OBJECTIVES Emerging evidence suggests that intermuscular adipose tissue is a risk factor for insulin resistance, but the underlying mechanism still remains unclear. We investigated whether the levels of leptin, adiponectin, and monocyte chemoattractant protein-1 are associated with intermuscular adipose tissue in obese subjects. DESIGN AND METHODS A cross-sectional study was performed on 77 obese Korean women. Areas of visceral adipose tissue, subcutaneous adipose tissue, and intermuscular adipose tissue were measured by computed tomography scan, and serum concentrations of adipokines were measured by enzyme-linked immunosorbent assays. Correlation between the levels of adipokines and the fat areas was assessed using Pearson correlation and covariate-adjusted multivariable regression. RESULTS Leptin was positively correlated with subcutaneous adipose tissue (r=0.452, P<0.001), fasting insulin (r=0.403, P<0.001), and homeostasis model assessment of insulin resistance (r=0.360, P=0.001), whereas monocyte chemoattractant protein-1 was positively correlated with intermuscular adipose tissue (r=0.483, P<0.001). After adjustment for age, height, and other body composition metrics, leptin was still related to subcutaneous adipose tissue (β=0.390, P=0.001). Monocyte chemoattractant protein-1 was associated with intermuscular adipose tissue (β=0.433, P=0.001) after adjustment for visceral adipose tissue. CONCLUSIONS Intermuscular adipose tissue was correlated with monocyte chemoattractant protein-1, suggesting its role in the development of insulin resistance.

中文翻译：

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肌间脂肪组织与单核细胞趋化蛋白-1相关，独立于内脏脂肪组织。

目的新兴证据表明，肌间脂肪组织是胰岛素抵抗的危险因素，但其潜在机制仍不清楚。我们研究了肥胖受试者中瘦素，脂联素和单核细胞趋化蛋白-1的水平是否与肌间脂肪组织有关。设计与方法对77名肥胖的韩国女性进行了横断面研究。通过计算机断层摄影术测量内脏脂肪组织，皮下脂肪组织和肌间脂肪组织的面积，并通过酶联免疫吸附测定法测量血清脂肪因子的浓度。使用皮尔森相关性和协变量调整后的多元回归分析评估脂肪因子水平与脂肪区域之间的相关性。结果瘦素与皮下脂肪组织（r = 0.452，P <0.001），空腹胰岛素（r = 0.403，P <0.001）和胰岛素抵抗稳态模型评估（r = 0.360，P = 0.001）呈正相关。趋化蛋白-1与肌间脂肪组织呈正相关（r = 0.483，P <0.001）。调整年龄，身高和其他身体成分指标后，瘦素仍与皮下脂肪组织有关（β= 0.390，P = 0.001）。调整内脏脂肪组织后，单核细胞趋化蛋白-1与肌间脂肪组织相关（β= 0.433，P = 0.001）。结论肌间脂肪组织与单核细胞趋化蛋白-1相关，提示其在胰岛素抵抗的发生中起重要作用。0.001）和胰岛素抵抗的稳态模型评估（r = 0.360，P = 0.001），而单核细胞趋化蛋白-1与肌间脂肪组织正相关（r = 0.483，P <0.001）。调整年龄，身高和其他身体成分指标后，瘦素仍与皮下脂肪组织有关（β= 0.390，P = 0.001）。调整内脏脂肪组织后，单核细胞趋化蛋白-1与肌间脂肪组织相关（β= 0.433，P = 0.001）。结论肌间脂肪组织与单核细胞趋化蛋白-1相关，提示其在胰岛素抵抗的发生中起重要作用。0.001）和稳态模型评估胰岛素抵抗（r = 0.360，P = 0.001），而单核细胞趋化蛋白-1与肌间脂肪组织正相关（r = 0.483，P <0.001）。调整年龄，身高和其他身体成分指标后，瘦素仍与皮下脂肪组织有关（β= 0.390，P = 0.001）。调整内脏脂肪组织后，单核细胞趋化蛋白-1与肌间脂肪组织相关（β= 0.433，P = 0.001）。结论肌间脂肪组织与单核细胞趋化蛋白-1相关，提示其在胰岛素抵抗的发生中起重要作用。P ＜0.001）。调整年龄，身高和其他身体成分指标后，瘦素仍与皮下脂肪组织有关（β= 0.390，P = 0.001）。调整内脏脂肪组织后，单核细胞趋化蛋白-1与肌间脂肪组织相关（β= 0.433，P = 0.001）。结论肌间脂肪组织与单核细胞趋化蛋白-1相关，提示其在胰岛素抵抗的发生中起重要作用。P ＜0.001）。调整年龄，身高和其他身体成分指标后，瘦素仍与皮下脂肪组织有关（β= 0.390，P = 0.001）。调整内脏脂肪组织后，单核细胞趋化蛋白-1与肌间脂肪组织相关（β= 0.433，P = 0.001）。结论肌间脂肪组织与单核细胞趋化蛋白-1相关，提示其在胰岛素抵抗的发生中起重要作用。