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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。
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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 |
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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