Nutritional epigenomics of metabolic syndrome : New perspective against the epidemic

• Published in: Diabetes (New York, N.Y.) Vol. 54; no. 7; pp. 1899 - 1906
• Main Authors: GALLOU-KABANI, Catherine, JUNIEN, Claudine
• Format: Journal Article
• Language: English
• Published: Alexandria, VA American Diabetes Association 01.07.2005
• Subjects: Animals; Apoptosis; Biological and medical sciences; Breastfeeding & lactation; Cardiovascular disease; Codes; Diabetes; Diabetes. Impaired glucose tolerance; Diet; DNA methylation; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Epigenetic inheritance; Epigenetics; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Gene expression; Genetic engineering; Genotype & phenotype; Health Promotion; Humans; Hypertension; Medical sciences; Metabolic diseases; Metabolic syndrome; Metabolic Syndrome - epidemiology; Metabolic Syndrome - genetics; Metabolic Syndrome - physiopathology; Metabolic syndrome X; Metabolites; Miscellaneous; Models, Animal; Neoplasms - genetics; Nutrients; Nutrition; Nutritional aspects; Nutritional Physiological Phenomena - physiology; Observations; Other metabolic disorders; Overweight; France; Endocrinopathy; Cardiovascular disease; Metabolic diseases; X Syndrome; Diabetes mellitus
• ISSN: 0012-1797; 1939-327X
• DOI: 10.2337/diabetes.54.7.1899

Human epidemiological studies and appropriately designed dietary interventions in animal models have provided considerable evidence to suggest that maternal nutritional imbalance and metabolic disturbances, during critical time windows of development, may have a persistent effect on the health of the offspring and may even be transmitted to the next generation. We now need to explain the mechanisms involved in generating such responses. The idea that epigenetic changes associated with chromatin remodeling and regulation of gene expression underlie the developmental programming of metabolic syndrome is gaining acceptance. Epigenetic alterations have been known to be of importance in cancer for approximately 2 decades. This has made it possible to decipher epigenetic codes and machinery and has led to the development of a new generation of drugs now in clinical trials. Although less conspicuous, epigenetic alterations have also been progressively shown to be relevant to common diseases such as atherosclerosis and type 2 diabetes. Imprinted genes, with their key roles in controlling feto-placental nutrient supply and demand and their epigenetic lability in response to nutrients, may play an important role in adaptation/evolution. The combination of these various lines of research on epigenetic programming processes has highlighted new possibilities for the prevention and treatment of metabolic syndrome.