Document Detail


Maternal and in utero determinants of type 2 diabetes risk in the young.
MedLine Citation:
PMID:  24292969     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
The global prevalence of diabetes mellitus has reached epidemic proportions. In 2010, it was estimated that 6.4 % of the adult population (285 million) have diabetes. In recent years, the incidence of type 2 diabetes (T2D), a condition traditionally associated with aging, has been steadily increasing among younger individuals. It is now a well-established notion that the early-life period is a critical window of development and that influences during this period can "developmentally prime" the metabolic status of the adult. This review discusses the role of maternal and in utero influences on the developmental priming of T2D risk. Both human epidemiological studies and experimental animal models are beginning to demonstrate that early dietary challenges can accelerate the onset of age-associated metabolic disturbances, including insulin resistance, T2D, obesity, hypertension, and cardiovascular disease. These findings show that poor maternal nutrition can prime a prediabetes phenotype, often manifest as insulin resistance, by very early stages of life. Thus, the maternal diet is a critical determinant of premature T2D risk. While the mechanisms that link early nutrition to age-associated metabolic decline are currently unclear, preliminary findings suggest perturbations in a number of processes involved in cellular aging, such as changes in longevity-associated Sirtuin activity, epigenetic regulation of key metabolic genes, and mitochondrial dysfunction. Preliminary studies show that pharmacological interventions in utero and dietary supplementation in early postnatal life may alleviate insulin resistance and reduce T2D risk. However, further studies are warranted to fully understand the relationship between the early environment and long-term effects on metabolism. Such mechanistic insights will facilitate strategic interventions that prevent accelerated metabolic decline and the premature onset of T2D in the current and future generations.
Authors:
Kimberley D Bruce
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Current diabetes reports     Volume:  14     ISSN:  1539-0829     ISO Abbreviation:  Curr. Diab. Rep.     Publication Date:  2014 Jan 
Date Detail:
Created Date:  2013-12-02     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101093791     Medline TA:  Curr Diab Rep     Country:  United States    
Other Details:
Languages:  eng     Pagination:  446     Citation Subset:  IM    
Affiliation:
Department of Metabolism and Aging, The Scripps Research Institute, Jupiter, FL, 33458, USA, Kbruce@scripps.edu.
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