Rigalleau V, Beylot M, Laville M, Pachiaudi C, Normand S, Nlend E, Gin H
Service de Nutrition et Diabétologie, Hôpital Haut-lévêque, Pessac, France.
Metabolism. 1999 Mar;48(3):278-84. doi: 10.1016/s0026-0495(99)90072-0.
Resistance to the glucoregulatory action of insulin is a common finding in obesity and may affect thermogenesis. In 13 healthy subjects, we studied the influence of acute insulin resistance induced by a lipid infusion on thermogenesis without any glucose load (n = 4) or during a euglycemic-hyperinsulinemic clamp (n = 5) and an oral glucose tolerance test (OGTT, n = 8). When substrates were not administered at the same time, the energy cost of storage was significantly (P < .05) lower for lipids (3.9%+/-0.9%) than for glucose (11.9%+/-0.5% during the clamp and 14.9%+/-4.0% during the OGTT, NS). The lipid infusion decreased glucose storage during the clamp (control, 3.99+/-0.40 mg x kg(-1) x min(-1); lipid infusion, 0.92+/-0.39; P < .05) but increased it during the OGTT (control, 1.76+/-0.22 mg x kg(-1) x min(-1); lipid infusion, 2.94+/-0.27; P < .05). Infused lipids were stored more (clamp, 3.31+/-0.16; OGTT, 2.65+/-0.11 mg x kg(-1) x min(-1); P < .01) and oxidized less (clamp, 0.64+/-0.21; OGTT, 1.02+/-0.09 mg x kg(-1) x min(-1); P < .05) during the clamp than during the OGTT. When lipids were infused, the energy cost of substrate storage was lower during the clamp versus the OGTT (clamp, 3.2%+/-0.8%; OGTT, 7.3%+/-1.0%; P < .05). This effect was attributed to a lipid-induced impairment of glucose tolerance, which overcomes the inhibitory effect of lipid infusion on glucose storage observed in euglycemia. A slight elevation of plasma glucose in response to a lipid infusion impairs thermogenesis by redirecting the storage of substrates from lipids to glucose, which has a higher energy cost.
胰岛素对糖代谢调节作用的抵抗在肥胖人群中很常见，并且可能影响产热。在13名健康受试者中，我们研究了脂质输注诱导的急性胰岛素抵抗在无任何葡萄糖负荷情况下（n = 4）、正常血糖-高胰岛素钳夹期间（n = 5）以及口服葡萄糖耐量试验（OGTT，n = 8）对产热的影响。当底物不同时给予时，脂质储存的能量消耗（3.9%±0.9%）显著低于葡萄糖（钳夹期间为11.9%±0.5%，OGTT期间为14.9%±4.0%，无显著性差异）（P < 0.05）。脂质输注在钳夹期间降低了葡萄糖储存（对照组，3.99±0.40 mg·kg⁻¹·min⁻¹；脂质输注组，0.92±0.39；P < 0.05），但在OGTT期间增加了葡萄糖储存（对照组，1.76±0.22 mg·kg⁻¹·min⁻¹；脂质输注组，2.94±0.27；P < 0.05）。在钳夹期间，输注的脂质储存更多（钳夹，3.31±0.16；OGTT，2.65±0.11 mg·kg⁻¹·min⁻¹；P < 0.01），氧化更少（钳夹，0.64±0.21；OGTT，1.02±0.09 mg·kg⁻¹·min⁻¹；P < 0.05）。当输注脂质时，钳夹期间底物储存的能量消耗低于OGTT期间（钳夹，3.2%±0.8%；OGTT，7.3%±1.0%；P < 0.05）。这种效应归因于脂质诱导的葡萄糖耐量受损，它克服了在正常血糖情况下观察到的脂质输注对葡萄糖储存的抑制作用。脂质输注引起的血浆葡萄糖轻微升高通过将底物储存从脂质转向能量消耗更高的葡萄糖而损害产热。
