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作 者:陈璐璐[1] 王保平[1] 曾天舒[1] 王咏波[1] 周慜
机构地区:[1]华中科技大学同济医学院附属协和医院内分泌科,武汉430022
出 处:《中国糖尿病杂志》2007年第2期104-106,共3页Chinese Journal of Diabetes
基 金:湖北省自然科学基金资助项目(2003ABA143)
摘 要:目的观察胰岛素治疗对高脂喂养的糖尿病(DM)大鼠胰腺内脂质及葡萄糖刺激后胰岛素分泌(GSIS)的影响。方法Wistar大鼠随机分为正常对照组(NC),DM高脂饲养组(DH)及DM高脂饲养胰岛素治疗组(DHI)。测定血糖、胰岛素、FFA、TG、胰腺内TG和FFA、胰岛素蛋白表达和相对β细胞数量、计算ΔI30/ΔG30及β细胞胰岛素分泌指数(MBCI)。结果与DH相比,DHI血TG和FFA下降虽无统计学意义,但胰腺内TG和FFA含量明显下降(P<0.01),ΔI30/ΔG30、MBCI、胰岛素表达和相对β细胞数量得到明显改善(P<0.05或P<0.01)。结论长期高脂喂养DM大鼠可导致脂质异位沉积于胰腺,并进一步损伤GSIS。GSIS受损可能与胰岛素合成降低,β细胞数量减少有关。胰岛素治疗对高脂所致的上述改变有一定的改善作用。Objective To investigate the effect of insulin treatment on lipid content in pancreas and on GSIS of diabetic (DM) rats fed by long-term high fat diet. Methods Wistar rats were randomly divided into groups of normal control (NC), diabetic high fat diet (DH) and diabetic high fat diet plus insulin therapy (DHI). The FFA and TG in the plasma and pancreas, △I30/△G30, MBCI, the amount of insulin and the relative β cell volume were measured. Results Though there is no obvious decrease in plasma TG and FFA, the contents of the TG and FFA in pancreas were decreased dramatically(P〈0.01), the disorders of △I30/△G30 , MBCI, the amount of insulin and relative β cell volume were also improved(P〈0.05-〈0.01) in DHI group compared with DH group. Conclusions Long-term high fat diet can cause ectopic lipid accumulation in pancreas and further harm the GSIS. The decrease of insulin content in β-cell and relative β-cell volume are likely to contribute to the impairment of GSIS. Insulin treatment could attenuate the damage of ectopic lipids in β-cell.
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