HYPERGLYCEMIA INDUCES ACCUMULATION OF GLUCOSE IN HUMAN SKELETAL-MUSCLE
HYPERGLYCEMIA INDUCES ACCUMULATION OF GLUCOSE IN HUMAN SKELETAL-MUSCLE
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DOI：
10.1152/ajpregu.1991.260.4.r698
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发表时间：
1991-04-01
影响因子：
--
通讯作者：
MOTT, DM
中科院分区：
文献类型：
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作者：
KATZ, A;RAZ, I;MOTT, DM
研究了高血糖对全身底物利用和骨骼肌代谢的影响。8名糖耐量正常男性患者静脉注射生长抑素(S)190min。在S静脉滴注的最后120min内，静脉滴注葡萄糖，使血药浓度稳定在26 mmoL/L，分别于诱导高血糖前、诱导高血糖后35min和120min取股四头肌组织标本。高血糖时的稳态葡萄糖代谢平均为(+/-SE)33.8+/-3.2mmol.kg脱脂质量-1.min-1，约70%的葡萄糖代谢是由骨骼肌完成的。细胞内血糖从S时的0.9+/-0.2 mmol/kg干重增加到高血糖时的9.5+/-2.5(P<；0.01)。据估计，在120分钟的高血糖中，肌肉摄取的葡萄糖中约有35%没有被磷酸化。肌肉中α-D-葡萄糖1，6-二磷酸、D-葡萄糖6-磷酸、ATP、ADP和AMP(两者都基于磷酸肌酸与肌酸的比率)在体外被证明能抑制己糖激酶的含量，在高血糖期间没有显著变化，也没有任何其他磷酸果糖激酶后中间产物D-2，6-二磷酸果糖和柠檬酸的显著变化。高血糖不改变糖原合成酶或磷酸化酶的部分活性，也不改变总的磷酸化酶活性。然而，高血糖导致糖原合成酶特异性活性增加55%(P<；0.01)。结论：高血糖会导致肌肉血糖的显著升高。研究表明，肌肉中葡萄糖的积累是葡萄糖转运速率超过己糖激酶在体内对葡萄糖磷酸化的速率的结果。
The effect of hyperglycemia on whole body substrate utilization and the metabolic profile of skeletal muscle has been investigated. Eight glucose-tolerant men were infused with somatostatin (S) for 190 min. During the last 120 min of S infusion, glucose was infused to achieve a steady-state plasma level of 26 mmol/l. Biopsies were obtained from the quadriceps femoris muscle immediately before and 35 and 120 min after induction of hyperglycemia. Steady-state glucose disposal during hyperglycemia averaged (+/- SE) 33.8 +/- 3.2-mu-mol.kg fat-free mass-1.min-1, and approximately 70% of the glucose disposal was accounted for by skeletal muscle. Intracellular glucose increased from 0.9 +/- 0.2 mmol/kg dry wt during S to 9.5 +/- 2.5 during hyperglycemia (P < 0.01). It was estimated that approximately 35% of the glucose taken up by muscle during 120 min of hyperglycemia was not phosphorylated. Muscle contents of alpha-D-glucose 1,6-diphosphate, D-glucose 6-phosphate, ATP, ADP, and AMP (both of which are based on the phosphocreatine-to-creatine ratio), which have been shown to inhibit hexokinase in vitro, did not change significantly during hyperglycemia, nor were there any significant changes in any of the other postphosphofructokinase intermediates, D-fructose 2,6-diphosphate, and citrate. Hyperglycemia did not alter the fractional activities of glycogen synthase or phosphorylase, nor total phosphorylase activity. However, hyperglycemia resulted in a 55% increase in glycogen synthase-specific activity (P < 0.01). It is concluded that hyperglycemia results in a marked increase in muscle glucose. It is suggested that the accumulation of glucose in muscle is a consequence of a glucose transport rate that exceeds the rate at which hexokinase phosphorylates glucose in vivo.