Metabolism of methionine in vivo: impact of pregnancy, protein restriction, and fatty liver disease.
The coexistence of intrauterine and neonatal malnutrition and the development of obesity, type 2 diabetes and related comorbidities have been confirmed in a number of studies in humans and animal models. Data from studies in animals suggest that epigenetic changes as a result of altered methylation of the genomic DNA may be responsible for such metabolic patterning. Methionine, an essential amino acid, plays a critical role in the methyltranferases involved in the methylation by providing the one-carbon units via the methionine transmethylation cycle. Because of its interaction with a number of vitamins (B12, folate, pyridoxine), its regulation by hormones, i.e. insulin and glucagon, and by the changes in redox state, methionine metabolism is effected by nutrient and environmental influences and by altered physiological states. In the present review the impact of human pregnancy, dietary protein restriction and fatty liver disease on methionine metabolism is discussed. The role of methionine in metabolic programming in a commonly used model of intrauterine growth retardation and in propagation of fatty liver disease is briefly described.
Kalhan
Satish C
SC
Department of Gastroenterology, Cleveland Clinic, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA.
D000818:Animals; D018753:Diet, Protein-Restricted; D004195:Disease Models, Animal; D005234:Fatty Liver / Q000378:metabolism*; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology; D005492:Folic Acid / Q000378:metabolism; D006801:Humans; D007333:Insulin Resistance; D008715:Methionine / Q000378:metabolism*; D023421:Models, Animal; D011247:Pregnancy
D005492:Folic Acid; D008715:Methionine