title: Epigenetic alterations caused by nutritional stress during fetal programming of the endocrine pancreas.
abstract: Nutrition during critical periods of development is one of the pivotal factors in establishing a lifelong healthy metabolism. Different nutritional deficiencies such as a low availability of proteins in the maternal diet produce alterations in offspring that include changes in insulin and glucose metabolism, a decrease in the size and number of cells of pancreatic islets of Langerhans, and premature ageing of the secretory function of pancreatic β cells. Moreover, it has been reported that chronic nutritional stress is associated with epigenetic alterations in mechanisms of gene regulation during pancreatic development and function. These alterations can lead to dysfunctional states in pancreatic β cells, which in the long run are responsible for the onset of metabolic diseases like type 2 diabetes. The present review summarizes the most important evidence in relation to the participation of epigenetic mechanisms in the regulation of gene expression during the intrauterine programming of the endocrine pancreas in animal models. Such mechanisms include DNA methylation as well as modifications of histones and microRNAs (miRNAs).
authors: Departamento de Biología de la Reproducción, Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán", Vasco de Quiroga No. 15, Tlalpan, México, D.F., México.
authors: Tonantzin C
authors: TC
authors: Sosa-Larios
authors: Facultad de Química, Departamento de Biología, and Instituto Nacional de Perinatología, Isidro Espinoza de los Monteros, Universidad Nacional Autónoma de México, México, D.F., México.
authors: Marco A
authors: MA
authors: Cerbón
authors: Departamento de Biología de la Reproducción, Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán", Vasco de Quiroga No. 15, Tlalpan, México, D.F., México. Electronic address: sumiko.morimotom@incmnsz.mx.
authors: Sumiko
authors: S
authors: Morimoto
mesh_terms: D019588:Aging, Premature / Q000378:metabolism; D000818:Animals; D019175:DNA Methylation / Q000235:genetics; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics; D004032:Diet; D004044:Dietary Proteins / Q000494:pharmacology; D044127:Epigenesis, Genetic / Q000235:genetics*; D005260:Female; D047109:Fetal Development / Q000235:genetics*; D005786:Gene Expression Regulation; D018507:Gene Expression Regulation, Developmental / Q000235:genetics*; D005947:Glucose / Q000378:metabolism; D006657:Histones / Q000235:genetics; D006801:Humans; D007328:Insulin / Q000378:metabolism; D050417:Insulin-Secreting Cells / Q000166:cytology* / Q000378:metabolism; D044342:Malnutrition / Q000378:metabolism; D008659:Metabolic Diseases / Q000235:genetics*; D035683:MicroRNAs / Q000235:genetics; D023421:Models, Animal
chemical_list: D004044:Dietary Proteins; D006657:Histones; D007328:Insulin; D035683:MicroRNAs; D005947:Glucose
keywords: DNA methylation; Developmental programming; Histones; Malnutrition; miRNAs; β cells