糖尿病小鼠肝脏胰岛素表达对脂质代谢的影响

Effect of hepatic insulin expression on lipid metabolism in diabetic mice
   BACKGROUND: Hypertriglyceridemia is a common lipid disorder that is characterized by elevated plasma levels of triglyceride (TG)-rich particles, such as very low-density lipoprotein (VLDL), in poorly controlled diabetes. The aim of the present study was to determine the potential therapeutic effect of hepatic insulin production on hypertriglyceridemia in mice. METHODS: Mice were induced diabetic and hypertriglyceridemic by streptozotocin (STZ) treatment. Using an adenovirus-mediated gene transfer approach, we delivered rat preproinsulin cDNA into the liver of diabetic mice and then determined plasma TG metabolism. To investigate the mechanism by which hepatic insulin improves TG metabolism, we determined hepatic expression of apolipoprotein C-III (ApoC-III), a structural moiety and functional inhibitor of VLDL-TG catabolism. RESULTS: Plasma VLDL-TG levels were markedly elevated in STZ-treated mice, and were accompanied by hyperglycemia and hypertriglyceridemia. These metabolic abnormalities were restored to near normal following hepatic insulin production in insulin vector-treated diabetic mice. In contrast, hypertriglyceridemia and hyperglycemia persisted in control vector-treated diabetic animals. Hepatic ApoC-III expression became deregulated secondary to insulin deficiency, contributing to impaired TG metabolism in diabetic mice. Hepatic insulin production suppressed excessive hepatic ApoC-III production to basal levels. CONCLUSION: Hepatic insulin production is efficacious in correcting hypertriglyceridemia associated with insulin deficiency in diabetic mice.


糖尿病小鼠肝脏胰岛素表达对脂质代谢的影响
   背景：在控制不佳的糖尿病中，高甘油三酯血症是一种常见的脂质代谢紊乱，其特征为富含甘油三酯（triglyceride，TG）的颗粒，例如极低密度脂蛋白（very low-density lipoprotein，VLDL）的血浆水平明显升高。当前这项研究的目的是在小鼠中测定肝脏胰岛素表达对高甘油三酯血症的潜在治疗效果。方法：小鼠使用链脲霉素（streptozotocin，STZ）治疗后诱导出了糖尿病与高甘油三酯血症。使用腺病毒介导的基因转移方法，我们将大鼠的前胰岛素原cDNA转移到糖尿病小鼠的肝脏中，接着测定血浆中的TG代谢。为了研究肝脏胰岛素改善TG代谢的机制，我们测定了肝脏表达的载脂蛋白C- III（ApoC-III），这是VLDL-TG的一种结构成分，并且具有抑制VLDL-TG分解代谢的功能。结果：在STZ诱导的小鼠中血浆VLDL-TGshui平显著升高，并且伴随着高血糖与高甘油三酯血症。糖尿病小鼠经过胰岛素媒介治疗后随着肝脏胰岛素的表达这些代谢异常可以恢复到接近正常。相比之下，使用对照媒介治疗的糖尿病小鼠却持续存在高甘油三酯血症与高血糖。在糖尿病小鼠中由于胰岛素的缺乏可使肝脏ApoC-III的表达出现异常，zui终导致TG代谢受损。肝脏胰岛素表达可以抑制肝脏ApoC-III的过度表达使其接近基础水平。结论：在糖尿病小鼠中肝脏胰岛素表达可以有效地纠正胰岛素缺乏所导致的高甘油三酯血症。


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