论文部分内容阅读
目的探讨吡格列酮(Pio)对脂质诱导的胰岛素抵抗(IR)大鼠糖代谢、血浆脂联素和抵抗素浓度及组织抵抗素水平的影响。方法采用清醒状态大鼠进行扩展高胰岛素-正糖钳夹术,检测4h脂质灌注升高血浆游离脂肪酸(FFA)引起的IR状态下,肝糖及外周组织糖代谢,血浆脂联素和抵抗素浓度,肝、肌肉、脂肪组织抵抗素水平的变化,以及经Pio处理后的影响。结果在钳夹稳态期,脂质灌注组(L组)和Pio处理+脂质灌注组(P/L组)FFA水平明显较对照组升高。P/L组葡萄糖输注率(GIR)较对照组降低[(20.6±0.9vs 33.6±1.5)mg·kg~(-1)·min~(-1),JP＜0.01],而L组又低于P/L组[(12.6±1.7)vs (20.6±0.9)mg·kg~(-1)·min~(-1),P＜0.01]；对照组和P/L组肝糖输出(HGP)与基础值相比被抑制85%,在L组胰岛素对HGP的抑制作用明显障碍。L组和P/L组葡萄糖清除率(G_(Rd))低于对照组(P＜0.01)。P/L组基础血浆抵抗素水平低于对照组[(7.8±1.3vs 29.1±3.1)μL,P＜0.01]。脂质灌注后P/L组抵抗素浓度明显升高,但仍低于L组[(18.1±3.8vs 47.0±2.2)μg/L,P＜0.01]。P/L组基础血浆脂联素水平明显高于对照组和L组[(3.9±0.2vs 2.8±0.1和2.6±0.2)mg/L,P＜0.01]。但在钳夹结束后,L和P/L组血浆脂联素水平降低(均P＜0.05)。P/L组肝脏抵抗素水平低于对照组和L组(均P＜0.05)；L组骨骼肌抵抗素水平高于对照组和P/L组(均P＜0.05)；各组脂肪组织抵抗素水平差异无统计学意义。结论脂质灌注在体内诱导了一种急性IR。Pio干预部分阻断了脂质诱导的IR。抵抗素和脂联素的变化在IR的发生和发展中可能发挥了一定的作用。
Objective To investigate the effects of pioglitazone on the glucose metabolism, plasma adiponectin and resistin levels and tissue resistin levels in lipid-induced insulin resistance (IR) rats. Methods Wistar rats were used to expand the hyperinsulinemic-to-glucose clamp, and the glucose metabolism, plasma adiponectin and plasma adiponectin in peripheral blood and glycometabolism induced by lipid perfused with free fatty acid (FFA) at 4h were measured. Changes in the levels of insulin, liver, muscle, and adipose tissue resistin, and the effect of Pio treatment. Results During steady-state clamp, FFA levels in lipid-perfusion group (L group) and Pio-treated group (P / L group) were significantly higher than those in control group. The glucose infusion rate (GIR) in P / L group was lower than that in control group [(20.6 ± 0.9 vs 33.6 ± 1.5) mg · kg -1 · min -1, JP <0.01] (P <0.01), and was lower than that in P / L group [(12.6 ± 1.7) vs (20.6 ± 0.9) mg · kg -1 · min -1, P <0.01] HGP) was inhibited by 85% compared with the basal value, and the inhibitory effect of insulin in group L on HGP was obviously disturbed. Glucose clearance (G Rd) in L group and P / L group was lower than that in control group (P <0.01). The basal plasma resistin level in P / L group was lower than that in control group [(7.8 ± 1.3 vs 29.1 ± 3.1) μL, P <0.01]. The concentrations of resistin in P / L group were significantly higher than those in L group [(18.1 ± 3.8 vs 47.0 ± 2.2) μg / L, P <0.01] after lipid perfused. The level of plasma adiponectin in P / L group was significantly higher than that in control group and L group [(3.9 ± 0.2 vs 2.8 ± 0.1 and 2.6 ± 0.2) mg / L, P <0.01]. However, at the end of the clamp, plasma adiponectin levels decreased in the L and P / L groups (all P <0.05). The level of resistin in P / L group was lower than that in control group and L group (all P <0.05). The resistin level in L group was higher than that in control group and P / L group (P <0.05) There was no significant difference between the two groups Conclusion Lipid infusion induces an acute IR in the body. Pio intervention partially blocked lipid-induced IR. Resistin and adiponectin changes in the occurrence and development of IR may play a role.