Plasma homocysteine level and hepatic sulfur amino acid metabolism in mice fed a high-fat diet

Eur J Nutr. 2013 Feb;52(1):127-34. doi: 10.1007/s00394-011-0294-0. Epub 2012 Jan 1.

Abstract

Purpose: Obesity, a feature of metabolic syndrome, is a risk factor for cardiovascular disease, and elevated plasma homocysteine is associated with increased cardiovascular risk. However, little published information is available concerning the effect of obesity on homocysteine metabolism.

Methods: Hepatic homocysteine metabolism was determined in male C57BL/6 mice fed a high-fat diet for 12 weeks.

Results: High-fat diet increased plasma homocysteine but decreased hepatic homocysteine levels. Hepatic S-adenosylhomocysteine hydrolase levels were down-regulated in the obese mice, which was in part responsible for the decrease in hepatic S-adenosylmethionine/S-adenosylhomocysteine, which served as an index of transmethylation potential. Despite the decrease in hepatic cysteine, hepatic taurine synthesis was activated via up-regulation of cysteine dioxygenase. Hepatic levels of methionine adenosyltransferase I/III, methionine synthase, methylene tetrahydrofolate reductase, and gamma-glutamylcysteine ligase catalytic subunit were unchanged. Obese mice showed elevated betaine-homocysteine methyltransferase and decreased cystathionine beta-synthase activities, although the quantities of these enzymes were unchanged.

Conclusion: This study suggests that plasma homocysteine level is increased in obesity-associated hepatic steatosis, possibly as a result of increased hepatic homocysteine efflux along with an altered sulfur amino acid metabolism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase / genetics
  • 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase / metabolism
  • Adenosylhomocysteinase / genetics
  • Adenosylhomocysteinase / metabolism
  • Amino Acids, Sulfur / metabolism*
  • Animals
  • Cardiovascular Diseases / complications
  • Cystathionine beta-Synthase / genetics
  • Cystathionine beta-Synthase / metabolism
  • Cysteine Dioxygenase / genetics
  • Cysteine Dioxygenase / metabolism
  • Diet, High-Fat*
  • Dipeptides / genetics
  • Dipeptides / metabolism
  • Down-Regulation
  • Homocysteine / blood*
  • Lipid Peroxidation
  • Liver / drug effects*
  • Liver / metabolism
  • Male
  • Methionine Adenosyltransferase / genetics
  • Methionine Adenosyltransferase / metabolism
  • Methylenetetrahydrofolate Reductase (NADPH2) / genetics
  • Methylenetetrahydrofolate Reductase (NADPH2) / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Risk Factors
  • S-Adenosylhomocysteine / metabolism
  • S-Adenosylmethionine / genetics
  • S-Adenosylmethionine / metabolism
  • Triglycerides / blood
  • Up-Regulation

Substances

  • Amino Acids, Sulfur
  • Dipeptides
  • Triglycerides
  • Homocysteine
  • S-Adenosylmethionine
  • S-Adenosylhomocysteine
  • Cysteine Dioxygenase
  • Methylenetetrahydrofolate Reductase (NADPH2)
  • 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase
  • Methionine Adenosyltransferase
  • Adenosylhomocysteinase
  • Cystathionine beta-Synthase
  • gamma-glutamylcysteine