| Retinoic acid and glucocorticoid treatment induce hepatic glycine N-methyltransferase and lower plasma homocysteine concentrations in rats and rat hepatoma cells. | |
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MedLine Citation:
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PMID: 14608049 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Perturbation of folate and methyl group metabolism is associated with a number of pathological conditions, including cardiovascular disease and neoplastic development. Glycine N-methyltransferase (GNMT) is a key protein that functions to regulate the supply and utilization of methyl groups for S-adenosylmethionine (SAM)-dependent transmethylation reactions. Factors or conditions that have the ability to regulate GNMT and the generation of homocysteine, a product of transmethylation, have important implications in the potential perturbation of methyl group metabolism. We showed that retinoid compounds induce active hepatic GNMT, resulting in compromised transmethylation processes. Because retinoids can stimulate gluconeogenesis, a condition known to alter methyl group and homocysteine metabolism, the current study was undertaken to determine the relationship between all-trans-retinoic acid (RA) and gluconeogenic hormones on these metabolic pathways. Intact adrenal function was not required for RA to induce and activate hepatic GNMT; however, treatment of rats with dexamethasone (DEX) was as effective as RA in inducing GNMT in rat liver. The marked increase in plasma total homocysteine levels observed in adrenalectomized rats was reduced to normal levels by treatment with either RA or DEX, indicating that the transsulfuration and/or remethylation pathways may be enhanced. Moreover, coadministration of RA and DEX had an additive effect on GNMT induction. Similar findings were also observed in a rat hepatoma cell culture model using H4IIE cells. Taken together, these results demonstrate that both RA and DEX independently induce GNMT, thereby having substantial implications for the potential interaction of retinoid administration with diabetes. |
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Authors:
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Matthew J Rowling; Kevin L Schalinske |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. |
Journal Detail:
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Title: The Journal of nutrition Volume: 133 ISSN: 0022-3166 ISO Abbreviation: J. Nutr. Publication Date: 2003 Nov |
Date Detail:
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Created Date: 2003-11-10 Completed Date: 2004-08-24 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0404243 Medline TA: J Nutr Country: United States |
Other Details:
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Languages: eng Pagination: 3392-8 Citation Subset: IM |
Affiliation:
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Department of Food Science and Human Nutrition, Iowa State University, Ames, IA 50011, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adrenalectomy Animals Bucladesine / pharmacology Carcinoma, Hepatocellular Dexamethasone / pharmacology* Enzyme Induction / drug effects Glucocorticoids / pharmacology* Glycine N-Methyltransferase Homocysteine / blood* Liver / enzymology, metabolism* Liver Neoplasms Male Methyltransferases / biosynthesis, metabolism* Rats Rats, Sprague-Dawley Tretinoin / pharmacology* Tumor Cells, Cultured |
| Chemical | |
Reg. No./Substance:
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0/Glucocorticoids; 302-79-4/Tretinoin; 362-74-3/Bucladesine; 454-28-4/Homocysteine; 50-02-2/Dexamethasone; EC 2.1.1.-/Methyltransferases; EC 2.1.1.20/Glycine N-Methyltransferase; EC 2.1.1.20/Gnmt protein, rat |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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