Venturi C, Zoppini G, Zamboni C, Muggeo M
Division of Endocrinology and Metabolic Disease, University of Verona Medical School, Verona, Italy.
Nutr Metab Cardiovasc Dis. 2004 Aug;14(4):200-4. doi: 10.1016/s0939-4753(04)80005-x.
Hepatic steatosis has recently been associated with insulin resistance and other metabolic abnormalities as a possible feature of the metabolic syndrome, but it is still uncertain how hepatic steatosis and insulin sensitivity are connected. Furthermore, obesity is a well characterized insulin resistant condition that is often associated with hepatic steatosis. The aim of this study was to verify whether hepatic steatosis further worsens insulin sensitivity in obese subjects by comparing the degree of insulin sensitivity in obese subjects with normal glucose tolerance on the basis of the presence or absence of hepatic steatosis.
We analyzed 86 obese patients whose alcohol intake was less than 20 g/day and who showed no signs of viral hepatopathy. All of the subjects had normal glucose tolerance as shown by an oral glucose tolerance test. Insulin resistance was estimated using the homeostasis model assessment (HOMA) method and the diagnosis of steatosis was determined by an ultrasound scan of the liver. The subjects were comparable in terms of body mass index (BMI), lipid profile and serum uric acid levels; those with hepatic steatosis were slightly older and tended to have higher systolic blood pressure and fasting glycemia levels. The HOMA values were significantly higher in the group with hepatic steatosis (4.48 +/- 2.22 vs 3.11 +/- 1.47, p=0.002). There was no linear correlation between HOMA and alanine aminotransferase (ALT) levels, but a close linear correlation between HOMA and BMI (r=0.40; p<0.001). The effect of hepatic steatosis on HOMA remained significant after adjusting for age and gender (covariance analysis, p=0.006). When BMI was added to the covariance analysis, hepatic steatosis retained its statistical significance.
Our data suggest that hepatic steatosis can increase insulin resistance independently of obesity.
肝脂肪变性最近被认为与胰岛素抵抗及其他代谢异常相关,可能是代谢综合征的一个特征,但肝脂肪变性与胰岛素敏感性之间的联系仍不明确。此外,肥胖是一种典型的胰岛素抵抗状态,常与肝脂肪变性相关。本研究的目的是通过比较存在或不存在肝脂肪变性的糖耐量正常肥胖受试者的胰岛素敏感性程度,来验证肝脂肪变性是否会进一步加重肥胖受试者的胰岛素敏感性。
我们分析了86例酒精摄入量小于20克/天且无病毒性肝病迹象的肥胖患者。所有受试者经口服葡萄糖耐量试验显示糖耐量正常。采用稳态模型评估(HOMA)法评估胰岛素抵抗,通过肝脏超声扫描确定脂肪变性的诊断。受试者在体重指数(BMI)、血脂谱和血清尿酸水平方面具有可比性;有肝脂肪变性的受试者年龄稍大,收缩压和空腹血糖水平往往较高。肝脂肪变性组的HOMA值显著更高(4.48±2.22对3.11±1.47,p = 0.002)。HOMA与丙氨酸氨基转移酶(ALT)水平之间无线性相关性,但HOMA与BMI之间存在密切的线性相关性(r = 0.40;p < 0.001)。在调整年龄和性别后,肝脂肪变性对HOMA的影响仍然显著(协方差分析,p = 0.006)。当将BMI添加到协方差分析中时,肝脂肪变性仍具有统计学意义。
我们的数据表明,肝脂肪变性可独立于肥胖增加胰岛素抵抗。