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Stevanovic 2019 MiPschool Coimbra

From Bioblast
Gestational physical exercise offers prolonged protection to liver mitochondrial function of female offspring against deleterious effects of maternal gestational diabetes.

Link: MitoEAGLE

Stevanovic J, Beleza J, Coxito P, Pereira R, Pereira SP, Palmeira CM, Moreno AJ, Oliveira PJ, Ascensao A, Magalhaes J (2019)

Event: MiPschool Coimbra 2019


Impaired glucose tolerance and insulin resistance during pregnancy may predispose development of gestational diabetes mellitus (GDM). Compromised metabolic burden may be transmitted to offspring (F1), which shows an increased risk for developing some associated metabolic disorders, including non-alcoholic fatty liver disease (NAFLD). The aim of our study was to assess the effects of maternal physical exercise (PE) during pregnancy and maternal diet on adult female F1 (16 wks-old) liver mitochondrial function in an animal model of GDM and NAFLD.

Female pregnant Sprague-Dawley on control diet (C) or high-fat high-sucrose diet (HFHS) were submitted to PE during 3 weeks. Oral glucose tolerance test was performed before and during the pregnancy to confirm GDM metabolic alterations. All F1 were sedentary and fed with C. F1 body weight (BW) alterations were monitored weekly. Liver mitochondrial function in 16 weeks old female F1 was assessed using complex I and II-related substrates.

Impaired glucose tolerance characteristic for GDM was observed only during, but not before pregnancy, in HFHS groups, regardless of exercise. Moreover, maternal BW gain during gestation was increased only in sedentary HFHS group comparing to C group. Likewise, sedentary HFHS mothers bred larger litter than sedentary C or exercised HFHS mothers. Furthermore, F1 of HFHS mothers had higher after-weaning BW compared to F1 of C mothers, while PE during pregnancy lessened the adverse effect of HFHS on F1 BW. Regarding F1 liver mitochondrial function, no alterations were found in complex I-sustained state 3 and state 4 respiration. While the respiratory control ratio (RCR) with complex I substrates was decreased as the consequence of maternal HFHS, liver mitochondrial function of HFHS-mothers’ F1 was improved by gestational PE. No alterations in state 3/state 4 respiration, and RCR was noticed when complex II-related substrates were used.

Maternal HFHS induced GDM-related glucose metabolism impairment and further deleteriously affected after-weaning BW, as well as liver mitochondrial function in 16-weeks old female offspring. Even though F1 was not submitted to PE, foetal exposure to maternal gestational PE only during 3 weeks was enough to protect female F1 liver mitochondrial function against negative impact of maternal fed condition.

Bioblast editor: Plangger M O2k-Network Lab: PT Coimbra Laranjinha J

Labels: MiParea: Respiration, Developmental biology, Exercise physiology;nutrition;life style 

Organism: Rat  Tissue;cell: Liver 

HRR: Oxygraph-2k 

Affiliations and support

Stevanovic J(1), Beleza J(1), Coxito P(1), Pereira R(1), Pereira SP(2), Palmeira CM(2), Moreno AJ(2,3), Oliveira PJ(2), Ascensão A(1), Magalhães J(1)
  1. LaMetEx — Lab Metabolism Exercise, CIAFEL — Research Centre Physical Activity, Health Leisure, Fac Sport, Univ Porto, Portugal
  2. CNC — Centre Neuroscience Cell Biology, UC-Biotech
  3. Dept Life Sciences, School Sciences Technology; Univ Coimbra, Portugal
Funding: EU’s Horizon 2020 Research and Innovation programme Marie Sklodowska-Curie (No.722619, FOIE GRAS; No.734719, mtFOIE GRAS); UID/DTP/00617/2013; POCI-01- 0145-FEDER-016690 - PTDC/DTP-DES/7087/2014; POCI-01-0145-FEDER-016657 - PTDC/DTP-DES/1082/2014; SFRH/BD/129645/2017, SFRH/BPD/116061/2016.