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Developmental Origins of Obesity: Programmed Adipogenesis

Overview
Journal Curr Diab Rep
Publisher Current Science
Specialty Endocrinology
Date 2012 Nov 29
PMID 23188593
Citations 74
Authors
Affiliations
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Abstract

The metabolic syndrome epidemic, including a marked increase in the prevalence of obesity and gestational diabetes mellitus (GDM) among pregnant women, represents a significant public health problem. There is increasing recognition that the risk of adult obesity is clearly influenced by prenatal and infant environmental exposures, particularly nutrition. This tenet is the fundamental basis of developmental programming. Low birth weight, together with infant catch-up growth, is associated with a significant risk of adult obesity. Exposure to maternal obesity, with or without GDM, or having a high birth weight also represents an increased risk for childhood and adult obesity. Animal models have replicated human epidemiologic findings and elucidated potential programming mechanisms that include altered organ development, cellular signaling responses, and epigenetic modifications. Prenatal care has made great strides in optimizing maternal, fetal, and neonatal health, and now has the opportunity to begin interventions which prevent or reduce childhood/adult obesity. Guidelines that integrate optimal pregnancy nutrition and weight gain, management of GDM, and newborn feeding strategies with long-term consequences on adult obesity, remain to be elucidated.

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References
1.
Desai M, Gayle D, Babu J, Ross M . Permanent reduction in heart and kidney organ growth in offspring of undernourished rat dams. Am J Obstet Gynecol. 2005; 193(3 Pt 2):1224-32. DOI: 10.1016/j.ajog.2005.05.041. View

2.
Wabitsch M . The acquisition of obesity: insights from cellular and genetic research. Proc Nutr Soc. 2000; 59(2):325-30. DOI: 10.1017/s0029665100000367. View

3.
Shamseddeen H, Getty J, Hamdallah I, Ali M . Epidemiology and economic impact of obesity and type 2 diabetes. Surg Clin North Am. 2011; 91(6):1163-72, vii. DOI: 10.1016/j.suc.2011.08.001. View

4.
Yee J, Lee W, Ross M, Lane R, Han G, Vega J . Peroxisome proliferator-activated receptor gamma modulation and lipogenic response in adipocytes of small-for-gestational age offspring. Nutr Metab (Lond). 2012; 9(1):62. PMC: 3495639. DOI: 10.1186/1743-7075-9-62. View

5.
Weiss R, Dziura J, Burgert T, Tamborlane W, Taksali S, Yeckel C . Obesity and the metabolic syndrome in children and adolescents. N Engl J Med. 2004; 350(23):2362-74. DOI: 10.1056/NEJMoa031049. View