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Maternal Physical Activity and Sex Impact Markers of Hepatic Mitochondrial Health.
Med Sci Sports Exerc 2018; 50(10):2040-2048MS

Abstract

INTRODUCTION

Maternal exercise and physical activity during the gestational period can be protective against maternal high-fat diet-induced hepatic steatosis in older offspring. However, it is unknown whether these protective effects are seen in younger offspring. In this study, we investigated whether maternal physical activity would attenuate maternal western diet (WD)-induced steatosis in young adult rats.

METHODS

Female Wistar rats (7-8 wk of age) were randomized into WD (42% fat, 27% sucrose) or normal chow diet (ND), and further randomized into physical activity (RUN) or sedentary (SED) conditions for a total of four groups. Dams returned to ND/SED conditions after parturition. Postweaning, offspring were maintained in ND/SED conditions for 18 wk.

RESULTS

Maternal WD-induced increases in male offspring body mass was attenuated in the WD/RUN offspring (P < 0.05). Maternal WD feeding significantly increased hepatic steatosis in male (but not female offspring), which was not attenuated by maternal RUN. However, maternal RUN increased (P < 0.05) hepatic markers of mitochondrial biogenesis and mitophagy (mitochondrial transcription factor A, peroxisome proliferator activator receptor γ, and nuclear factor E2-related factor 2) in all offspring and the mitophagy marker BCL2-interacting protein 3 in WD/RUN offspring. Interestingly, hepatic markers of de novo lipogenesis (fatty acid synthase and acetyl coenzyme A carboxylase), mitophagy (autophagy-related gene 12:5, BCL2-interacting protein 3, P62, and LC3 II/I), and mitochondria biogenesis/content (mitochondrial transcription factor A and OXPHOS-Complex II) were significantly increased in female versus male offspring.

CONCLUSION

Although maternal physical activity did not attenuate maternal WD-induced hepatic steatosis as has been previously reported in older adult offspring, it did significantly increase hepatic markers of mitochondrial biogenesis and mitophagy. Furthermore, female offspring had elevated hepatic markers of mitochondrial health, possibly explaining why female rats are protected against maternal WD-induced hepatic steatosis. Future studies are warranted to shed light on the time line of hepatic steatosis development under the influence of maternal physical activity.

Authors+Show Affiliations

Research Service, Harry S Truman Memorial Veterans Medical Center, Columbia, MO. Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO.Research Service, Harry S Truman Memorial Veterans Medical Center, Columbia, MO. Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO.Research Service, Harry S Truman Memorial Veterans Medical Center, Columbia, MO. Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO. Division of Gastroenterology and Hepatology, Department of Medicine, University of Missouri, Columbia, MO.Department of Biomedical Sciences, University of Missouri, Columbia, MO.Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO. Department of Biomedical Sciences, University of Missouri, Columbia, MO.Research Service, Harry S Truman Memorial Veterans Medical Center, Columbia, MO. Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO. Division of Gastroenterology and Hepatology, Department of Medicine, University of Missouri, Columbia, MO.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

29787476

Citation

Cunningham, Rory P., et al. "Maternal Physical Activity and Sex Impact Markers of Hepatic Mitochondrial Health." Medicine and Science in Sports and Exercise, vol. 50, no. 10, 2018, pp. 2040-2048.
Cunningham RP, Moore MP, Meers GM, et al. Maternal Physical Activity and Sex Impact Markers of Hepatic Mitochondrial Health. Med Sci Sports Exerc. 2018;50(10):2040-2048.
Cunningham, R. P., Moore, M. P., Meers, G. M., Ruegsegger, G. N., Booth, F. W., & Rector, R. S. (2018). Maternal Physical Activity and Sex Impact Markers of Hepatic Mitochondrial Health. Medicine and Science in Sports and Exercise, 50(10), pp. 2040-2048. doi:10.1249/MSS.0000000000001675.
Cunningham RP, et al. Maternal Physical Activity and Sex Impact Markers of Hepatic Mitochondrial Health. Med Sci Sports Exerc. 2018;50(10):2040-2048. PubMed PMID: 29787476.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Maternal Physical Activity and Sex Impact Markers of Hepatic Mitochondrial Health. AU - Cunningham,Rory P, AU - Moore,Mary P, AU - Meers,Grace M, AU - Ruegsegger,Gregory N, AU - Booth,Frank W, AU - Rector,R Scott, PY - 2018/5/23/pubmed PY - 2018/5/23/medline PY - 2018/5/23/entrez SP - 2040 EP - 2048 JF - Medicine and science in sports and exercise JO - Med Sci Sports Exerc VL - 50 IS - 10 N2 - INTRODUCTION: Maternal exercise and physical activity during the gestational period can be protective against maternal high-fat diet-induced hepatic steatosis in older offspring. However, it is unknown whether these protective effects are seen in younger offspring. In this study, we investigated whether maternal physical activity would attenuate maternal western diet (WD)-induced steatosis in young adult rats. METHODS: Female Wistar rats (7-8 wk of age) were randomized into WD (42% fat, 27% sucrose) or normal chow diet (ND), and further randomized into physical activity (RUN) or sedentary (SED) conditions for a total of four groups. Dams returned to ND/SED conditions after parturition. Postweaning, offspring were maintained in ND/SED conditions for 18 wk. RESULTS: Maternal WD-induced increases in male offspring body mass was attenuated in the WD/RUN offspring (P < 0.05). Maternal WD feeding significantly increased hepatic steatosis in male (but not female offspring), which was not attenuated by maternal RUN. However, maternal RUN increased (P < 0.05) hepatic markers of mitochondrial biogenesis and mitophagy (mitochondrial transcription factor A, peroxisome proliferator activator receptor γ, and nuclear factor E2-related factor 2) in all offspring and the mitophagy marker BCL2-interacting protein 3 in WD/RUN offspring. Interestingly, hepatic markers of de novo lipogenesis (fatty acid synthase and acetyl coenzyme A carboxylase), mitophagy (autophagy-related gene 12:5, BCL2-interacting protein 3, P62, and LC3 II/I), and mitochondria biogenesis/content (mitochondrial transcription factor A and OXPHOS-Complex II) were significantly increased in female versus male offspring. CONCLUSION: Although maternal physical activity did not attenuate maternal WD-induced hepatic steatosis as has been previously reported in older adult offspring, it did significantly increase hepatic markers of mitochondrial biogenesis and mitophagy. Furthermore, female offspring had elevated hepatic markers of mitochondrial health, possibly explaining why female rats are protected against maternal WD-induced hepatic steatosis. Future studies are warranted to shed light on the time line of hepatic steatosis development under the influence of maternal physical activity. SN - 1530-0315 UR - https://www.unboundmedicine.com/medline/citation/29787476/Maternal_Physical_Activity_and_Sex_Impact_Markers_of_Hepatic_Mitochondrial_Health_ L2 - http://Insights.ovid.com/pubmed?pmid=29787476 DB - PRIME DP - Unbound Medicine ER -