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硬脂酰辅酶 A 去饱和酶-1 与病态肥胖患者的胰岛素抵抗有关。

Stearoyl-CoA desaturase-1 is associated with insulin resistance in morbidly obese subjects.

机构信息

CIBER Diabetes and Associated Metabolic Disorders, ISCIII, Spain.

出版信息

Mol Med. 2011 Mar-Apr;17(3-4):273-80. doi: 10.2119/molmed.2010.00078. Epub 2010 Nov 5.

DOI:10.2119/molmed.2010.00078
PMID:21060977
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3060976/
Abstract

Animal studies have revealed the association between stearoyl-CoA desaturase 1 (SCD1) and obesity and insulin resistance. However, only a few studies have been undertaken in humans. We studied SCD1 in visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) from morbidly obese patients and their association with insulin resistance, sterol regulatory element binding protein-1 (SREBP-1) and ATPase p97, proteins involved in SCD1 synthesis and degradation. The insulin resistance was calculated in 40 morbidly obese patients and 11 overweight controls. Measurements were made of VAT and SAT SCD1, SREBP-1 and ATPase p97 mRNA expression and protein levels. VAT and SAT SCD1 mRNA expression levels in the morbidly obese patients were significantly lower than in the controls (P = 0.006), whereas SCD1 protein levels were significantly higher (P < 0.001). In the morbidly obese patients, the VAT SCD1 protein levels were decreased in patients with higher insulin resistance (P = 0.007). However, SAT SCD1 protein levels were increased in morbidly obese patients with higher insulin resistance (P < 0.05). Multiple linear regressions in the morbidly obese patients showed that the variable associated with the SCD1 protein levels in VAT was insulin resistance, and the variables associated with SCD1 protein levels in SAT were body mass index (BMI) and ATPase p97. In conclusion, these data suggest that the regulation of SCD1 is altered in individuals with morbid obesity and that the SCD1 protein has a different regulation in the two adipose tissues, as well as being closely linked to the degree of insulin resistance.

摘要

动物研究揭示了硬脂酰辅酶 A 去饱和酶 1(SCD1)与肥胖和胰岛素抵抗之间的关联。然而,仅有少数研究在人类中进行。我们研究了病态肥胖患者内脏脂肪组织(VAT)和皮下脂肪组织(SAT)中的 SCD1 及其与胰岛素抵抗、固醇调节元件结合蛋白-1(SREBP-1)和 ATPase p97 的关系,这些蛋白参与 SCD1 的合成和降解。在 40 名病态肥胖患者和 11 名超重对照者中计算了胰岛素抵抗。测量了 VAT 和 SAT 的 SCD1、SREBP-1 和 ATPase p97 mRNA 表达和蛋白水平。病态肥胖患者的 VAT 和 SAT SCD1 mRNA 表达水平明显低于对照组(P = 0.006),而 SCD1 蛋白水平明显升高(P < 0.001)。在病态肥胖患者中,VAT SCD1 蛋白水平在胰岛素抵抗较高的患者中降低(P = 0.007)。然而,SAT SCD1 蛋白水平在胰岛素抵抗较高的病态肥胖患者中增加(P < 0.05)。病态肥胖患者的多元线性回归显示,与 VAT 中 SCD1 蛋白水平相关的变量是胰岛素抵抗,与 SAT 中 SCD1 蛋白水平相关的变量是体重指数(BMI)和 ATPase p97。总之,这些数据表明,病态肥胖个体中 SCD1 的调节发生了改变,并且 SCD1 蛋白在两种脂肪组织中的调节方式不同,并且与胰岛素抵抗的程度密切相关。

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