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进餐吸收过程中氨基酸和胰岛素对蛋白质合成代谢的作用。

Contribution of amino acids and insulin to protein anabolism during meal absorption.

作者信息

Volpi E, Lucidi P, Cruciani G, Monacchia F, Reboldi G, Brunetti P, Bolli G B, De Feo P

机构信息

Department of Internal Medicine, Endocrine and Metabolic Sciences, University of Perugia, Italy.

出版信息

Diabetes. 1996 Sep;45(9):1245-52. doi: 10.2337/diab.45.9.1245.

DOI:10.2337/diab.45.9.1245
PMID:8772730
Abstract

The contribution of dietary amino acids and endogenous hyperinsulinemia to prandial protein anabolism still has not been established. To this end, leucine estimates ([1-14C]leucine infusion, plasma alpha-ketoisocaproic acid [KIC] specific activity [SA] as precursor pool SA) of whole-body protein kinetics and fractional secretory rates (FSRs) of albumin, fibrinogen, antithrombin III, and immunoglobulin G (IgG) were measured in three groups of healthy volunteers during intragastric infusion of water (controls, n = 5), liquid glucose-lipid-amino acid (AA) meal (meal+AA, n = 7), or isocaloric glucose-lipid meal (meal-AA, n = 7) that induced the same insulin response as the meal+AA. The results of this study demonstrate that 1) by increasing (P < 0.01) whole-body protein synthesis and decreasing (P < 0.01) proteolysis, dietary amino acids account for the largest part (approximately 90%) of postprandial protein anabolism; 2) the ingestion of an isocaloric meal deprived of amino acids exerts a modest protein anabolic effect (10% of postprandial protein anabolism) by decreasing amino acid oxidation and increasing (P < 0.01) albumin synthesis; 3) albumin FSR is increased (approximately 20%) by postprandial hyperinsulinemia (meal-AA) and additionally increased (approximately 50%) by amino acid intake (meal+AA); 4) IgG FSR is stimulated (approximately 40%) by amino acids, not by insulin; and 5) fibrinogen and antithrombin III FSR are not regulated by amino acids or insulin.

摘要

膳食氨基酸和内源性高胰岛素血症对餐后蛋白质合成代谢的作用尚未明确。为此,在三组健康志愿者胃内输注水(对照组,n = 5)、液体葡萄糖 - 脂质 - 氨基酸(AA)餐(餐 + AA,n = 7)或等热量葡萄糖 - 脂质餐(餐 - AA,n = 7)期间,测量了全身蛋白质动力学的亮氨酸估计值([1 - 14C]亮氨酸输注,血浆α - 酮异己酸[KIC]比活性[SA]作为前体池SA)以及白蛋白、纤维蛋白原、抗凝血酶III和免疫球蛋白G(IgG)的分数分泌率(FSR),其中等热量葡萄糖 - 脂质餐诱导的胰岛素反应与餐 + AA相同。本研究结果表明:1)通过增加(P < 0.01)全身蛋白质合成并减少(P < 0.01)蛋白质分解,膳食氨基酸占餐后蛋白质合成代谢的最大部分(约90%);2)摄入不含氨基酸的等热量餐通过减少氨基酸氧化并增加(P < 0.01)白蛋白合成,发挥适度的蛋白质合成代谢作用(餐后蛋白质合成代谢的10%);3)餐后高胰岛素血症(餐 - AA)使白蛋白FSR增加(约20%),氨基酸摄入(餐 + AA)使其进一步增加(约50%);4)IgG FSR受氨基酸刺激(约40%),而非胰岛素;5)纤维蛋白原和抗凝血酶III的FSR不受氨基酸或胰岛素调节。

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