Developmental programming of type 2 diabetes: early nutrition and epigenetic mechanisms

Autor(es)

Ong, Thomas P. ^{[1, 2, 3, 4]} ; Ozanne, Susan E. ^{[2, 3]}

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Fac Pharmaceut Sci, Dept Food & Expt Nutr, Sao Paulo - Brazil

^[2] Univ Cambridge, Inst Metab Sci, Cambridge CB2 0QQ - England

^[3] Univ Cambridge, MRC, Metab Dis Unit, Cambridge CB2 0QQ - England

^[4] Food Res Ctr FoRC, Sao Paulo - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE; v. 18, n. 4, p. 354-360, JUL 2015.
• Citações Web of Science: 24

Resumo

Purpose of review The environment experienced during critical windows of development can `programme' long-term health and risk of metabolic diseases such as type 2 diabetes in the offspring. The purpose of this review is to discuss potential epigenetic mechanisms involved in the developmental programming of type 2 diabetes by early nutrition. Recent findings Maternal and more recently paternal nutrition have been shown to play key roles in metabolic programming of the offspring. Although the exact mechanisms are still not clear, epigenetic processes have emerged as playing a plausible role. Epigenetic dysregulation is associated with several components that contribute to type 2 diabetes risk, including altered feeding behaviour, insulin secretion and insulin action. It may also contribute to transgenerational risk transmission. Summary Epigenetic processes may represent a central underlying mechanism of developmental programming of type 2 diabetes. During embryonic and foetal development, extensive epigenetic remodelling takes place not only in somatic but also in primordial germ cells. Therefore, concerns have been raised that epigenetic dysregulation induced by a suboptimal early environment could programme altered phenotypes not only in the first generation but also in the subsequent ones. Characterizing these altered epigenetic marks has great implications for identifying individuals at an increased disease risk as well as potentially leading to novel preventive and treatment strategies. (AU)

• Processo FAPESP: 13/07914-8 - FoRC - Centro de Pesquisa em Alimentos
• Beneficiário: Bernadette Dora Gombossy de Melo Franco
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs