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7336845 
Journal Article 
Benefits of l-alanine or l-arginine supplementation against adiposity and glucose intolerance in monosodium glutamate-induced obesity 
Araujo, TR; Freitas, IN; Vettorazzi, JF; Batista, TM; Santos-Silva, JC; Bonfleur, ML; Balbo, SL; Boschero, AC; Carneiro, EM; Ribeiro, RA 
2017 
Yes 
European Journal of Nutrition
ISSN: 1436-6207
EISSN: 1436-6215 
Dr. Dietrich Steinkopff Verlag GmbH and Co. KG 
56 
6 
2069-2080 
English 
Purpose: l-alanine (Ala) and l-arginine (Arg) have been reported to regulate pancreatic β-cell physiology and to prevent body fat accumulation in diet-induced obesity. Here, we assessed growth and adiposity parameters, glucose tolerance, insulin secretion and the expression of insulin and nutrient-regulated proteins in monosodium glutamate (MSG)-obese mice supplemented with either Ala or Arg. Methods: Male newborn C57Bl/6 mice received a daily subcutaneous injection of MSG or saline solution (CTL group), during the first 6 days of life. From 30 to 90 days of age, MSG and CTL mice received or not 2.55 % Ala (CAla or MArg groups) or 1.51 % Arg-HCl (CArg or MArg groups) in their drinking water. Results: Adult MSG mice displayed higher adiposity associated with lower phosphorylation of the adipogenic enzyme, ACC, in adipose tissue. Glucose intolerance in MSG mice was linked to lower insulin secretion and to lower expression of IRβ in adipose tissue, as well as AS160 phosphorylation in skeletal muscle. Perigonadal fat depots were smaller in Ala and Arg mice, while retroperitoneal fat pads were decreased by Ala supplementation only. Both Ala and Arg improved fed-state glycemia as well as IRβ and pAS160 content, but only Ala led to improved glucose tolerance and insulin secretion. Adipostatic signals were increased in MAla mice, as indicated by enhanced AMPK phosphorylation and pACC content in fat depots. Conclusions: Ala supplementation led to more pronounced metabolic improvements compared to Arg, possibly due to suppression of lipogenesis through activation of the AMPK/ACC pathway. © 2016, Springer-Verlag Berlin Heidelberg. 
AMP-activated kinase; Insulin secretion; l-alanine supplementation; l-arginine supplementation; MSG obesity; Neuroendocrine disorder; alanine; albumin; antiobesity agent; arginine; cholesterol; drinking water; glucose; glutamate sodium; insulin; insulin receptor; insulin receptor beta; protein kinase B; synth; triacylglycerol; unclassified drug; alanine; arginine; cholesterol; glutamate sodium; guanosine triphosphatase activating protein; insulin; insulin receptor; serum albumin; Tbc1d4 protein, mouse; triacylglycerol; adipogenesis; adipose tissue; adult; albumin blood level; animal experiment; animal model; animal tissue; Article; body height; cholesterol blood level; controlled study; diet supplementation; experimental obesity; fat pad; food intake; gastrocnemius muscle; glucose blood level; glucose homeostasis; glucose intolerance; glucose tolerance; insulin blood level; insulin release; lipid storage; male; mouse; newborn; nonhuman; protein expression; protein phosphorylation; retroperitoneal fat; triacylglycerol blood level; animal; blood; C57BL mouse; chemically induced; dietary supplement; drug effect; gene expression regulation; genetics; glucose intolerance; homeostasis; metabolism; mouse mutant; obesity; phosphorylation; secretion (process); Adiposity; Alanine; Animals; Arginine; Blood Glucose; Cholesterol; Dietary Supplements; Gene Expression Regulation; Glucose Intolerance; GTPase-Activating Proteins; Homeostasis; Insulin; Male; Mice; Mice, Inbred C57BL; Mice, Obese; Obesity; Phosphorylation; Receptor, Insulin; Serum Albumin; Sodium Glutamate; Triglycerides