Influence of Maternal Exercise on Glucose and Lipid Metabolism in Offspring Stem Cells: ENHANCED by Mom

Author:

Chaves Alec123ORCID,Weyrauch Luke A123ORCID,Zheng Donghai123ORCID,Biagioni Ericka M123,Krassovskaia Polina M123,Davidson Breanna L123,Broskey Nicholas T123,Boyle Kristen E45,May Linda E123,Houmard Joseph A123ORCID

Affiliation:

1. Department of Kinesiology, East Carolina University , Greenville, NC 27834 , USA

2. Human Performance Laboratory, East Carolina University , Greenville, NC 27834 , USA

3. East Carolina Diabetes and Obesity Institute, East Carolina University , Greenville, NC 27834 , USA

4. The Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center , Aurora, CO 80045 , USA

5. Department of Pediatrics, University of Colorado School of Medicine , Aurora, CO 80045 , USA

Abstract

Abstract Context Recent preclinical data suggest exercise during pregnancy can improve the metabolic phenotype not only of the mother, but of the developing offspring as well. However, investigations in human offspring are lacking. Objective To characterize the effect of maternal aerobic exercise on the metabolic phenotype of the offspring’s mesenchymal stem cells (MSCs). Design Randomized controlled trial. Setting Clinical research facility. Patients Healthy female adults between 18 and 35 years of age and ≤ 16 weeks’ gestation. Intervention Mothers were randomized into 1 of 2 groups: aerobic exercise (AE, n = 10) or nonexercise control (CTRL, n = 10). The AE group completed 150 minutes of weekly moderate-intensity exercise, according to American College of Sports Medicine guidelines, during pregnancy, whereas controls attended stretching sessions. Main Outcome Measures Following delivery, MSCs were isolated from the umbilical cord of the offspring and metabolic tracer and immunoblotting experiments were completed in the undifferentiated (D0) or myogenically differentiated (D21) state. Results AE-MSCs at D0 had an elevated fold-change over basal in insulin-stimulated glycogen synthesis and reduced nonoxidized glucose metabolite (NOGM) production (P ≤ 0.05). At D21, AE-MSCs had a significant elevation in glucose partitioning toward oxidation (oxidation/NOGM ratio) compared with CTRL (P ≤ 0.05). Immunoblot analysis revealed elevated complex I expression in the AE-MSCs at D21 (P ≤ 0.05). Basal and palmitate-stimulated lipid metabolism was similar between groups at D0 and D21. Conclusions These data provide evidence of a programmed metabolic phenotype in human offspring with maternal AE during pregnancy.

Funder

American Heart Association

Publisher

The Endocrine Society

Subject

Biochemistry (medical),Clinical Biochemistry,Endocrinology,Biochemistry,Endocrinology, Diabetes and Metabolism

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