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2015 ; 35
(4
): ä Nephropedia Template TP
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High homocysteine induces betaine depletion
#MMPMID26182429
Imbard A
; Benoist JF
; Esse R
; Gupta S
; Lebon S
; de Vriese AS
; de Baulny HO
; Kruger W
; Schiff M
; Blom HJ
Biosci Rep
2015[Apr]; 35
(4
): ä PMID26182429
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Betaine is the substrate of the liver- and kidney-specific betaine-homocysteine
(Hcy) methyltransferase (BHMT), an alternate pathway for Hcy remethylation. We
hypothesized that BHMT is a major pathway for homocysteine removal in cases of
hyperhomocysteinaemia (HHcy). Therefore, we measured betaine in plasma and
tissues from patients and animal models of HHcy of genetic and acquired cause.
Plasma was collected from patients presenting HHcy without any Hcy interfering
treatment. Plasma and tissues were collected from rat models of HHcy induced by
diet and from a mouse model of cystathionine ?-synthase (CBS) deficiency.
S-adenosyl-methionine (AdoMet), S-adenosyl-homocysteine (AdoHcy), methionine,
betaine and dimethylglycine (DMG) were quantified by ESI-LC-MS/MS. mRNA
expression was quantified using quantitative real-time (QRT)-PCR. For all
patients with diverse causes of HHcy, plasma betaine concentrations were below
the normal values of our laboratory. In the diet-induced HHcy rat model, betaine
was decreased in all tissues analysed (liver, brain, heart). In the mouse CBS
deficiency model, betaine was decreased in plasma, liver, heart and brain, but
was conserved in kidney. Surprisingly, BHMT expression and activity was decreased
in liver. However, in kidney, BHMT and SLC6A12 expression was increased in
CBS-deficient mice. Chronic HHcy, irrespective of its cause, induces betaine
depletion in plasma and tissues (liver, brain and heart), indicating a global
decrease in the body betaine pool. In kidney, betaine concentrations were not
affected, possibly due to overexpression of the betaine transporter SLC6A12 where
betaine may be conserved because of its crucial role as an osmolyte.
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