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目的探讨脂肪酸合成酶(FAS)及其调节因子碳水化合物反应元件结合蛋白(ChREBP)在T1DM小鼠肾脏的表达及胰岛素对其调节的作用。方法将15只C57BL/6小鼠分为对照(Con)组、糖尿病(DM)组和胰岛素治疗(Ins)组,各5只。腹腔注射STZ诱导T1DM小鼠模型,观察FAS、ChREBP在其肾脏的表达,以及胰岛素对其的调节。结果 Con、DM、Ins组TG水平为(0.99±0.46),(2.25±0.66),(1.29±0.24)mmol/L,TC水平为(1.62±0.10),(1.90±0.12),(1.68±0.11)mmol/L(P<0.05);肾脏FAS及ChREBP蛋白均相对集中表达于肾皮质的肾小管上皮细胞;DM组肾组织中FAS和ChREBP蛋白水平较Con组降低,胰岛素可使糖尿病小鼠肾脏以上2种蛋白含量有所回升;DM组肾脏FAS含量在mRNA水平也较Con组低,下降约50%(P<0.01)。胰岛素治疗可使糖尿病小鼠肾脏FAS含量上升0.34倍(P<0.01);与Con组相比,糖尿病小鼠肾脏ChREBP含量在mRNA水平降低,下降约70%(P<0.01),胰岛素治疗可使糖尿病小鼠肾脏ChREBP含量上升1.96倍(P<0.01)。结论糖尿病小鼠肾脏FAS和ChREBP的表达量较非糖尿病小鼠降低,胰岛素可上调糖尿病小鼠肾脏FAS和ChREBP的表达水平。
Objective To investigate the expression of fatty acid synthase (FAS) and its regulatory factor carbohydrate response element binding protein (ChREBP) in the kidney of T1DM mice and the effect of insulin on it. Methods Fifteen C57BL / 6 mice were divided into control group (Con), diabetes mellitus group (DM) and Ins group (5 rats). The model of T1DM was induced by intraperitoneal injection of STZ. The expression of FAS and ChREBP in their kidneys and the regulation by insulin were observed. Results The levels of TC in the Con, DM and Ins groups were (1.99 ± 0.46), (2.25 ± 0.66), (1.29 ± 0.24) mmol / L and 1.62 ± 0.10, 1.90 ± 0.12, 1.68 ± 0.11 ) mmol / L (P <0.05). The expression of FAS and ChREBP protein in renal cortex was relatively concentrated in renal tubular epithelial cells. The levels of FAS and ChREBP protein in DM group were lower than those in Con group The protein content of the above two kinds of protein increased. The content of FAS in DM group was lower than that of Con group by about 50% (P <0.01). Compared with Con group, the level of ChREBP in kidney of diabetic mice decreased by about 70% (P <0.01), insulin treatment could increase the FAS level in diabetic mice by 0.34 times (P <0.01) Diabetic mice kidney ChREBP increased 1.96 times (P <0.01). Conclusion The expression of FAS and ChREBP in kidney of diabetic mice is lower than that in non-diabetic mice, and insulin can up-regulate the expression of FAS and ChREBP in the kidney of diabetic mice.