title: Vitamin A deficiency increases protein catabolism and induces urea cycle enzymes in rats.
abstract: Chronic vitamin A deficiency induces a substantial delay in the rates of weight and height gain in both humans and experimental animals. This effect has been associated with an impaired nutrient metabolism and loss of body protein. Therefore, we analyzed the effect of vitamin A deficiency on endogenous proteolysis and nitrogen metabolism and its reversibility with all-trans retinoic acid (RA). Male weanling rats, housed in pairs, were pair-fed a vitamin A-deficient (VAD) or control diet until they were 60 d old. A group of deficient rats were further treated with daily intraperitoneal injections of all-trans RA for 10 d. Final body and tissue (i.e. liver and heart) weights were significantly lower and tissue:body weight ratios were similar in VAD rats and in controls. Conversely, the epididymal white fat:body weight ratio and the plasma concentrations of alanine aminotransferase and adiponectin were significantly higher in VAD rats, which also had hepatic macrovesicular lipid accumulations. Plasma and gastrocnemius muscle 3-methylhistidine, urine nitrogen, and plasma and urine urea concentrations were all significantly higher in the VAD group. The expression of the genes encoding urea cycle enzymes and their activities increased in VAD livers. These changes were partially reverted by all-trans RA. We propose that fuel partitioning in vitamin A deficiency may shift from fatty acids to protein catabolism as an energy source. Our results emphasize the importance of vitamin A on the energy balance control system and they provide an explanation for the role of vitamin A in protein turnover, development, and growth.
authors.affiliation: Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de Valencia, Valencia, Spain.
authors.forename: Guillermo
authors.initials: G
authors.lastname: Esteban-Pretel
authors.forename: M Pilar
authors.initials: MP
authors.lastname: Marín
authors.forename: Francisco
authors.initials: F
authors.lastname: Cabezuelo
authors.forename: Verónica
authors.initials: V
authors.lastname: Moreno
authors.forename: Jaime
authors.initials: J
authors.lastname: Renau-Piqueras
authors.forename: Joaquín
authors.initials: J
authors.lastname: Timoneda
authors.forename: Teresa
authors.initials: T
authors.lastname: Barber
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D004790:Enzyme Induction; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000201:enzymology / Q000378:metabolism* / Q000648:ultrastructure; D008297:Male; D008762:Methylhistidines / Q000097:blood / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D009584:Nitrogen / Q000378:metabolism; D051381:Rats; D012176:Retinoids / Q000097:blood / Q000378:metabolism; D014212:Tretinoin / Q000494:pharmacology / Q000627:therapeutic use*; D014280:Triglycerides; D014508:Urea / Q000378:metabolism*; D014802:Vitamin A Deficiency / Q000188:drug therapy / Q000201:enzymology / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D008762:Methylhistidines; D012176:Retinoids; D014280:Triglycerides; D014212:Tretinoin; D014508:Urea; C028118:3-methylhistidine; D009584:Nitrogen