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Maternal exercise during pregnancy in prevention of disease in the offspring

Type 2 diabetes and heart disease are leading causes of morbidity and mortality with a common origin in gene-environment interactions. Numerous studies have uncovered enduring association of parental conditions to disease susceptibility in the offspring, presenting a dangerous cycle of amplification of disease prevalence and hence the current pandemics. Parental obesity has been shown to predisposit the offspring to the metabolic syndrome, whereas exercise during pregnancy can mitigate it effectively; however, the underlying mechanism is unknown. Peroxisome proliferator activated receptor g co-activator-1α (PGC-1α) gene, a master regulator of mitochondrial biogenesis and oxidative metabolis, has been shown to be hypermethylated under the condition of diabetes in skeletal muscle. The Yan Lab hypothesizes that maternal exercise during pregnancy prevents hypermethylation of the Pgc-1a gene in offspring skeletal muscle, preventing age-dependent metabolic dysfunction. The lab is using powerful molecular genetics combined with diet-induced obesity and exercise training to test the hypothesis. The studies will likely provide mechanistic insights into the prevention of parental-offspring transmission of the metabolic syndrome by maternal exercise.


Laker RC, Wlodek ME, Connelly JJ, Yan Z. Epigenetic origins of metabolic disease: The impact of the maternal condition to the offspring epigenome and later health consequences. Food Science and Human Wellness . 2013; 2(1):1-11.

Laker RC, Lillard T, Okutsu M, Zhang M, Hoehn LK, Connelly JJ, Yan Z. Exercise prevents maternal high-fat diet-induced hypermethylation of the Pgc-1α gene and age-dependent metabolic dysfunction in the offspring. Diabetes. 2014 Jan 15. [Epub ahead of print] PMID: 24430439. PubMed - in process Link

Laker RC, Connelly JJ, Yan Z. Response to comment on Laker et al. Exercise prevents maternal high-fat diet-induced hypermethylation of the pgc-1α gene and age-dependent metabolic dysfunction in the offspring. Diabetes 2014;63:1605-1611. Diabetes. 2014 May;63(5):e6-7. doi: 10.2337/db14-0135. PubMed PMID: 24757208 Link.

oxidative stress