Skip to main content
ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #331249

Title: Effect of diet-induced maternal obesity on fetal skeletal development

item CHEN, JIN-RAN - Arkansas Children'S Nutrition Research Center (ACNC)

Submitted to: Book Chapter
Publication Type: Book / Chapter
Publication Acceptance Date: 11/30/2015
Publication Date: 3/21/2016
Citation: Chen, J. 2016. Effect of diet-induced maternal obesity on fetal skeletal development. In: Watson, R.R., Mahadevan, D., editors. Handbook of Nutrition and Diet in Therapy of Bone Diseases. The Netherlands: Wageningen Academic. p. 67-79.

Interpretive Summary:

Technical Abstract: The maternal environment, in particular nutritional status and diet composition during pregnancy, can alter the developmental trajectory of the fetus and change the risk for chronic disease processes such as cardiovascular disease, obesity, diabetes and cancer in the offspring. This knowledge supports the concept of developmental origins of health and diseases. Many of these maternal 'programming' effects appear to be transmitted between several generations suggesting an epigenetic basis, and difficulties for disease prevention. The fetal skeleton may represent another target for developmental programming. Epigenetic changes in genes regulating skeletal development could result in changes in attainment of peak bone mass or alter the risk of osteoporosis in later life. Because both mature osteoblasts and adipocytes originate from the same pool of mesenchymal stem cells, the causal mechanisms or the underlying root of diet-induced obesity and impaired bone development is thought to be interchangeable. However, there is dearth of evidence of the mechanisms connecting diet-induced maternal obesity and impaired fetal bone development. One that has been previously suggested is that increased circulating non-esterified free fatty acids (NEFA) released from maternal fat stores after development of obesity may be essential to explain altered differentiation potential of a stem cell although other hormones and inflammatory cytokines may act in concert with maternal NEFA.