Pereira 2018 MiPschool Tromso C1

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Pereira Susana P
Obesity-induced mitochondrial hepatic changes during pregnancy.

Link: MitoEAGLE

Pereira SP, Grilo L, Cavallaro CH, Martins JD, Cardoso I, Baldeiras I, Cunha-Oliveira T, Ford S, Nathanielsz PW, Oliveira PJ (2018)

Event: MiPschool Tromso-Bergen 2018


Pregnancy represents a unique maternal metabolic challenge [1]. Liver disease in pregnancy occurs in 3-10% of cases causing maternal morbidity and mortality [2]. High maternal BMI exacerbates metabolic and hepatic complications. Mitochondrial substrate oxidation supports the maternal and fetal metabolic demands. Mitochondrial defects have been associated with maternal and fetal complications [3]. A better understanding of MO induced maternal physiological changes is needed to prevent adverse outcomes during pregnancy. Our aim was to characterize liver mitochondrial profile and redox network in term pregnant MO ewes.

Rambouillet:Columbia ewes consumed either an obesogenic (MO: 150% of NRC requirements; n=8), or control diet (C: 100% NRC; n=10) from 60 days prior to conception and through pregnancy. Maternal livers were removed at 0.9 gestation for right lobe measurements. Mitochondrial and antioxidant defense system proteins were determined by Western blot. Mitochondrial respiratory chain complex activities were determined in isolated fractions. Using whole liver tissue we determined catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase activities by spectrophotometry and reduced and oxidized glutathione. Lipid peroxidation was assessed by fluorometry by malondialdehyde (MDA) formation. Data expressed as mean±SE and comparison between groups performed by Mann-Whitney test, P-value<0.05 as significant.

In MO mothers we found increased maternal hepatic MDA indicating greater lipid peroxidation and decreased reduced glutathione, indicating imbalance of endogenous antioxidant defenses. Despite unchanged MO mtDNA copy number, content of proteins implicated in mitochondrial metabolism was altered, with decreased succinate dehydrogenase complex subunit B, increased VDAC1, cyclophilin D and cytochrome c. Complex I activity was decreased in MO-livers.

MO in pregnancy alters maternal hepatic mitochondrial biology impairing redox state, eventually predisposing mothers to metabolic diseases including non-alcoholic fatty liver disease.

Bioblast editor: Plangger M

Labels: MiParea: Exercise physiology;nutrition;life style 

Organism: Other mammals  Tissue;cell: Liver 

Event: C1, Oral 

Affiliations and support

Pereira SP(1,2), Grilo L(1), Cavallaro CH(1), Martins JD(1), Cardoso I(1), Baldeiras I(1,3), Cunha-Oliveira T(1), Ford S(4), Nathanielsz PW(4), Oliveira PJ(1)

  1. Center Neuroscience Cell Biology, UC-Biotech, Biocant Park, Univ Coimbra
  2. Research Centre Physical Activity Health Leisure, Fac Sports, Univ Porto
  3. Neurological Clinic, Fac Medicine, Univ Coimbra; Portugal
  4. Dept Animal Science, Univ Wyoming, Laramie, WY, USA

Funded by FEDER/COMPETE/FCT-Portugal (PTDC/DTP-DES/1082/2014, POCI-01-0145-FEDER-007440, OCI-01-0145-FEDER-016657, SFRH/BPD/116061/2016 and SFRH/BPD/101169/2014), and NIH (R01HD070096-01A1).


  1. Rodríguez-González GL, Castro-Rodríguez DC, Zambrano E (2018) Pregnancy and lactation: A window of opportunity to improve individual health. Methods Mol Biol 1735:115–44.
  2. Ahmed KT, Almashhrawi AA, Rahman RN, Hammoud GM, Ibdah JA (2013) Liver diseases in pregnancy: diseases unique to pregnancy. World J Gastroenterol 19:7639–46.
  3. Say RE, Whittaker RG, Turnbull HE, McFarland R, Taylor RW, Turnbull DM (2011) Mitochondrial disease in pregnancy: a systematic review. Obstet Med 4:90–4.