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Characterization of homocysteine and methyl group metabolism in female non‐obese diabetic (NOD) mice
Author(s) -
Nieman Kristin M,
McGuire Annette S,
Schalinske Kevin L
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.557.5
Subject(s) - nod , homocysteine , nod mice , endocrinology , medicine , diabetes mellitus , metabolism , methyltransferase , methylation , biology , chemistry , biochemistry , gene
Methyl groups are critical for numerous biological reactions and proper regulation of methyl group and homocysteine (hcy) metabolism is essential for disease prevention. The hepatic protein glycine N ‐methyltransferase (GNMT) is a key regulator of supply and utilization of methyl groups from the primary donor, S ‐adenosylmethionine. Chemically‐induced type 1 diabetes has been shown to alter hcy and methyl group metabolism, resulting in a methyl deficient state, including DNA hypomethylation. The objective of this study was to characterize hcy and methyl group metabolism using a genetic model of diabetes, the non‐obese diabetic (NOD) mouse, which spontaneously develops autoimmune‐mediated type 1 diabetes. NOD mice and their controls (ICR), were sacrificed at 12, 18, and 24 wk of age for collection of blood and liver tissue. Plasma hcy concentrations in NOD mice were only 63% of the control values in 18 wk old ICR animals. NOD mice exhibited a 1.4‐fold increase in GNMT activity compared to ICR mice at 18 wk. Neither metabolic parameter was altered in 12 wk old animals. The NOD mouse, a genetic model for type 1 diabetes, exhibits similar perturbations in methyl group and hcy metabolism as the chemically‐induced rat model. This validation will be important in future studies directed at understanding the relation between diabetes, perturbation of methyl groups, and specific pathologies (Support: NIH HD057315 ‐02).