Shadid Samyah, Stehouwer Coen D A, Jensen Michael D
Endocrine Research Unit, 5-194 Joseph, Mayo Clinic, 200 1st Street SW, Rochester, Minnesota 55905, USA.
J Clin Endocrinol Metab. 2006 Sep;91(9):3418-25. doi: 10.1210/jc.2006-0015. Epub 2006 Jun 27.
Plasma adipokine concentrations are variably related to fatness/insulin resistance and may act via endocrine mechanisms. We assessed the relationship among plasma adipokine concentrations and their relationship with insulin sensitivity and body composition in obese adults before and after insulin sensitization accomplished using diet/exercise or pioglitazone.
Plasma adipokine concentrations, insulin sensitivity, and body composition were assessed in 39 upper-body obese insulin-resistant, nondiabetic adults before and after 19 wk of diet/exercise or 30 mg/d pioglitazone.
Diet/exercise reduced body fat and visceral fat and improved insulin sensitivity parameters; pioglitazone improved insulin sensitivity to a similar degree but increased body fat. Adiponectin increased more after pioglitazone (4770 +/- 487 vs. 8351 +/- 693.6 ng/ml, P < 0.001) than after diet/exercise (4704 +/- 367 to 5426 +/- 325.3 ng/ml, P < 0.01), whereas TNFalpha, IL-6, and resistin did not change. C-reactive protein decreased with diet/exercise. Adipokine concentrations were not correlated with each other at baseline or after insulin sensitization, except TNFalpha and IL-6 (r = 0.43, P < 0.05); IL-6 was inversely correlated with resistin. Only adiponectin was correlated (P < 0.05) with indices of insulin sensitivity. Adiponectin concentrations were inversely correlated with visceral fat and with sc fat depots in men but positively correlated with sc fat in women.
Plasma adipokine concentrations were not consistently interrelated, and only adiponectin displayed the expected relationship with insulin sensitivity and sensitization. These findings do not support an endocrine role for resistin, TNFalpha, and IL-6 in mediating changes in insulin resistance after diet/exercise or pioglitazone.
血浆脂肪因子浓度与肥胖/胰岛素抵抗存在不同程度的关联,可能通过内分泌机制发挥作用。我们评估了肥胖成年人在通过饮食/运动或吡格列酮实现胰岛素增敏前后血浆脂肪因子浓度之间的关系,以及它们与胰岛素敏感性和身体组成的关系。
对39名上半身肥胖、胰岛素抵抗的非糖尿病成年人在进行19周饮食/运动或每日30毫克吡格列酮治疗前后,评估其血浆脂肪因子浓度、胰岛素敏感性和身体组成。
饮食/运动减少了体脂和内脏脂肪,改善了胰岛素敏感性参数;吡格列酮在相似程度上改善了胰岛素敏感性,但增加了体脂。吡格列酮治疗后脂联素增加幅度(4770±487对8351±693.6纳克/毫升,P<0.001)大于饮食/运动治疗后(4704±367至5426±325.3纳克/毫升,P<0.01),而肿瘤坏死因子α(TNFα)、白细胞介素-6(IL-6)和抵抗素未发生变化。饮食/运动使C反应蛋白降低。在基线或胰岛素增敏后,除TNFα和IL-6(r=0.43,P<0.05)外,脂肪因子浓度彼此之间无相关性;IL-6与抵抗素呈负相关。只有脂联素与胰岛素敏感性指标相关(P<0.05)。脂联素浓度与男性内脏脂肪和皮下脂肪储存呈负相关,但与女性皮下脂肪呈正相关。
血浆脂肪因子浓度并非始终相互关联,只有脂联素表现出与胰岛素敏感性和增敏作用的预期关系。这些发现不支持抵抗素、TNFα和IL-6在介导饮食/运动或吡格列酮治疗后胰岛素抵抗变化中发挥内分泌作用。