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Low birth weight in the pathophysiology of type 2 diabetes: A focus onmetabolic and epigenetic aspects

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  1. Prediction of carotid intima-media thickness and its relation to cardiovascular events in persons with type 2 diabetes

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  2. Epigenetic markers associated with metformin response and intolerance in drug-naïve patients with type 2 diabetes

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  3. Dyslipidemia at diagnosis of childhood acute lymphoblastic leukemia

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The prevalence of diabetes is increasing worldwide and constitutes a major threat to global health. A number of novel type 2 diabetes susceptibility genes have been identified in recent genomewide association studies (GWA). Nevertheless only up to 10% of the risk of type 2 diabetes can be explained by these genes, placing the focus on non-genetic environmental factors. It is well recognized that an adverse intrauterine environment leads to a compensatory programming of fetal metabolism that may be beneficial for short-term survival, but can be detrimental in the long term. This phenomenon is particularly detrimental if the prenatal nutrient restriction is followed by a postnatal nutrient abundance, leading to rapid catch-up growth and increased risk of later development of obesity and type 2 diabetes, including the metabolic syndrome. Many defects present in patients with overt type 2 diabetes are detectable at the age around 20 years in lean and otherwise healthy young men born with a low birth weight, strongly suggestive of an important role of intrauterine programming in the etiology and pathophysiology of type 2 diabetes. In this review we will focus on the complicated physiological and molecular mechanisms as well as abnormalities of metabolism linking low birth weight (LBW) with an increased risk of type 2 diabetes several decades later in life.

Original languageEnglish
Title of host publicationHandbook of Growth and Growth Monitoring in Health and Disease
Number of pages22
PublisherSpringer New York 2014
Publication date1 Jan 2012
ISBN (Print)9781441917942
ISBN (Electronic)9781441917959
Publication statusPublished - 1 Jan 2012

ID: 59278232