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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #305633
Title: In utero exposure to prepregnancy maternal obesity and postweaning high-fat diet impair regulators of mitochondrial dynamics in rat placenta and offspring

Author
item BORENGASSER, SARAH - Arkansas Children'S Nutrition Research Center (ACNC)
item FASKE, JENNIFER - Arkansas Children'S Nutrition Research Center (ACNC)
item KANG, PING - Arkansas Children'S Nutrition Research Center (ACNC)
item BLACKBURN, MICHAEL - Arkansas Children'S Nutrition Research Center (ACNC)
item Badger, Thomas - Arkansas Children'S Nutrition Research Center (ACNC)
item SHANKAR, KARTIK - Arkansas Children'S Nutrition Research Center (ACNC)

Submitted to: Physiological Genomics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/15/2014
Publication Date: 12/1/2014
Citation: Borengasser, S.J., Faske, J., Kang, P., Blackburn, M.L., Badger, T.M., Shankar, K. 2014. In utero exposure to prepregnancy maternal obesity and postweaning high-fat diet impair regulators of mitochondrial dynamics in rat placenta and offspring. Physiological Genomics. 46(23):841-850.

Interpretive Summary: More women are becoming overweight or obese prior to becoming pregnant, and there is compelling evidence suggesting that mother's weight during pregnancy may be an important factor in baby's health. Maternal obesity and maternal diets (under- and over-nourished) have been shown to adversely alter the offspring's metabolism. Recent research has suggested that imbalance of processes in the power-houses of cells called mitochondria, may be responsible for changes in metabolism. In the present study, we examined the influences of maternal obesity and diets high in fat on key how mitochondria are affected. Our results indicated that specific factors associated involved in creating healthy mitochondria were reduced in the placenta and important tissues of rat offspring consistent with an impaired ability to burn fat. Reductions of some of these factors were also evident in human placenta from overweight mothers. Overall, mother’s obesity detrimentally alters the energy producing powerhouses in cells and that may contribute to impaired increased obesity susceptibility in later life.

Technical Abstract: The proportion of obese women who become pregnant continues to rise. Compelling evidence suggests the intrauterine environment is an important determinant of offspring health. Maternal obesity and unhealthy diets are shown to promote metabolic programming in the offspring. Mitochondria are maternally inherited, and we have previously shown impaired mitochondrial function in rat offspring exposed to maternal obesity in utero. Mitochondrial health is maintained by mitochondrial dynamics, or the processes of fusion and fission, which serve to repair damaged mitochondria, remove irreparable mitochondria, and maintain mitochondrial morphology. Moreover, an imbalance between fusion and fission has been associated with detrimental health outcomes such as obesity, insulin resistance, and reproduction complications. In the present study, we examine the influence of maternal obesity and post-weaning high fat diet (HFD) on key regulators of mitochondrial fusion and fission in rat offspring at important developmental milestones prior to and after the development of obesity. Further, we determine if gestational obesity leads to changes in mitochondrial plasticity in term placental tissue from lean and overweight/obese (OW/OB) pregnant women. Our results indicate that putative transcriptional regulators (PGC1a, PGC1beta, and ERRa) of mitochondrial dynamics and mitofusins (Mfn1 and Mfn2) were reduced in rat placenta and rat offspring liver and skeletal muscle consistent with indirect calorimetry findings revealing reduced energy expenditure and impaired fat utilization. Reductions of PGC1beta and ERRa were also evident in human placenta from OW/OB mothers. Overall, maternal obesity detrimentally alters mitochondrial targets that may contribute to impaired mitochondrial health and increased obesity susceptibility in later life.