载体介导的果糖摄取对人类骨骼肌中的碳水化合物代谢有显著贡献。
Carrier-mediated fructose uptake significantly contributes to carbohydrate metabolism in human skeletal muscle.
作者信息
Zierath J R, Nolte L A, Wahlström E, Galuska D, Shepherd P R, Kahn B B, Wallberg-Henriksson H
机构信息
Department of Clinical Physiology, Karolinska Hospital, Stockholm, Sweden.
出版信息
Biochem J. 1995 Oct 15;311 ( Pt 2)(Pt 2):517-21. doi: 10.1042/bj3110517.
To determine whether fructose can be utilized as a metabolic substrate for skeletal muscle in man, we investigated its incorporation into glycogen, its oxidation and lactate production in isolated human skeletal muscle. Rates of fructose oxidation and incorporation into glycogen increased in the presence of increasing fructose concentrations (0.1-1.0 mM). Lactate production increased 3-fold when extracellular fructose was increased from 0.1 to 0.5 mM. Cytochalasin B, a competitive inhibitor of hexose transport mediated by the GLUT1 and GLUT4 facilitative glucose transporters, completely inhibited insulin-stimulated glucose incorporation into glycogen and glucose oxidation (P < 0.01), but did not alter fructose incorporation into glycogen or fructose oxidation. Insulin (1000 mu-units/ml) increased glucose incorporation into glycogen 2.7-fold and glucose oxidation 2.3-fold, whereas no effect on fructose incorporation into glycogen or fructose oxidation was noted. A physiological concentration of glucose (5 mM) decreased the rate of 0.5 mM fructose incorporation into glycogen by 60% (P < 0.001), whereas fructose oxidation was not altered in the presence of 5 mM glucose. Irrespective of fructose concentration, the majority of fructose taken up underwent non-oxidative metabolism. Lactate production accounted for approx. 80% of the fructose metabolism in the basal state and approx. 70% in the insulin (1000 mu-units/ml)-stimulated state. In the presence of 5 mM glucose, physiological concentrations of fructose could account for approximately 10-30% of hexose (glucose + fructose) incorporation into glycogen under non-insulin-stimulated conditions. In conclusion, fructose appears to be transported into human skeletal muscle via a carrier-mediated system that does not involve GLUT4 or GLUT1. Furthermore, under physiological conditions, fructose can significantly contribute to carbohydrate metabolism in human skeletal muscle.
为了确定果糖是否可作为人体骨骼肌的代谢底物，我们研究了其在分离的人体骨骼肌中合成糖原、氧化以及生成乳酸的情况。随着果糖浓度（0.1 - 1.0 mM）升高，果糖氧化及合成糖原的速率增加。当细胞外果糖浓度从0.1 mM增至0.5 mM时，乳酸生成增加了3倍。细胞松弛素B是由GLUT1和GLUT4易化型葡萄糖转运体介导的己糖转运的竞争性抑制剂，它完全抑制胰岛素刺激的葡萄糖合成糖原及葡萄糖氧化（P < 0.01），但不改变果糖合成糖原或果糖氧化。胰岛素（1000 μ单位/毫升）使葡萄糖合成糖原增加2.7倍，葡萄糖氧化增加2.3倍，而对果糖合成糖原或果糖氧化无影响。生理浓度的葡萄糖（5 mM）使0.5 mM果糖合成糖原的速率降低60%（P < 0.001），而在5 mM葡萄糖存在时果糖氧化未改变。无论果糖浓度如何，摄取的大部分果糖都进行非氧化代谢。在基础状态下，乳酸生成约占果糖代谢的80%，在胰岛素（1000 μ单位/毫升）刺激状态下约占70%。在5 mM葡萄糖存在时，生理浓度的果糖在非胰岛素刺激条件下可占己糖（葡萄糖 + 果糖）合成糖原的约10 - 30%。总之，果糖似乎通过一种不涉及GLUT4或GLUT1的载体介导系统转运至人体骨骼肌。此外，在生理条件下，果糖可显著促进人体骨骼肌中的碳水化合物代谢。
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