putz Darcy M, Goldner Whitney S, Bar Robert S, Haynes William G, Sivitz William I
Department of Internal Medicine, Division of Endocrinology, Iowa City Veterans Affairs Medical Center, IA 52246, USA.
Metabolism. 2004 Nov;53(11):1454-61. 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.
为了进一步了解糖尿病中调节脂肪因子的因素，我们检测了年龄匹配的特征明确的几组个体的空腹血浆脂联素和C反应蛋白（CRP）浓度，这些个体分为：（1）2型糖尿病；（2）空腹血糖受损或轻度糖尿病（IFG/轻度DM）；（3）肥胖，体重指数（BMI）匹配；（4）非肥胖。对糖尿病患者还进行了如下研究：未接受药物治疗时、随机接受二甲双胍或格列本脲治疗3个月后，以及交叉使用另一种药物治疗3个月后。第1组至第4组受试者的CRP逐渐降低，脂联素逐渐升高。CRP与体脂百分比（r = 0.45）、总脂肪量（r = 0.50）、胰岛素敏感性[S(I)，r = -0.39]或胰岛素抵抗稳态模型评估[HOMA(IR)，r = -0.36]以及糖化血红蛋白（HbA(1c)，r = 0.41）显著相关。CRP与体脂百分比的关系似乎呈对数关系，且log CRP随体脂百分比变化，与性别无关。脂联素浓度与胰岛素敏感性[S(I)，r = 0.55]或HOMA(IR)（r = -0.46）显著相关。总体而言，女性的脂联素浓度较高（包括所有组），但2型糖尿病女性的脂联素浓度不高。尽管与肥胖者相比，非肥胖者的平均脂联素水平较高，但与瘦素（先前报道的数据）和CRP形成鲜明对比的是，脂联素作为肥胖的函数时变化显著。多元回归模型证实了脂联素与胰岛素敏感性之间的密切关系，以及CRP与肥胖和胰岛素敏感性之间的关系。格列本脲治疗糖尿病可降低CRP，即使体重增加时也是如此。我们得出结论，CRP和脂联素均与S(I)密切相关。与脂联素不同，CRP更依赖于肥胖。CRP（如瘦素）与性别的关系取决于CRP相对于肥胖的表达方式。我们的数据增加了糖尿病中脂联素性别差异可能消失的可能性。最后，糖尿病的药物治疗可能独立于肥胖调节CRP。
