Environmental and genetic contributions to diabetes
- PMID: 31610851
- DOI: 10.1016/j.metabol.2019.153952
Environmental and genetic contributions to diabetes
Abstract
Diabetes mellitus (DM) is a heterogeneous group of disorders characterized by persistent hyperglycemia. Its two most common forms are type 1 diabetes (T1D) and type 2 diabetes (T2D), for which genetic and environmental risk factors act in synergy. Because it occurs in children and involves infectious, autoimmune or toxic destruction of the insulin-secreting pancreatic beta-cells, type 1 diabetes has been called juvenile or insulin-deficient diabetes. In type 2, patients can still secrete some insulin but its effectiveness may be attenuated by 'insulin resistance.' There is also a group of rare forms of diabetes in the young which are inherited as monogenetic diseases. Whether one calls the underlying process 'genes vs. environment' or 'nature vs nurture', diabetes occurs at the interface of the two domains. Together with our genetic background we are born tabula rasa-a blank slate upon which the story of life, with all its environmental inputs will be written. There is one proviso: the influence of epigenetic inheritance must also be considered. Thus, in the creation of databases that include "big data" originating from genomic as well as exposome (defined as: the totality of environmental exposure from conception to death), a broad perspective is crucial as these factors act in concert in such chronic illnesses as diabetes that, for example, are likely to require adoption of an appropriate lifestyle change. Also, it is becoming increasingly evident that epigenetic factors can modulate the interplay between genes and environment. Consequently, throughout the life of an individual nature and nurture interact in a complex manner in the development of diabetes. This review addresses the question of the contribution of gene and environment and their interactions in the development of diabetes.
Keywords: Diabetes; Epigenetics; Gene–environment interactions (G × E); MODY; T1D; T2D.
Copyright © 2019. Published by Elsevier Inc.
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