糖尿病小鼠肝髒胰島素表達對脂質代謝的影響

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.


糖尿病小鼠肝髒胰島素表達對脂質代謝的影響
   背景：在控制不佳的糖尿病中，高甘油三酯血症是一種常見的脂質代謝紊亂，其特征爲富含甘油三酯（triglyceride，TG）的顆粒，例如極低密度脂蛋白（very low-density lipoprotein，VLDL）的血漿水平明顯升高。當前這項研究的目的是在小鼠中測定肝髒胰島素表達對高甘油三酯血症的潛在治療效果。方法
：小鼠使用鏈脲黴素（streptozotocin，STZ）治療後誘導出瞭糖尿病與高甘油三酯血症。使用腺病毒介導的基因轉移方法，我們将大鼠的前胰島素原cDNA轉移到糖尿病小鼠的肝髒中，接著測定血漿中的TG代謝。爲瞭研究肝髒胰島素改善TG代謝的機制，我們測定瞭肝髒表達的載脂蛋白C- III（ApoC-III），這是VLDL-TG的一種結構成分，並且具有抑制VLDL-TG分解代謝的功能。結果：在STZ誘導的小鼠中血漿VLDL-TGshui平顯著升高，並且伴随著高血糖與高甘油三酯血症。糖尿病小鼠經過胰島素媒介治療後随著肝髒胰島素的表達這些代謝異常可以恢複到接近正常。相比之下，使用對照媒介治療的糖尿病小鼠卻持續存在高甘油三酯血症與高血糖。在糖尿病小鼠中由於胰島素的缺乏可使肝髒ApoC-III的表達出現異常
，zui終導緻TG代謝受損。肝髒胰島素表達可以抑制肝髒ApoC-III的過度表達使其接近基礎水平。結論：在糖尿病小鼠中肝髒胰島素表達可以有效地糾正胰島素缺乏所導緻的高甘油三酯血症。


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