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Beleza 2019 MiPschool Coimbra

From Bioblast
Jorge Beleza
Gestational exercise counteracts the deleterious consequences imposed by diabetes mellitus developed during pregnancy on 16 weeks old male offspring liver mitochondrial function.

Link: MitoEAGLE

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

Event: MiPschool Coimbra 2019


The development of gestational diabetes mellitus (GDM) during pregnancy is associated with impaired glucose tolerance and insulin resistance, which may be transgenerationally inherited by the offspring (F1). The aim of our study was to assess the effects of maternal physical exercise (PE) during pregnancy on F1 (16 wks-old) liver mitochondrial function in a model of GDM.

Female Sprague-Dawley fed with control (C) or high-fat-high-sugar (HFHS) diets were submitted to PE during the 3 weeks of pregnancy. Oral glucose tolerance tests (OGTT) were performed before and during pregnancy to assess the GMD condition. F1 body weight (BW) was weekly monitored and liver mitochondrial function was determined at 16th wks of age using complex I and II-related substrates.

No pre-mating OGTT differences were observed between C and HFHS groups. In contrast, increased impaired glucose tolerance was detected during pregnancy in HFHS groups, regardless of PE. Although F1 of HFHS mothers had significantly higher BW compared to C, PE during pregnancy decreased this adverse effect of HFHS. Regarding F1 liver mitochondrial function, no alterations were found in state 3 and 4 respiration between groups, using complex I and II-related substrates, while a decrease in the respiratory control ratio (RCR) of the HFHS animals compared to C was observed using substrates for complex I. The PE program was able to improve the F1-related RCR in the HFHS animals back to C values.

In conclusion, HFHS during pregnancy induced GDM; however, the negative impact of this fed condition during pregnancy on liver mitochondrial function was significantly attenuated by the PE program.

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

Labels: MiParea: Respiration, Developmental biology  Pathology: Diabetes 

Organism: Rat  Tissue;cell: Liver 

Coupling state: LEAK, OXPHOS  Pathway: N, S 

Affiliations and support

Beleza J(1), Stevanovic J(1), Coxito P(1), Pereira R(1), Pereira SP(1,2), 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
  2. CNC — Centre Neuroscience Cell Biology, UC-Biotech, Univ Coimbra
  3. DepT Life Sciences, School Sciences Technology, Univ Coimbra; Portugal
Funding: SFRH/BD/129645/2017;SFRH/BPD/116061/2016;UID/DTP/00617/2013;POCI-01-0145-FEDER-016690-PTDC/DTP-DES/7087/2014;POCI-01-0145-FEDER-016657-PTDC/DTP-DES/1082/2014;EU’s Horizon 2020 Research and Innovation programme Marie Skłodowska-Curie (No.722619,FOIE GRAS;No.734719,mtFOIE GRAS).