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Tan B.,Chinese Academy of Sciences | Li X.,Hunan Institute of Animal Husbandry and Veterinary Medicine | Wu G.,Chinese Academy of Sciences | Wu G.,China Agricultural University | And 6 more authors.
Amino Acids | Year: 2012

This study tested the hypothesis that an increase in arginine concentration in the portal vein may affect blood flow and oxygen consumption in the portal-drained viscera (PDV) of swine. Eight barrows (70 kg body weight) were surgically fitted with chronic catheters in the portal vein, ileal vein, and carotid artery. Thirteen days after the surgery, pigs that had been fasted for 12 h were randomly allocated to receive administration of either L-Alanine (103 mg/kg body weight, isonitrogenous control) or L-Arginine-HCl (61 mg/kg body weight) via the portal vein. Portal vein blood flow (PVBF) was measured with infusion of p-Aminohippuric acid into the ileal vein, and blood samples were simultaneously obtained every 0.5 h for 4 h. Compared with the control, arginine infusion increased PVBF at 30-90 min after infusion but decreased PDV oxygen consumption at 60-150 min after infusion (P\0.05). Plasma concentrations of glutamate at infusion times of 180-240 min and of arginine at infusion times of 60-240 min in arginine-infused pigs were higher than those for the control group (P\0.05). Plasma concentrations of insulin and glucagon at the infusion times of 30-90 min were higher and of free fatty acids at the infusion times of 60-120 min were lower than those for the control pigs (P\0.05). These results indicate that increasing arginine concentration in the portal vein enhances PDV blood flow, reduces PDV oxygen consumption, and beneficially alters the metabolic profile in swine, an established animal model for studying human nutrition and metabolism. © Springer-Verlag 2012. Source


Tan B.,CAS Institute of Subtropical Agriculture | Tan B.,University of Chinese Academy of Sciences | Tan B.,Texas College | Yin Y.,CAS Institute of Subtropical Agriculture | And 17 more authors.
Journal of Nutritional Biochemistry | Year: 2011

Obesity is a major health crisis worldwide and new treatments are needed to fight this epidemic. Using the swine model, we recently reported that dietary l-arginine (Arg) supplementation promotes muscle gain and reduces body-fat accretion. The present study tested the hypothesis that Arg regulates expression of key genes involved in lipid metabolism in skeletal muscle and white adipose tissue. Sixteen 110-day-old barrows were fed for 60 days a corn- and soybean-meal-based diet supplemented with 1.0% Arg or 2.05% l-alanine (isonitrogenous control). Blood samples, longissimus dorsi muscle and overlying subcutaneous adipose tissue were obtained from 170-day-old pigs for biochemical studies. Serum concentrations of leptin, alanine and glutamine were lower, but those for Arg and proline were higher in Arg-supplemented pigs than in control pigs. The percentage of oleic acid was higher but that of stearic acid and linoleic acid was lower in muscle of Arg-supplemented pigs, compared with control pigs. Dietary Arg supplementation increased mRNA levels for fatty acid synthase in muscle, while decreasing those for lipoprotein lipase, glucose transporter-4, and acetyl-coenzyme A carboxylase-α in adipose tissue. Additionally, mRNA levels for hormone sensitive lipase were higher in adipose tissue of Arg-supplemented pigs compared with control pigs. These results indicate that Arg differentially regulates expression of fat-metabolic genes in skeletal muscle and white adipose tissue, therefore favoring lipogenesis in muscle but lipolysis in adipose tissue. Our novel findings provide a biochemical basis for explaining the beneficial effect of Arg in improving the metabolic profile in mammals (including obese humans). © 2011 Elsevier Inc. Source


Tan B.,CAS Institute of Subtropical Agriculture | Tan B.,Texas A&M University | Tan B.,University of Chinese Academy of Sciences | Yin Y.,CAS Institute of Subtropical Agriculture | And 8 more authors.
Amino Acids | Year: 2010

This study tested the hypothesis that l-arginine (Arg) may stimulate cell proliferation and prevent lipopolysaccharide (LPS)-induced death of intestinal cells. Intestinal porcine epithelial cells (IPEC-1) were cultured for 4 days in Arg-free Dulbecco's modified Eagle's-F12 Ham medium (DMEM-F12) containing 10, 100 or 350 μM Arg and 0 or 20 ng/ml LPS. Cell numbers, protein concentrations, protein synthesis and degradation, as well as mammalian target of rapamycin (mTOR) and Toll-like receptor 4 (TLR4) signaling pathways were determined. Without LPS, IPEC-1 cells exhibited time- and Arg-dependent growth curves. LPS treatment increased cell death and reduced protein concentrations in IPEC-1 cells. Addition of 100 and 350 μM Arg to culture medium dose-dependently attenuated LPS-induced cell death and reduction of protein concentrations, in comparison with the basal medium containing 10 μM Arg. Furthermore, supplementation of 100 and 350 μM Arg increased protein synthesis and reduced protein degradation in both control and LPS-treated IPEC-1 cells. Consistent with the data on cell growth and protein turnover, addition of 100 or 350 μM Arg to culture medium increased relative protein levels for phosphorylated mTOR and phosphorylated ribosomal protein S6 kinase-1, while reducing the relative levels of TLR4 and phosphorylated levels of nuclear factor-κB in LPS-treated IPEC-1 cells. These results demonstrate a protective effect of Arg against LPS-induced enterocyte damage through mechanisms involving mTOR and TLR4 signaling pathways, as well as intracellular protein turnover. © 2009 The Author(s). Source


Tan B.,CAS Institute of Subtropical Agriculture | Li X.,Hunan Institute of Animal Husbandry and Veterinary Medicine | Yin Y.,CAS Institute of Subtropical Agriculture | Wu Z.,China Agricultural University | And 5 more authors.
Frontiers in Bioscience | Year: 2012

As the nitrogenous precursor of nitric oxide, Larginine 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 proliferatoractivated receptor-gamma coactivator-1 alpha (PGC-1 alpha), mitochondrial biogenesis, and the growth of brown adipose tissue growth. Furthermore, arginine regulates adipocytemuscle crosstalk and energy partitioning via the secretion of cytokines and hormones. In addition, arginine enhances AMPactivated 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. Source

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