Chetty V Tony, Damjanovic Suzana, Gerstein Hertzel, Singh Nina, Yusuf Salim, Anand Sonia S, Sharma Arya M
McMaster University , Hamilton, Ontario , Canada.
Blood Press. 2014 Feb;23(1):54-60. doi: 10.3109/08037051.2013.791411. Epub 2013 Jun 3.
BACKGROUND. Abdominal obesity, characterized by ectopic fat deposition in skeletal muscle and liver tissue, has been associated with insulin resistance and increased risk for type 2 diabetes mellitus. The aim of this study was to evaluate whether treatment with the angiotensin II type 1 (AT-1) receptor blocker telmisartan can reduce intramyocellular lipid (IMCL) and hepatic fat storage, thereby improving insulin sensitivity among individuals with abdominal obesity. METHODS. Ninety-five adults with abdominal obesity (body mass index ≥ 30 kg/m(2) and waist circumference > 102 cm in men and > 88 cm in women) were randomized to double-blind treatment with telmisartan or placebo for 24 weeks. Following 4 weeks of 80 mg telmisartan per day, the dose was increased to 160 mg telmisartan for the duration of the study. Soleus muscle IMCL and liver fat content were assessed by (1)H-magnetic resonance imaging ((1)H-MRI) spectroscopy. Secondary outcomes included changes in body composition, plasma lipids, glucose profiles, insulin sensitivity, beta-cell function and total adiponectin levels. RESULTS. There was no significant effect of telmisartan in abdominally obese individuals consuming either a low or high glycemic diet, on IMCL content (5.73 ± 1.11 vs 6.11 ± 1.11; p = 0.13) or liver fat (0.08 ± 0.05 vs 0.09 ± 0.05; p = 0.60). Body composition, lipid and glucose profiles, insulin sensitivity and adiponectin were likewise unaffected. Beta-cell function, as determined by the insulinogenic index (IGI), improved significantly (19.3 ± 13.7 vs 22.5 ± 17.6; p = 0.03; 16.5% increase from baseline in the telmisartan group). CONCLUSIONS. Telmisartan increased beta-cell function but did not decrease IMCL or liver fat content or other metabolic parameters among individuals with abdominal obesity.
背景。腹部肥胖的特征是骨骼肌和肝组织中存在异位脂肪沉积,与胰岛素抵抗及2型糖尿病风险增加有关。本研究的目的是评估血管紧张素II 1型(AT-1)受体阻滞剂替米沙坦治疗是否能减少肌细胞内脂质(IMCL)和肝脏脂肪储存,从而改善腹部肥胖个体的胰岛素敏感性。方法。95名腹部肥胖的成年人(男性体重指数≥30kg/m²且腰围>102cm,女性体重指数≥30kg/m²且腰围>88cm)被随机分为替米沙坦或安慰剂双盲治疗24周。在每天服用80mg替米沙坦4周后,在研究期间剂量增加至160mg替米沙坦。通过氢磁共振成像((1)H-MRI)光谱评估比目鱼肌IMCL和肝脏脂肪含量。次要结局包括身体成分、血脂、血糖谱、胰岛素敏感性、β细胞功能和总脂联素水平的变化。结果。在食用低糖或高糖饮食的腹部肥胖个体中,替米沙坦对IMCL含量(5.73±1.11 vs 6.11±1.11;p = 0.13)或肝脏脂肪(0.08±0.05 vs 0.09±0.05;p = 0.60)均无显著影响。身体成分、血脂和血糖谱、胰岛素敏感性和脂联素同样未受影响。由胰岛素生成指数(IGI)确定的β细胞功能显著改善(19.3±13.7 vs 22.5±17.6;p = 0.03;替米沙坦组较基线增加16.5%)。结论。替米沙坦可增加腹部肥胖个体的β细胞功能,但不会降低IMCL或肝脏脂肪含量或其他代谢参数。