Beneficial effects of L-arginine on reducing obesity: potential mechanisms and important implications for human health.

Department of Animal Science, Faculty of Nutrition, Texas A&M University, College Station, TX 77843, USA.
Amino Acids (Impact Factor: 3.65). 05/2010; 39(2):349-57. DOI: 10.1007/s00726-010-0598-z
Source: PubMed

ABSTRACT Over the past 20 years, growing interest in the biochemistry, nutrition, and pharmacology of L-arginine has led to extensive studies to explore its nutritional and therapeutic roles in treating and preventing human metabolic disorders. Emerging evidence shows that dietary L-arginine supplementation reduces adiposity in genetically obese rats, diet-induced obese rats, finishing pigs, and obese human subjects with Type-2 diabetes mellitus. The mechanisms responsible for the beneficial effects of L-arginine are likely complex, but ultimately involve altering the balance of energy intake and expenditure in favor of fat loss or reduced growth of white adipose tissue. Recent studies indicate that L-arginine supplementation stimulates mitochondrial biogenesis and brown adipose tissue development possibly through the enhanced synthesis of cell-signaling molecules (e.g., nitric oxide, carbon monoxide, polyamines, cGMP, and cAMP) as well as the increased expression of genes that promote whole-body oxidation of energy substrates (e.g., glucose and fatty acids) Thus, L-arginine holds great promise as a safe and cost-effective nutrient to reduce adiposity, increase muscle mass, and improve the metabolic profile in animals and humans.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Amino acids (AA) have enormous physiological importance, serving as building blocks for proteins and substrates for synthesis of low-molecular-weight substances. Based on growth or nitrogen balance, AA were traditionally classified as nutritionally essential or nonessential for animals. Although those AA that are not synthesized in eukaryotes (nutritionally essential AA, EAA) must be present in animal diets, nutritionally nonessential AA (NEAA) have long been ignored for all species. Emerging evidence shows that nonruminants cannot adequately synthesize NEAA or conditionally essential AA (CEAA) to realize their growth or anti-infection potential. Likewise, all preformed AA are needed for high-producing cows and rapidly growing ruminants. Many NEAA and CEAA (e.g., arginine, glutamine, glutamate, glycine, and proline) and certain EAA (e.g., leucine and tryptophan) participate in cell signaling, gene expression, and metabolic regulation. Thus, functions of AA beyond protein synthesis must be considered in dietary formulations to improve efficiency of nutrient use, growth, development, reproduction, lactation, and well-being in animals.
    02/2014; 2:387-417. DOI:10.1146/annurev-animal-022513-114113
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Arginine, an α-amino acid, has been reported to exert beneficial effects that ameliorate health problems and prevent excessive fat deposition. In this study, we investigated whether the activation of cell signaling by arginine can induce osteogenic differentiation and modulate excessive adipogenic differentiation in human mesenchymal stem cells (MSCs). Arginine potently induced the expression of type Iα1 collagen, osteocalcin, and ALP in a dose-dependent manner without causing cytotoxicity. Arginine significantly increased the mRNA expression of the osteogenic transcription factors runt-related transcription factor 2 (Runx2), DIx5, and osterix. Furthermore, arginine demonstrated its antiadipogenicity by decreasing adipocyte formation and triglyceride (TG) content in MSCs and inhibiting the mRNA expression of the adipogenic transcription factors peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα), and fatty acid binding protein 4 (Fabp4). This effect was associated with increased expression of Wnt5a, and nuclear factor of activated T-cells (NFATc), and was abrogated by antagonists of Wnt and NFATc, which indicated a role of Wnt and NFATc signaling in the switch from adipogenesis to osteoblastogenesis induced by arginine. In conclusion, this is the first report of the dual action of arginine in promoting osteogenesis and inhibiting adipocyte formation through involving Wnt5a and NFATc signaling pathway.
    International Journal of Molecular Sciences 07/2014; 15(7):13010-29. DOI:10.3390/ijms150713010 · 2.46 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Numerous studies have demonstrated the impact of functional fibers on gut microbiota and metabolic health but some less well-studied fibers and/or fractions of foods known to be high in fiber still warrant examination. The aim of this study was to assess the effect of yellow pea-derived fractions varying in fiber and protein content on metabolic parameters and gut microbiota in diet induced obese (DIO) rats. We hypothesized that the yellow pea fiber fraction would improve glycemia and alter gut microbiota. Rats were randomized to 1 of 5 isocaloric dietary treatments for 6 weeks: (1) control; (2) oligofructose (OFS); (3) yellow pea fiber (PF); (4) yellow pea flour (PFL); or (5) yellow pea starch (PS). Glycemia, plasma gut hormones, body composition, hepatic triglyceride content, gut microbiota and mRNA expression of genes related to hepatic fat metabolism were examined. PFL attenuated weight gain compared to control, PF, and PS (P < 0.05). PFL, PS and OFS had significantly lower final percent body fat compared to control. OFS but not the pea fraction diets reduced food intake compared to control (P < 0.05). PF resulted in lower fasting glucose and glucose area under the curve compared to control. Changes in gut microbiota were fraction-specific and included a decrease in Firmicutes (%) for OFS, PF, and PFL compared to control (P < 0.05). The Firmicutes/Bacteroidetes ratio was reduced with OFS, PF, and PFL when compared to PS (P < 0.05). Taken together, this work suggests that yellow pea-derived fractions are able to distinctly modulate metabolic parameters and gut microbiota in obese rats.
    Nutrition Research 08/2014; 34(8). DOI:10.1016/j.nutres.2014.07.016 · 2.59 Impact Factor