Regulatory roles for L-arginine in reducing white adipose tissue

Abstract

As the nitrogenous precursor of nitric oxide, L-arginine regulates multiple metabolic pathways involved in the metabolism of fatty acids, glucose, amino acids, and proteins through cell signaling and gene expression. Specifically, arginine stimulates lipolysis and the expression of key genes responsible for activation of fatty acid oxidation to CO2 and water. The underlying mechanisms involve increases in the expression of peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha), mitochondrial biogenesis, and the growth of brown adipose tissue growth. Furthermore, arginine regulates adipocyte-muscle crosstalk and energy partitioning via the secretion of cytokines and hormones. In addition, arginine enhances AMP-activated protein kinase (AMPK) expression and activity, thereby modulating lipid metabolism and energy balance toward the loss of triacylglycerols. Growing evidence shows that dietary supplementation with arginine effectively reduces white adipose tissue in Zucker diabetic fatty rats, diet-induced obese rats, growing-finishing pigs, and obese patients with type II diabetes. Thus, arginine can be used to prevent and treat adiposity and the associated metabolic syndrome.

Nutritional epigenetics with a focus on amino acids: implications for the development and treatment of metabolic syndrome

“…In a rodent model of a low-protein diet, arginine supplementation contributed to increased insulin sensitivity and whole-body energy expenditure [56]. Growing evidence suggests an important role for arginine in 10 stimulating lipolysis and oxidation of fatty acids in the whole body, thereby reducing white adipose tissue [56,57]. These beneficial effects of arginine may also be associated with growth and development of brown adipose tissue in the fetus and postnatal mammals, as demonstrated by studies involving nutrient-restricted sheep and diet-induced obese sheep [58,59] as well as diet-induced obese rats and diabetic rats [60].…”

Особливості Вуглеводного Обміну У хворих На хронічне Обструктивне Захворювання Легень За коморбідного Перебігу Хронічного Панкреатиту

“…Саме пероксинітрит як мета-боліт NO викликає ушкодження -клітин підшлун-кової залози, безпосередньо впливаючи на ДНК цих клітин [11]. З іншого боку, аргінін, що є по-передником NO, стимулює секрецію глюкагону -клітинами острівцевого апарату підшлункової залози, який, у свою чергу, стимулює секрецію інсуліну -клітинами підшлункової залози [4,19]. Гіперінсулінемія через адаптивне зниження екс-пресії інсулінових рецепторів при «ситому» стані клітин також може сприяти розвитку ІР [12].…”

Ultraviolet radiation, vitamin D and the development of obesity, metabolic syndrome and type-2 diabetes

“…In addition to the protective effects of UVRinduced release of nitric oxide from storage forms in the skin (described above), improved insulin sensitivity and metabolic profiles, [40][41][42][43][44] reduced adiposity (reviewed by 42,45,46 ), increased energy expenditure 42 and improved liver function. 44 NOS inhibitors such as L-NAME (N ω nitro-L-arginine methyl ester), lowered endogenous nitric oxide production and reduced circulating levels of nitric oxide metabolites, 47,48 but had inconsistent effects on the development of obesity and metabolic dysfunction.…”