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Nutrition and its role in epigenetic inheritance of obesity and diabetes across generations.

Mamm. Genome 31, 119–133 (2020)
Verlagsversion DOI
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
Nutritional constraints including not only caloric restriction or protein deficiency, but also energy-dense diets affect metabolic health and frequently lead to obesity and insulin resistance, as well as glucose intolerance and type 2 diabetes. The effects of these environmental factors are often mediated via epigenetic modifiers that target the expression of metabolic genes. More recently, it was discovered that such parentally acquired metabolic changes can alter the metabolic health of the filial and grand-filial generations. In mammals, this epigenetic inheritance can either follow an intergenerational or transgenerational mode of inheritance. In the case of intergenerational inheritance, epimutations established in gametes persist through the first round of epigenetic reprogramming occurring during preimplantation development. For transgenerational inheritance, epimutations persist additionally throughout the reprogramming that occurs during germ cell development later in embryogenesis. Differentially expressed transcripts, genomic cytosine methylations, and several chemical modifications of histones are prime candidates for tangible marks which may serve as epimutations in inter- and transgenerational inheritance and which are currently being investigated experimentally. We review, here, the current literature in support of epigenetic inheritance of metabolic traits caused by nutritional constraints and potential mechanisms in man and in rodent model systems.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter High-fat-diet; Induced Paternal Obesity; Exposure In-utero; Maternal High-fat; Prenatal Exposure; Dna Methylation; Transgenerational Inheritance; Calorie Restriction; Gene-expression; Histone Modifications
ISSN (print) / ISBN 0938-8990
e-ISSN 1432-1777
Zeitschrift Mammalian Genome
Quellenangaben Band: 31, Heft: , Seiten: 119–133 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort One New York Plaza, Suite 4600, New York, Ny, United States
Begutachtungsstatus Peer reviewed