Abdominal subcutaneous and visceral adipose tissue and insulin resistance in the Framingham heart study.

Abdominal subcutaneous and visceral adipose tissue and insulin resistance in the Framingham heart study.
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DOI:
10.1038/oby.2010.59
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发表时间:
2010-11
期刊:
Obesity (Silver Spring, Md.)
影响因子:
--
通讯作者:
Fox CS
Fox CS
中科院分区:
其他
文献类型:
--
作者:
Preis SR;Massaro JM;Robins SJ;Hoffmann U;Vasan RS;Irlbeck T;Meigs JB;Sutherland P;D'Agostino RB Sr;O'Donnell CJ;Fox CS

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胰岛素抵抗与中心性肥胖和心血管疾病风险增加有关。我们的目的是研究腹部皮下脂肪组织(SAT)和内脏脂肪组织(VAT)与胰岛素抵抗之间的关系,以确定哪种脂肪储存与胰岛素抵抗的相关性更强,并评估SAT,VAT和年龄,性别或BMI之间是否存在相互作用。对来自FHS的无糖尿病受试者进行了评估,他们接受了多探测器计算机断层扫描以评估SAT和VAT(n = 3,093; 48%为女性;平均年龄50.4岁;平均BMI 27.6 kg/m2)。使用稳态模型测量胰岛素抵抗,并定义为HOMAIR ≥第75百分位数。Logistic回归模型,调整年龄,性别,吸烟,饮酒,绝经状态,激素替代治疗的使用,用于评估脂肪措施和胰岛素抵抗之间的关联。SAT每增加一个标准差,胰岛素抵抗的比值比(OR)为2.5(95%置信区间(CI):2.2 - 2.7; P <0.0001),而VAT每增加一个标准差,胰岛素抵抗的OR为3.5(95% CI:3.1 - 3.9; P <0.0001)。总体而言,VAT与胰岛素抵抗的相关性强于SAT(SAT与VAT比较P <0.0001)。调整BMI后,胰岛素抵抗与增值税的OR为2.2(95%CI:1.9 - 2.5; P <0.0001)。我们观察到VAT和BMI之间的胰岛素(P交互= 0.0004),胰岛素原(P交互= 0.003)和HOMAIR(P交互= 0.003)的相互作用,其中VAT在肥胖个体中具有更强的相关性。总之,SAT和VAT都是胰岛素抵抗的相关因素;然而,VAT比SAT与胰岛素抵抗的相关性更强。
Insulin resistance is associated with central obesity and an increased risk of cardiovascular disease. Our objective is to examine the association between abdominal subcutaneous (SAT) and visceral adipose tissue (VAT) and insulin resistance, to determine which fat depot is a stronger correlate of insulin resistance, and to assess whether there was an interaction between SAT, VAT, and age, sex, or BMI. Participants without diabetes from the Framingham Heart Study (FHS), who underwent multidetector computed tomography to assess SAT and VAT (n = 3,093; 48% women; mean age 50.4 years; mean BMI 27.6 kg/m2), were evaluated. Insulin resistance was measured using the homeostasis model and defined as HOMAIR ≥75th percentile. Logistic regression models, adjusted for age, sex, smoking, alcohol, menopausal status, and hormone replacement therapy use, were used to assess the association between fat measures and insulin resistance. The odds ratio (OR) for insulin resistance per standard deviation increase in SAT was 2.5 (95% confidence interval (CI): 2.2–2.7; P < 0.0001), whereas the OR for insulin resistance per standard deviation increase in VAT was 3.5 (95% CI: 3.1–3.9; P < 0.0001). Overall, VAT was a stronger correlate of insulin resistance than SAT (P < 0.0001 for SAT vs. VAT comparison). After adjustment for BMI, the OR of insulin resistance for VAT was 2.2 (95% CI: 1.9–2.5; P < 0.0001). We observed an interaction between VAT and BMI for insulin (P interaction = 0.0004), proinsulin (P interaction = 0.003), and HOMAIR (P interaction = 0.003), where VAT had a stronger association in obese individuals. In conclusion, SAT and VAT are both correlates of insulin resistance; however, VAT is a stronger correlate of insulin resistance than SAT.
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