Lipid-dependent control of hepatic glycogen stores in healthy humans
Lipid-dependent control of hepatic glycogen stores in healthy humans
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DOI：
10.1007/s001250051579
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发表时间：
2001-01-01
期刊：
影响因子：
8.2
通讯作者：
Roden, M
中科院分区：
文献类型：
--
作者：
Stingl, H;Krss치k, M;Roden, M
目标/假设。非酯化脂肪酸和甘油可以刺激糖异生，也有助于调节肝糖原储备。我们检测了它们对人体肝糖原分解的影响。禁食一夜后，健康受试者分别给予脂/肝素(血浆非酯化脂肪酸：2.2+/-0.1mol/L；甘油：0.5+/-0.03mol/L；n=7)、甘油(0.4/-0.1mol/L；1.5+/-0.2mol/L；n=5)和生理盐水(对照组：0.5/-0.1mol/L；0.2RT0.02mol/L；n=7)。用C-13核磁共振波谱计算肝糖原在9h内的净降解率。用D-[6，6-H-2(2)]葡萄糖输注测定内源性葡萄糖产量。在注射脂肪和生理盐水(p<；0.005)时，内源性葡萄糖的产生减少了约25%，但在注射甘油(p<；0.001 vs脂肪和生理盐水)时并没有。血浆非酯化脂肪酸或甘油的增加分别使净糖原分解减少约84%至0.001.6/-0.3m ol·kg(-1)分(p<；0.001 vs生理盐水：3.7+/-0.5mol.kg(-1)m in(-1))和约46%至2.0/-0.4m ol·kg(-1)m in(p<；0.0 1vs生理盐水和脂肪)。糖异生速率增加到11.5+/-0.8mol.kg(-1)min(-1)(p<；0.01)和12.8+/-1.0mol.kg(-1).min(-1)(p<；0.01vs生理盐水：8.2+/-0.7mol.1(-1).min(-1)。结论/解读：非酯化脂肪酸的增加明显抑制了肝糖原的净分解，促进了糖异生，而葡萄糖的产生与对照条件没有差别。我们认为，这种效果不是由于甘油可利用性的增加，而是由于对肝糖原储备的脂依赖控制。
Aims/hypothesis. Non-esterified fatty acids and glycerol could stimulate gluconeogenesis and also contribute to regulating hepatic glycogen stores. We examined their effect on liver glycogen breakdown in humans.Methods. After an overnight fast healthy subjects participated in three protocols with lipid/heparin (plasma non-esterified fatty acids: 2.2 +/- 0.1 mol/l; plasma glycerol: 0.5 +/- 0.03mol/l; n=7), glycerol (0.4 +/- 0.1 mol/l; 1.5 +/- 0.2 mol/l; n = 5) and saline infusion (control; 0.5 +/- 0.1 mol/l; 0.2 rt 0.02 mol/l; n = 7). Net rates of glycogen breakdown were calculated from the decrease of liver glycogen within 9 h using C-13 nuclear magnetic resonance spectroscopy. Endogenous glucose production was measured with infusion of D-[6,6-H-2(2)]glucose,Results. Endogenous glucose production decreased by about 25 % during lipid and saline infusion (p < 0.005) but not during glycerol infusion (p < 0.001 vs lipid, saline). An increase of plasma non-esterified fatty acids or glycerol reduced the net glycogen breakdown by about 84 % to 0.6 +/- 0.3 mu mol.kg(-1) min(-1) (p < 0.001 vs saline: 3.7 +/- 0.5 mol.kg(-1) min(-1)) and by about 46 % to 2.0 +/- 0.4 mu mol.kg(-1) min(-1) (p < 0.01 vs saline and lipid), respectively. Rates of gluconeogenesis increased to 11.5 +/- 0.8 mol.kg(-1) min(-1) (p < 0.01) and 12.8 +/- 1.0 mol.kg(-1).min(-1) (p < 0.01 vs saline: 8.2 +/- 0.7 mol.1(-1).min(-1)), respectively.Conclusion/interpretation: An increase of non-esterified fatty acid leads to a pronounced inhibition of net hepatic glycogen breakdown and increases gluconeogenesis whereas glucose production does not differ from the control condition. We suggest that this effect is not due to increased availability of glycerol alone but rather to lipid-dependent control of hepatic glycogen stores.