Maslowska M, Vu H, Phelis S, Sniderman A D, Rhode B M, Blank D, Cianflone K
Mike Rosenbloom Laboratory for Cardiovascular Research, McGill University, Montreal, Quebec, Canada.
Eur J Clin Invest. 1999 Aug;29(8):679-86. doi: 10.1046/j.1365-2362.1999.00514.x.
Acylation stimulating protein (ASP) is a potent stimulator of TG synthesis in human adipocytes.
In the present study, we have analysed plasma ASP and adipsin levels and their relationships to plasma lipids in non-obese and obese groups.
The results show that the frequency distribution of ASP is skewed but that of adipsin is normal in both groups. In the non-obese population, the mean levels of plasma ASP and adipsin were 20.2 nmol L-1 (median) and 66.6 +/- 19 nmol L-1 (mean) respectively. No difference was observed between men and women for each of the parameters. In the obese population, the median plasma ASP was increased by 246% (69.9 nmol L-1) and adipsin by 31% (87.0 +/- 22.7 nmol L-1) above that of the control group. Although the levels for men and women were not statistically different for adipsin, the median ASP plasma concentration was 1.9-fold higher in obese women than in obese men (71.8 nmol L-1 vs. 37.6 nmol L-1, P < 0.05). Best subset regression analysis provided a model with variables that best predict plasma ASP [r2 = 0.160, P < 0.008 for body mass index (BMI), P < 0.05 for triacylglycerol (TG), P < 0.03 for free fatty acid (FFA)] and plasma adipsin (r2 = 0.057, P < 0.017 for BMI) in a non-obese population. In obese subjects, the model was different for plasma ASP (P = NS for any of the variables) and plasma adipsin (r2 = 0.356, P < 0.008 for FFA, P < 0.0002 for BMI, P < 0.02 for age). There was no correlation between ASP and adipsin in either the non-obese or the obese group.
The present data suggest involvement of the ASP/adipsin pathway in the pathogenesis of obesity.
酰化刺激蛋白(ASP)是人类脂肪细胞中甘油三酯(TG)合成的有效刺激物。
在本研究中,我们分析了非肥胖组和肥胖组的血浆ASP和脂肪酶水平及其与血脂的关系。
结果显示,两组中ASP的频率分布呈偏态,但脂肪酶的频率分布呈正态。在非肥胖人群中,血浆ASP和脂肪酶的平均水平分别为20.2 nmol/L(中位数)和66.6±19 nmol/L(平均值)。各参数在男性和女性之间未观察到差异。在肥胖人群中,血浆ASP中位数比对照组增加了246%(69.9 nmol/L),脂肪酶增加了31%(87.0±22.7 nmol/L)。尽管脂肪酶在男性和女性中的水平无统计学差异,但肥胖女性血浆ASP中位数浓度比肥胖男性高1.9倍(71.8 nmol/L对37.6 nmol/L,P<0.05)。最佳子集回归分析提供了一个模型,该模型中的变量能最佳预测非肥胖人群的血浆ASP[r2 = 0.160,体重指数(BMI)P<0.008,甘油三酯(TG)P<0.05,游离脂肪酸(FFA)P<0.03]和血浆脂肪酶(r2 = 0.057,BMI P<0.017)。在肥胖受试者中,血浆ASP(任何变量P =无显著性差异)和血浆脂肪酶的模型不同(r2 = 0.356,FFA P<0.008,BMI P<0.0002,年龄P<0.02)。非肥胖组或肥胖组中ASP与脂肪酶之间均无相关性。
目前的数据表明ASP/脂肪酶途径参与了肥胖的发病机制。