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741 results on '"Torres, Nimbe"'

205. Insulin and SGK1 reduce the function of Na+/monocarboxylate transporter 1 (SMCT1/SLC5A8).

Author

López-Barradas, Adriana, González-Cid, Tania, Vázquez, Norma, Gavi-Maza, Marisol, Reyes-Camacho, Adriana, Velázquez-Villegas, Laura A., Ramírez, Victoria, Zandi-Nejad, Kambiz, Mount, David B., Torres, Nimbe, Tovar, Armando R., Romero, Michael F., Gamba, Gerardo, and Plata, Consuelo

Subjects
INSULIN, SERINE/THREONINE kinases, MONOCARBOXYLATE transporters, AMINO acid metabolism, CELL metabolism
Abstract

SMCTs move several important fuel molecules that are involved in lipid, carbohydrate, and amino acid metabolism, but their regulation has been poorly studied. Insulin controls the translocation of several solutes that are involved in energetic cellular metabolism, including glucose. We studied the effect of insulin on the function of human SMCT1 expressed in Xenopus oocytes. The addition of insulin reduced α-keto-isocaproate (KIC)-dependent 22Na+ uptake by 29%. Consistent with this result, the coinjection of SMCT1 with SGK1 cRNA decreased the KIC-dependent 22Na+ uptake by 34%. The reduction of SMCT1 activity by SGK1 depends on its kinase activity, and it was observed that the coinjection of SMCT1 with S442D-SGK1 (a constitutively active mutant) decreased the KIC-dependent 22Na+ uptake by 50%. In contrast, an SMCT1 coinjection with K127M-SGK1 (an inactive mutant) had no effect on the KIC-dependent Na+ uptake. The decreasing SMCT1 function by insulin or SGK1 was corroborated by measuring [1-14C]acetate uptake and the electric currents of SMCT1-injected oocytes. Previously, we found that SMCT2/Slc5a12-mRNA, but not SMCT1/Slc5a8-mRNA, is present in zebrafish pancreas (by in situ hybridization); however, SLC5a8 gene silencing was associated with the development of human pancreatic cancer. We confirmed that the mRNA and protein of both transporters were present in rat pancreas using RT-PCR with specific primers, Western blot analysis, and immunohistochemistry. Additionally, significant propionate-dependent 22Na+ uptake occurred in pancreatic islets and was reduced by insulin treatment. Our data indicate that human SMCT1 is regulated by insulin and SGK1 and that both SMCTs are present in the mammalian pancreas. [ABSTRACT FROM AUTHOR]

Published
2016
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206. PPARα Downregulates Hepatic Glutaminase Expression in Mice Fed Diets with Different Protein:Carbohydrate Ratios.

Author

AVelázquez-Villegas, Laura, Charabati, Tania, Contreras, Alejandra V., Alemán, Gabriela, Torres, Nimbe, Tovar, Armando R., and Velázquez-Villegas, Laura A

Subjects
PEROXISOME proliferator-activated receptors, GLUTAMINASES, LABORATORY mice, AMINO acids, ENZYMES, PROTEIN metabolism, RNA metabolism, ANIMAL experimentation, BIOCHEMISTRY, CELL receptors, DIET, EPITHELIAL cells, CARBOHYDRATE content of food, GENES, HYDROLASES, LIVER, PHENOMENOLOGY, MICE, NUCLEOTIDES, PROTEINS, DIETARY proteins, RNA
Abstract

Background: Glutamine is catabolized in the liver by glutaminase 2 (GLS2). Evidence suggests that peroxisome proliferator-activated receptor α (PPARα) represses the expression of several amino acid-catabolizing enzymes, but for Gls2 this is unknown.Objective: The aim of the study was to assess whether PPARα regulates Gls2 expression.Methods: For 8 d, 7-9-wk-old male C57BL/6 wild-type (WT) and Ppara-null mice weighing 23.4 ± 0.5 g were fed diets with different dietary protein:carbohydrate (DP:DCH) ratios (6%:77%, 20%:63%, or 50%:33%). Liver samples were obtained after 16 h of feed deprivation or 3 h of refeeding, and microarrays were performed. Hepatic glutaminase expression was measured by quantitative polymerase chain reaction and Western blotting. Cotransfection analyses in hepatocellular carcinoma cell line (HepG2) cells with PPARα and hepatocyte nuclear factor 4α (HNF4α) expression vectors were performed.Results: The microarray results showed that Gls2 was the only upregulated gene in WT mice, but not in the Ppara-null mice. In the feed-deprived WT mice, the Gls2 mRNA and protein abundances in the 50%:33% group were 2.5- and 1.1-fold greater (P < 0.05), respectively, than those in the 20%:63% group, which were 2.3- and 0.4-fold greater than those in the 6%:77% group (P < 0.01). Gls2 mRNA expression in the 6%:77% group of feed-deprived Ppara-null mice was 33-fold greater than that in the same group of WT mice (P < 0.0001). GLS2 protein abundance in HepG2 cells was 78% greater than that in the controls (P < 0.0001) after HNF4α overexpression, and it was 99% greater after transfection with a short hairpin targeting PPARα.Conclusions: In Ppara-null mice, Gls2 mRNA expression was greater than in WT mice, regardless of the DP:DCH ratio. In HepG2 cells overexpressing HNF4α, Gls2 expression increased, an effect repressed by overexpression of PPARα. This suggests that Gls2 depends on the PPARα/HNF4α counterregulatory transcriptional control. [ABSTRACT FROM AUTHOR]

Published
2016
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215. Development of diet induced obesity models in rats, comparison of metabolic and genetic effects

Author

Hamdan-Perez, Nashla, primary, Torres, Nimbe, additional, Palacio, Armando Tovar, additional, Ordaz-Nava, Guillermo, additional, Torre-Villalvazo, Ivan, additional, Moran, Sofia, additional, Tovar-Palacio, Claudia, additional, Martinez, Braulio, additional, Hiriart, Marcia, additional, Santillan-Medina, Roberto, additional, and Torres-Villalobos, Gonzalo, additional

Published
2012
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235. Foreword

Author

Tovar, Armando R., primary, Torres, Nimbe, additional, Pardio, Jeanette, additional, and Arroyo, Pedro, additional

Published
2008
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