糖尿病酮症酸中毒大鼠的肌肉谷氨酰胺生成
Muscle glutamine production in diabetic ketoacidotic rats.
作者信息
Goldstein L, Perlman D F, McLaughlin P M, King P A, Cha C J
出版信息
Biochem J. 1983 Sep 15;214(3):757-67. doi: 10.1042/bj2140757.
The mechanism of activation of glutamine production by the hindlimb during diabetic ketoacidosis (DKA) was investigated in rats. Muscle glutamine production was estimated to account for over 90% of the total glutamine produced by the hindlimb. DKA produced significant increases in the concentrations of NH4+ and IMP in hindlimb muscles, suggesting that AMP deaminase is activated by DKA. NH4Cl- and HCl-induced acidosis did not produce these changes, indicating either that acidosis itself is not the stimulus for increased AMP deaminase activity or that the more severe degree of acidosis accompanying DKA is necessary for activation. Muscle glutamine concentrations were depressed in DKA. Experiments with isolated epitrochlearis muscle showed that the transport and permeability properties of the muscle cells (as judged by uptake and release of alpha-aminoisobutyrate and glutamine) were not altered by DKA. However, glutamine uptake by muscle cells was significantly inhibited by L-leucine, the concentration of which, along with other branched-chain amino acids, is markedly elevated in DKA.
在大鼠中研究了糖尿病酮症酸中毒（DKA）期间后肢激活谷氨酰胺生成的机制。据估计，肌肉谷氨酰胺生成占后肢生成的总谷氨酰胺的90%以上。DKA使后肢肌肉中NH4+和IMP的浓度显著增加，这表明DKA激活了AMP脱氨酶。NH4Cl和HCl诱导的酸中毒并未产生这些变化，这表明要么酸中毒本身不是AMP脱氨酶活性增加的刺激因素，要么DKA伴随的更严重程度的酸中毒是激活所必需的。DKA时肌肉谷氨酰胺浓度降低。对分离的肱三头肌进行的实验表明，DKA并未改变肌肉细胞的转运和通透性特性（通过α-氨基异丁酸和谷氨酰胺的摄取和释放来判断）。然而，肌肉细胞对谷氨酰胺的摄取受到L-亮氨酸的显著抑制，在DKA中，L-亮氨酸以及其他支链氨基酸的浓度显著升高。
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