Keller U, Szinnai G, Bilz S, Berneis K
Division of Endocrinology, Diabetology and Clinical Nutrition, Basel, Switzerland.
Eur J Clin Nutr. 2003 Dec;57 Suppl 2:S69-74. doi: 10.1038/sj.ejcn.1601904.
Alterations of cell volume induced by changes of extracellular osmolality have been reported to regulate intracellular metabolic pathways. Hypo-osmotic cell swelling counteracts proteolysis and glycogen breakdown in the liver, whereas hyperosmotic cell shrinkage promotes protein breakdown, glycolysis and glycogenolysis. To investigate the effect of acute changes of extracellular osmolality on whole-body protein, glucose and lipid metabolism in vivo, we studied 10 male subjects during three conditions: (i) hyperosmolality was induced by fluid restriction and intravenous infusion of hypertonic NaCl (2-5%, wt/vol) during 17 h; (ii) hypo-osmolality was produced by intravenous administration of desmopressin, liberal water drinking and infusion of hypotonic saline (0.4%); and (iii) the iso-osmolality study comprised oral water intake ad libitum. Plasma osmolality increased from 285+/-1 to 296+/-1 mosm/kg (P<0.001 during hyperosmolality, and decreased from 286+/-1 to 265+/-1 mosm/kg during hypo-osmolality (P<0.001). Total body leucine flux ([1-(13)C]leucine infusion technique), reflecting whole-body protein breakdown, as well as whole-body leucine oxidation rate (irreversible loss of amino acids) decreased significantly during hypo-osmolality. The glucose metabolic clearance rate during hyperinsulinaemic-euglycemic clamping increased significantly less during hypo-osmolality than iso-osmolality, indicating diminished peripheral insulin sensitivity. Glycerol turnover (2-[(13)C]glycerol infusion technique), reflecting whole-body lipolysis, increased significantly during hypo-osmolar conditions. The results demonstrate that the metabolic adaptation to acute hypo-osmolality resembles that of acute fasting, that is, it results in protein sparing associated with increased lipolysis, ketogenesis and lipid oxidation and impaired insulin sensitivity of glucose metabolism.
据报道,细胞外渗透压变化引起的细胞体积改变可调节细胞内代谢途径。低渗性细胞肿胀可抵消肝脏中的蛋白水解和糖原分解,而高渗性细胞皱缩则促进蛋白质分解、糖酵解和糖原分解。为了研究细胞外渗透压急性变化对体内全身蛋白质、葡萄糖和脂质代谢的影响,我们对10名男性受试者在三种情况下进行了研究:(i)在17小时内通过限制液体摄入和静脉输注高渗氯化钠(2 - 5%,重量/体积)诱导高渗状态;(ii)通过静脉注射去氨加压素、大量饮水和输注低渗盐水(0.4%)产生低渗状态;(iii)等渗性研究包括随意口服饮水。血浆渗透压在高渗状态下从285±1 mosm/kg升高至296±1 mosm/kg(P<0.001),在低渗状态下从286±1 mosm/kg降至265±1 mosm/kg(P<0.001)。反映全身蛋白质分解的全身亮氨酸通量([1 - (13)C]亮氨酸输注技术)以及全身亮氨酸氧化率(氨基酸不可逆损失)在低渗状态下显著降低。在正常血糖高胰岛素钳夹期间,低渗状态下的葡萄糖代谢清除率比等渗状态下显著增加得更少,表明外周胰岛素敏感性降低。反映全身脂肪分解的甘油周转率(2 - [(13)C]甘油输注技术)在低渗状态下显著增加。结果表明,对急性低渗状态的代谢适应类似于急性禁食状态下的适应,即它导致与脂肪分解增加、生酮作用和脂质氧化增加以及葡萄糖代谢的胰岛素敏感性受损相关的蛋白质节约。