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目的:探讨FK506对血糖调节的副作用,并研究其机制。方法:健康SD大鼠12只,随机分为2组:对照组(生理盐水,1 mL·kg-1·d-1)、给药组(FK506,1 mg·kg-1·d-1)。每天监测体重,每2 d测空腹血糖。在第15天取脂肪组织,实时荧光定量PCR检测脂联素(adiponectin)、瘦素(leptin)、内酯素(visfatin)、抵抗素(resistin)、视黄醇结合蛋白4(RBP4)及氧化物酶体增殖物激活受体γ(PPAR-γ)mRNA的表达;Western blotting检测PPAR-γ及脂联素蛋白的表达。结果:第10天开始,给药组大鼠空腹血糖逐渐升高,显著高于对照组(P<0.05);第14天,给药组空腹血糖由(5.10±0.62)mmol/L升到(7.73±0.73)mmol/L,对照组空腹血糖无明显变化;与对照组相比,给药组大鼠脂肪组织adiponectin和leptin mRNA的表达量显著降低(P<0.01),而visfatin、resistin和RBP4 mRNA表达明显升高(P<0.05);与对照组相比,给药组脂肪组织PPAR-γmRNA表达量降低(P<0.01);与对照组相比,给药组脂肪组织PPAR-γ及脂联素蛋白表达量明显降低(P<0.01)。结论:FK506可能通过抑制PPAR-γ的表达,影响脂肪因子的表达,影响血糖。
Objective: To investigate the side effects of FK506 on blood glucose regulation and to study its mechanism. Methods: Twelve healthy SD rats were randomly divided into 2 groups: control group (normal saline, 1 mL · kg-1 · d-1), administration group (FK506, 1 mg · kg-1 · d-1) . Daily weight monitoring, fasting blood glucose every 2 d. Adipose tissue was harvested on day 15, and adiponectin, leptin, visfatin, resistin, retinol binding protein 4 (RBP4) were detected by real-time fluorescence quantitative PCR. The expression of PPAR-γ mRNA was detected by Western blotting. The expression of PPAR-γ and adiponectin were detected by Western blotting. Results: On the 10th day, the fasting blood glucose of the rats in the treatment group increased gradually, which was significantly higher than that in the control group (P <0.05). On the 14th day, the fasting blood glucose increased (5.10 ± 0.62) mmol / L to 7.73 ± 0.73) mmol / L, while there was no significant change in fasting blood glucose in the control group. Compared with the control group, the expression of adiponectin and leptin mRNA in the adipose tissue of the treated group was significantly decreased (P <0.01), while visfatin, resistin and RBP4 (P <0.05). Compared with the control group, the expression of PPAR-γmRNA in the adipose tissue of the treated group was decreased (P <0.01). Compared with the control group, the PPAR-γ and lipid Diprotein expression was significantly reduced (P <0.01). Conclusion: FK506 may affect the expression of adipokines and affect blood glucose by inhibiting the expression of PPAR-γ.