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A Low-Protein,High-Carbohydrate Diet Increases Fatty Acid Uptake and Reduces Norepinephrine-Induced Lipolysis in Rat Retroperitoneal White Adipose Tissue
Authors:Maísa P. dos Santos  Suélem A. de França  José Tiago F. dos Santos  Samyra L. Buzelle  Gisele L. Bertolini  Maria Antonieta R. Garófalo  Isis C. do Kettelhut  Danúbia Frasson  Valéria E. Chaves  Nair H. Kawashita
Affiliation:1.Department of Chemistry,Federal University of Mato Grosso,Cuiabá,Brazil;2.Department of Basic Sciences in Health,Federal University of Mato Grosso,Cuiabá,Brazil;3.Department of Physiology,University of S?o Paulo,Ribeir?o Preto,Brazil;4.Department of Biochemistry, Immunology,University of S?o Paulo,Ribeir?o Preto,Brazil
Abstract:A low-protein, high-carbohydrate (LPHC) diet for 15 days increased the lipid content in the carcass and adipose tissues of rats. The aim of this work was to investigate the mechanisms of this lipid increase in the retroperitoneal white adipose tissue (RWAT) of these animals. The LPHC diet induced an approximately two- and tenfold increase in serum corticosterone and TNF-α, respectively. The rate of de novo fatty acid (FA) synthesis in vivo was reduced (50%) in LPHC rats, and the lipoprotein lipase activity increased (100%). In addition, glycerokinase activity increased (60%), and the phosphoenolpyruvate carboxykinase content decreased (27%). Basal [U-14C]-glucose incorporation into glycerol-triacylglycerol did not differ between the groups; however, in the presence of insulin, [U-14C]-glucose incorporation increased by 124% in adipocytes from only control rats. The reductions in IRS1 and AKT content as well as AKT phosphorylation in the RWAT from LPHC rats and the absence of an insulin response suggest that these adipocytes have reduced insulin sensitivity. The increase in NE turnover by 45% and the lack of a lipolytic response to NE in adipocytes from LPHC rats imply catecholamine resistance. The data reveal that the increase in fat storage in the RWAT of LPHC rats results from an increase in FA uptake from circulating lipoproteins and glycerol phosphorylation, which is accompanied by an impaired lipolysis that is activated by NE.
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