会社ロゴ Better Health Through Science
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糖尿病はプラズマアルギニン不足と神経伝達物質の一酸化窒素の合成を減少します。一酸化窒素が減少すると糖尿病とインシュリン抵抗の患者に虚血と突然死を招く可能性が上がります。
Diabetics Have Reduced Plasma Arginine and Reduced Nitric Oxide Production that is Improved with Oral Arginine Administration
Diabetes mellitus is associated with reduced plasma arginine concentrations and reduced nitric oxide synthesis by endothelial cells. The reduction of nitric oxide production by the blood vessels cells is thought to produce increased ischemia and sudden death rate in diabetics and patients with insulin resistance.The reduction of plasma arginine and reduced blood vessel production of nitric oxide has been shown in humans and animal models of diabetes mellitus. Moreover, ingestion of oral arginine results in increased blood vessel production of nitric oxide.This article uses a well defined animal model to explore the mechanism of improved nitric oxide synthesis by oral arginine administration in diabetes.The authors demonstrate that oral arginine administration increases plasma arginine and blood vessel production of nitric oxide. Also, the authors show that the improved nitric oxide synthesis occurs by stimulation of BH4, an important cofactor for nitric oxide production . The authors show that diabetes is associated with reduced arginine plasma levels and confirm the deficiency of arginine in diabetes and insulin resistance. There is a good bibliography documenting the human studies of arginine deficiency All patients who have diabetes or insulin resistance, including obesity, should receive oral arginine to improve their vascular function.The Editors
Dietary L-arginine supplementation enhances endothelial nitric oxide synthesis in streptozotocin-induced diabetic rats
Kohli,R.; Meininger,C.J.; Haynes,T.E.; Yan,W.; Self,J.T.; Wu,G.

Faculty of Nutrition and Department of Animal Science, Texas A&M University, College Station, TX 77843, USA

J. Nutrition 134:600-608:2004

This study tested the hypothesis that dietary arginine supplementation increases endothelial tetrahydrobiopterin (BH(4)) availability for nitric oxide (NO) synthesis in diabetic rats. Streptozotocin-induced diabetic rats either were given unrestricted access to a casein-based diet (Expt. 1) or were pair-fed the diet on the basis of the food intake per kg of body weight of nondiabetic rats (Expt. 2). Beginning 1 d after vehicle or streptozotocin injection, arginine-HCl (1.51%) or alanine (isonitrogenous control, 2.55%) was added daily to the drinking water for nondiabetic rats, whereas concentrations were adjusted (0.43% arginine-HCl and 0.73% alanine) in the drinking water for diabetic rats (which consumed more water) to ensure isonitrogenous provision. At 2 wk after the initiation of arginine supplementation, coronary endothelial cells and plasma were obtained for the measurement of NO synthesis and metabolites. In both experiments, plasma and endothelial concentrations of N(G)-monomethylarginine, asymmetric dimethylarginine, and symmetric dimethylarginine increased, but those of arginine as well as endothelial BH(4) availability and NO synthesis decreased in diabetic rats, compared with nondiabetic rats. In both diabetic and nondiabetic rats, arginine supplementation increased plasma concentrations of arginine and insulin, endothelial concentrations of arginine and BH(4), and endothelial NO synthesis, but did not affect plasma and endothelial concentrations of methylarginines or plasma concentrations of homocysteine. Dietary arginine supplementation or provision of a BH(4) precursor normalized endothelial NO synthesis in diabetic rats. Arginine supplementation did not affect plasma glucose levels in nondiabetic rats, but reduced body weight loss and plasma glucose levels in diabetic rats. Thus, dietary L-arginine supplementation stimulates endothelial NO synthesis by increasing BH(4) provision, which is beneficial for vascular function and glucose homeostasis in diabetic subjects
 
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