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- W54909899 abstract "The “thrifty phenotype” hypothesis proposes that the fetus adapts to an adverse intrauterine milieu by optimizing the use of a reduced nutrient supply to ensure survival, but by favoring the development of certain organs over that of others, this leads to persistent alterations in the growth and function of developing tissues. This concept has been somewhat controversial; however, recent epidemiological, clinical, and animal studies provide support for the developmental origins of disease hypothesis. Underlying mechanisms include reprogramming of the hypothalamic-pituitary-adrenal axis, islet development, and insulin signaling pathways. Emerging data suggests that oxidative stress and mitochondrial dysfunction may also play a critical role in the pathogenesis of type 2 diabetes in individuals who were growth retarded at birth.KeywordsMitochondrial DysfunctionFetal Growth RestrictionHepatic Glucose ProductionFetal Growth RetardationUterine Artery LigationThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves." @default.
- W54909899 created "2016-06-24" @default.
- W54909899 creator A5077604020 @default.
- W54909899 date "2014-01-01" @default.
- W54909899 modified "2023-09-24" @default.
- W54909899 title "Developmental Origins of Disease: The Role of Oxidative Stress" @default.
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- W54909899 doi "https://doi.org/10.1007/978-1-4939-1405-0_6" @default.
- W54909899 hasPublicationYear "2014" @default.
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