Vettor R, Pagano C, Granzotto M, Englaro P, Angeli P, Blum W F, Federspil G, Rohner-Jeanrenaud F, Jeanrenaud B
Endocrine-Metabolic Laboratory, Institute of Medical Semiotics, University of Padua, Italy.
Diabetologia. 1998 Nov;41(11):1361-7. doi: 10.1007/s001250051077.
Intracerebroventricular administration of neuropeptide Y to normal rats induces a syndrome characterised by obesity, hyperinsulinaemia, insulin resistance and over expression of the adipose tissue ob gene. Little is known about the effect of circulating neuropeptide Y on glucose metabolism, insulin secretion and leptin. We therefore aimed to evaluate the effect of an intravenous infusion of neuropeptide Y on glucose disposal, endogenous glucose production, whole body glycolytic flux, and glucose storage as assessed during euglycaemic hyperinsulinaemic clamp. In addition, the insulin-stimulated glucose utilisation index in individual tissues was measured by the 2-deoxy-[1-3H]-glucose technique. The effect of neuropeptide Y on insulin secretion was evaluated by hyperglycaemic clamp. Infusion did not induce any change in endogenous glucose production during basal conditions or at the end of the clamp. Glucose disposal was significantly increased in the rats given neuropeptide Y compared with controls (27.8 +/- 1.3 vs 24.3 +/- 1.6 mg x min(-1) x kg(-1); p < 0.05) as was the glycolytic flux (18.9 +/- 1.6 vs 14.4 +/- 0.8 mg x min(-1) x kg(-1); p < 0.05), while glucose storage was comparable in the two groups. In skeletal muscle, the glucose utilisation index was increased significantly in rats given neuropeptide Y. The glucose utilisation index in subcutaneous and epididimal adipose tissue was not significantly different between the two groups. Plasma leptin was significantly increased by hyperinsulinaemia, but was not affected by neuropeptide Y infusion. Both the early and late phase of the insulin response to hyperglycaemia were significantly reduced by neuropeptide Y. In conclusion neuropeptide Y infusion may increase insulin-induced glucose disposal in normal rats, accelerating its utilisation through the glycolytic pathway. Neuropeptide Y reduces both phases of the insulin response to hyperglycaemia.
向正常大鼠脑室内注射神经肽Y会诱发一种综合征，其特征为肥胖、高胰岛素血症、胰岛素抵抗以及脂肪组织ob基因的过度表达。关于循环神经肽Y对葡萄糖代谢、胰岛素分泌和瘦素的影响，人们了解甚少。因此，我们旨在评估静脉输注神经肽Y对葡萄糖处置、内源性葡萄糖生成、全身糖酵解通量以及在正常血糖高胰岛素钳夹期间评估的葡萄糖储存的影响。此外，通过2-脱氧-[1-3H]-葡萄糖技术测量各个组织中胰岛素刺激的葡萄糖利用指数。通过高血糖钳夹评估神经肽Y对胰岛素分泌的影响。在基础状态或钳夹结束时，输注未引起内源性葡萄糖生成的任何变化。与对照组相比，给予神经肽Y的大鼠的葡萄糖处置显著增加（27.8±1.3对24.3±1.6mg·min-1·kg-1；p<0.05），糖酵解通量也是如此（18.9±1.6对14.4±0.8mg·min-1·kg-1；p<0.05），而两组的葡萄糖储存相当。在骨骼肌中，给予神经肽Y的大鼠的葡萄糖利用指数显著增加。两组之间皮下和附睾脂肪组织中的葡萄糖利用指数没有显著差异。高胰岛素血症使血浆瘦素显著增加，但不受神经肽Y输注的影响。神经肽Y显著降低了对高血糖的胰岛素反应的早期和晚期阶段。总之，输注神经肽Y可能会增加正常大鼠中胰岛素诱导的葡萄糖处置，通过糖酵解途径加速其利用。神经肽Y降低了对高血糖的胰岛素反应的两个阶段。
