Diabetes and Metabolism Unit, Department of Medicine, Section of Endocrinology, Boston University Medical Center, Boston, MA 02118, U.S.A.
Biochem J. 2010 Sep 1;430(2):e1-4. doi: 10.1042/BJ20101062.
In recent years, it has become widely accepted that obesity is characterized by a chronic low-grade inflammation of adipose tissue that predisposes affected individuals to insulin resistance, Type 2 diabetes and other disorders associated with the metabolic syndrome. On the other hand, a subset of obese individuals appears to be protected against insulin resistance and the disorders to which it predisposes. The comparison between such insulin-sensitive and insulin-resistant obese individuals offers a unique opportunity to identify key factors that either contribute to or prevent the development of insulin resistance in humans, without the confounding effect of a major difference in fat mass. In the previous issue of the Biochemical Journal, Barbarroja et al. reported that insulin-sensitive obese individuals show less inflammation in their visceral adipose tissue than a group of insulin-resistant subjects matched for BMI (body mass index). This finding reinforces the concept that inflammation in adipose tissue may be a cause of insulin resistance in most obese individuals, although it does not prove it. Further studies will be required for this purpose, as well as to identify the pathogenetic factors that determine whether or not adipose tissue of an obese individual becomes inflamed.
近年来,人们普遍认为肥胖的特征是脂肪组织的慢性低度炎症,这使受影响的个体易患胰岛素抵抗、2 型糖尿病和其他与代谢综合征相关的疾病。另一方面,一部分肥胖个体似乎对胰岛素抵抗及其易患的疾病有一定的保护作用。这种胰岛素敏感和胰岛素抵抗肥胖个体之间的比较为我们提供了一个独特的机会,使我们能够在没有脂肪量主要差异的混杂影响下,确定导致或预防人类胰岛素抵抗的关键因素。在之前一期的《生物化学杂志》上,Barbarroja 等人报告说,与 BMI(体重指数)匹配的胰岛素抵抗组相比,胰岛素敏感的肥胖个体其内脏脂肪组织的炎症程度较低。这一发现进一步证实了这样一种观点,即脂肪组织的炎症可能是大多数肥胖个体发生胰岛素抵抗的原因,但这并不能证明这一点。为此目的,还需要进一步研究,以确定决定肥胖个体的脂肪组织是否发生炎症的发病因素。