Molecular mechanisms of diabetic lipemia in streptozotocin-treated mice

胰岛素缺乏状态下糖尿病脂血症的分子机制尚不完全清楚。我们先前已经发现，激素敏感脂肪酶(HSL)缺陷小鼠在用链脲佐菌素攻击时，其血浆甘油三酯水平低于野生型小鼠。本研究旨在通过对处于胰岛素缺乏状态的HSL基因缺陷小鼠的详细分析，阐明糖尿病血脂的分子机制。我们发现，在胰岛素缺乏状态下，野生型和HSL缺陷型小鼠脂蛋白脂酶(LPL)的酶活性和mRNA水平没有显著差异。调节体内LPL活性的其他因素或其他途径，如肠道脂肪吸收，可能解释了目前正在研究的表型差异。

The molecular mechanism of diabetic lipemia in the setting of insulin deficiency is not fully understood. We have previously found that the plasma level of triglycerides is lower in hormone-sensitive lipase (HSL) deficient mice than in wild-type mice when they are challenged with streptozotocin. The current study was aimed at elucidating the molecular mechanism of diabetic lipemia through the detailed analysis of HSL-deficient mice in the insulin-deficient status. We found that the enzymatic activity and mRNA levels of lipoprotein lipase (LPL) were not significantly different between wild-type and HSL-deficient mice in the insulin-deficient status. Other factors that regulate LPL activity in vivo or other pathways such as intestinal lipid absorption may explain the phenotypic difference, which are currently under investigation.