Corticoadrenal activity regulates in rat betaine-homocysteine <Emphasis Type="Italic">S</Emphasis>-methyltransferase expression with opposites effects in liver and kidney |
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Authors: | Osvaldo Fridman Analía V Morales Laura E Bortoni Paula C Turk-Noceto Elio A Prieto |
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Institution: | 1.Centro de Altos Estudios en Ciencias Humanas y de la Salud,Universidad Abierta Interamericana (UAI),Buenos Aires,Argentina;2.Instituto de Oncología ángel H Roffo,Buenos Aires,Argentina;3.Consejo Nacional de Investigaciones Científicas y Técnicas,Buenos Aires,Argentina |
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Abstract: | Betaine-homocysteine S-methyltransferase (BHMT) is an enzyme that converts homocysteine (Hcy) to methionine using betaine as a methyl donor. Betaine
also acts as osmolyte in kidney medulla, protecting cells from high extracellular osmolarity. Hepatic BHMT expression is regulated
by salt intake. Hormones, particularly corticosteroids, also regulate BHMT expression in rat liver. We investigated to know
whether the corticoadrenal activity plays a role in kidney BHMT expression. BHMT activity in rat kidneys is several orders
of magnitude lower than in rat livers and only restricted to the renal cortex. This study confirms that corticosteroids stimulate
BHMT activity in the liver and, for the first time in an animal model, also up-regulate the BHMT gene expression. Besides,
unlike the liver, corticosteroids in rat kidney down-regulate BHMT expression and activity. Given that the classical effect
of adrenocortical activity on the kidney is associated with sodium and water re-absorption by the distal tubule leading to
volume expansion, by promoting lesser use of betaine as a methyl donor, corticosteroids would preserve betaine for its other
role as osmoprotectant against changes in the extracellular osmotic conditions. We conclude that corticosteroids are, at least
in part, responsible for the inhibition of BHMT expression and activity in rat kidneys. |
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