Impact of fetal and neonatal environment on beta cell function and development of diabetes

Jens Høiriis Nielsen, Tobias Nørresøe Haase, Caroline Jaksch, Amarnadh Nalla, Birgitte Søstrup, Louise Larsen, Morten Rasmussen, Louise Torp Dalgaard, Louise Winkel Gaarn, Peter Thams, Hans Kofod, Nils Billestrup

    Research output: Contribution to journalReviewpeer-review

    Abstract

    The global epidemic of diabetes is a serious threat against health and healthcare expenses. Although genetics is important it does not explain the dramatic increase in incidence, which must involve environmental factors. Two decades ago the concept of the thrifty phenotype was introduced, stating that the intrauterine environment during pregnancy has an impact on the gene expression that may persist until adulthood and cause metabolic diseases like obesity and type 2 diabetes. As the pancreatic beta cells are crucial in the regulation of metabolism this article will describe the influence of normal pregnancy on the beta cells in both the mother and the fetus and how various conditions like diabetes, obesity, overnutrition and undernutrition during and after pregnancy may influence the ability of the offspring to adapt to changes in insulin demand later in life. The influence of environmental factors including nutrients and gut microbiota on appetite regulation, mitochondrial activity and the immune system that may affect beta cell growth and function directly and indirectly is discussed. The possible role of epigenetic changes in the transgenerational transmission of the adverse programming may be the most threatening aspect with regard to the global diabetes epidemics. Finally, some suggestions for intervention are presented
    Original languageEnglish
    JournalActa Obstetricia et Gynecologica Scandinavica
    Volume93
    Issue number11
    Pages (from-to)1109-1122
    Number of pages14
    ISSN0001-6349
    DOIs
    Publication statusPublished - Nov 2014

    Keywords

    • fetal programming
    • diabetes mellitus type 2
    • Beta-cell dysfunction

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