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Corticoadrenal activity regulates in rat betaine-homocysteine S-methyltransferase expression with opposites effects in liver and kidney

Authors
  • Fridman, Osvaldo1, 2, 3
  • Morales, Analía V1
  • Bortoni, Laura E2
  • Turk-Noceto, Paula C1
  • Prieto, Elio A1
  • 1 Universidad Abierta Interamericana (UAI), Centro de Altos Estudios en Ciencias Humanas y de la Salud, Buenos Aires, Argentina , Buenos Aires (Argentina)
  • 2 Instituto de Oncología Ángel H Roffo, Buenos Aires, Argentina , Buenos Aires (Argentina)
  • 3 Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina , Buenos Aires (Argentina)
Type
Published Article
Journal
Journal of Biosciences
Publisher
Springer-Verlag
Publication Date
Dec 30, 2011
Volume
37
Issue
1
Pages
115–123
Identifiers
DOI: 10.1007/s12038-011-9171-5
Source
Springer Nature
Keywords
License
Yellow

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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