Inflammation, insulin resistance, and adiposity - A study of first-degree relatives of type 2 diabetic subjects
Inflammation, insulin resistance, and adiposity - A study of first-degree relatives of type 2 diabetic subjects
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DOI：
10.2337/diacare.27.8.2033
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发表时间：
2004-08-01
期刊：
影响因子：
16.2
通讯作者：
Campbell, LV
中科院分区：
文献类型：
--
作者：
Kriketos, AD;Greenfield, JR;Campbell, LV
目的：炎症标志物如C反应蛋白（CRP）与胰岛素抵抗、肥胖和2型糖尿病有关。炎症是否引起胰岛素抵抗或肥胖的附带现象仍然没有解决。我们的目的是确定2型糖尿病受试者的一级亲属与无糖尿病家族史的对照受试者在胰岛素敏感性方面是否存在差异，2型糖尿病受试者的一级亲属与对照受试者在CRP、脂联素和补体水平方面是否存在差异，研究设计和方法-我们首先研究了19名血糖正常的非肥胖的年轻人，2型糖尿病受试者和22名年龄、性别和BMI相似的对照受试者的一级亲属。胰岛素敏感性（葡萄糖输注率[GIR]）通过正常血糖-高胰岛素钳夹测定。双能X线吸收法测定总脂肪和腹部脂肪。结果：2型糖尿病患者的一级亲属的GIR比对照组低20%（51.8 +/- 3.9 Vs. 64.9 +/- 4.6 mumol（.）min（-1）（.）kg去脂体重（-1），P = 0.04）。然而，2型糖尿病患者和无糖尿病家族史患者的一级亲属CRP、脂联素和补体蛋白水平正常且相当。CRP与GIR（r =-0.33，P0.04）、脂联素（r =-0.34，P = 0.03）呈负相关，与肥胖呈正相关（P <0.05）。04）。然而，CRP与GIR无关，与脂肪量无关。与C3（r = 0.41，P 0.009）和因子B（r = 0.43，P = 0.005）相反，CRP与因子D无关。结论-胰岛素抵抗状态与2型糖尿病高危受试者的炎症标志物或补体蛋白变化无关。我们的研究证实了CRP和脂肪量之间的密切关系。肥胖和胰岛素抵抗的增加可能会相互作用，导致CRP水平升高。
OBJECTIVE - Inflammatory markers such as C-reactive Protein (CRP) are associated With insulin resistance, adiposity, and type 2 diabetes. Whether inflammation causes insulin resistance or is an epiphenomenon of obesity remains Unresolved. We aimed to determine whether first-degree relatives of type 2 diabetic subjects differ in insulin sensitivity from control subjects without a family history of diabetes, whether first-degree relatives of type 2 diabetic subjects and control subjects differ in CRP, adiponectin, and complement levels, and whether CRP is related to insulin sensitivity independently of adiposity.RESEARCH DESIGN AND METHODS - We studied 19 young normoglycemic non-obese first-degree relatives of type 2 diabetic subjects and 22 control subjects who were similar for age, sex, and BMI. Insulin sensitivity (glucose infusion rate [GIR]) was measured by the euglycemic-hyperinsulinemic clamp. Dual-energy X-ray absorptiometry determined total and abdominal adiposity. Magnetic resonance imaging Measured abdominal adipose tissue volumes.RESULTS - First-degree relatives of type 2 diabetic subjects had a 20% lower GIR than the control group (51.8 +/- 3.9 Vs. 64.9 +/- 4.6 mumol (.) min(-1) (.) kg fat-free mass(-1), P = 0.04). However, first-degree relatives of subjects With type 2 diabetes and those Without a family history Of diabetes had normal and comparable levels of CRP, adiponectin, and complement proteins. When the cohort was examined as a whole, CRP was inversely related to GIR (r = -0.33, P 0.04) and adiponectin (r = -0.34, P = 0.03) and positively related to adiposity (P < 0. 04). However, CRP was not related to GIR independently of fat mass. In contrast to C3 (r = 0.41, P 0.009) and factor B (r = 0.43, P = 0.005), CRP was unrelated to factor D.CONCLUSIONS - The insulin-resistant state is not associated with changes in inflammatory markers or complement proteins in subjects at high risk of type 2 diabetes. Our study confirms a strong relationship between CRP and fat mass. Increasing adiposity and insulin resistance may interact to raise CRP levels.