GLUTAMINE NITROGEN KINETICS IN INSULIN-DEPENDENT DIABETIC HUMANS

被引:16
作者
DARMAUN, D
RONGIER, M
KOZIET, J
ROBERT, JJ
机构
[1] ST LAZARE HOSP,INSERM,U290,F-75010 PARIS,FRANCE
[2] SICK CHILDRENS HOSP,DEPT PEDIAT DIABETOL,F-75015 PARIS,FRANCE
[3] PERNOD RICARD RES LAB,F-94015 CRETEIL,FRANCE
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1991年 / 261卷 / 06期
关键词
TYPE-I DIABETES; AMINO ACIDS; STABLE ISOTOPES; ARTIFICIAL BETA-CELL; GLUCONEOGENESIS;
D O I
10.1152/ajpendo.1991.261.6.E713
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
To assess the effect of insulin deficiency on whole body glutamine kinetics, five young adults with type I (insulin-dependent) diabetes received 4-h primed continuous infusions of L-[1-C-13]leucine and L-[2-N-15]glutamine in the postabsorptive state after blood glucose had been clamped overnight at either a normoglycemic level (approximately 85 mg/dl) or a moderate hyperglycemic level (approximately 260 mg/dl) by means of an automated glucose control insulin infusion system. The hyperglycemic state was associated with a significant rise in leucine level [from 165 +/- 23 to 242 +/- 62 (SD) mu-M], appearance rate (from 125 +/- 11 to 142 +/- 17-mu-mol.kg-1.h-1), and oxidation (from 27 +/- 10 to 31 +/- 10-mu-mol.kg-1.h-1). In contrast, neither the plasma level nor the appearance rate of glutamine (333 +/- 51 vs. 318 +/- 58-mu-mol.kg-1.h-1) was affected. We conclude that insulin deficiency resulting in moderate hyperglycemia induces a 13% rise in whole body proteolysis and yet does not stimulate glutamine de novo synthesis, despite increased precursor availability.
引用
收藏
页码:E713 / E718
页数:6
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