Unchanged mitochondrial phenotype, but accumulation of lipids in the myometrium in obese pregnant women. (9th November 2017)

• Record Type: Journal Article
• Authors: Gam, Christiane Marie Bourgin Folke; Larsen, Lea Hüche; Mortensen, Ole Hartvig; Engelbrechtsen, Line; Poulsen, Steen Seier; Qvortrup, Klaus; Mathiesen, Elisabeth Reinhart; Damm, Peter; Quistorff, Bjørn
• Is Part Of: Journal of physiology. Volume 595:Number 23(2017)
• Page Start: 7109
• Page End: 7122
• Publication Date: 2017-11-09
• Subjects: mitochondria -- pregnancy -- obesity -- myometrium -- intramuscular fat; Physiology -- Periodicals; 612.005
• DOI: 10.1113/JP274838
• Languages: English
• ISSNs: 0022-3751

Abstract

Abstract : Key points: Obesity during pregnancy and childbirth is associated with labour dystocia leading to instrumental or operative delivery, but the underlying pathophysiological mechanisms remain unclear and insufficient uterine contractility has been suggested. This study examined whether reduced myometrial mitochondrial capacity or quantity could contribute as a pathophysiological mechanism to labour dystocia. Data did not support reduced myometrial mitochondrial capacity or quantity in the myometrium at term in obese women, but a reduced myocyte density with increased triglyceride content was demonstrated, which could lead to poorer uterine contractility. These results add to the understanding of systemic effects of obesity, placing also the myometrium at term as an affected non‐adipose tissue. Abstract: Obesity is known to increase the risk of labour dystocia and insufficient energy supply, due to reduced mitochondrial capacity or quantity, could be a possible mechanism leading to reduced efficiency of uterine contractility during labour. In the present study of 36 women having an elective Caesarean section at term, obesity did not change mitochondrial phenotype in the myometrial myocyte obtained from uterine biopsies taken at delivery. Respiration rates in isolated mitochondria were unaffected by obesity. No indication of reduced content, investigated by quantification of the complexes of the respiratory chain, or altered regulation, examined by myometrial mRNA levels of genes related to mitochondrial biogenesis and inflammation, was detected. Yet we found increased myometrial triglyceride content in the obese group (2.39 ± 0.26 vs . 1.56 ± 0.20 mm, P = 0.024), while protein content and citrate synthase activity per gram wet weight myometrium were significantly lower in the obese (109.2 ± 7.2 vs . 139.4 ± 5.6 mg g −1, P = 0.002, and 24.8 ± 1.0 vs . 29.6 ± 1.4 U g −1 wet wt, P = 0.008, respectively). These differences were substantiated by our histological findings where staining for nuclei, cytoplasm, glycogen and collagen supported the idea of a smaller muscle content in the myometrium in obese women. In conclusion no indication of myometrial mitochondrial dysfunction in the isolated state was found, but the observed increase of lipid content might play a role in the pathophysiological mechanisms behind labour dystocia in obese women. Key points: Obesity during pregnancy and childbirth is associated with labour dystocia leading to instrumental or operative delivery, but the underlying pathophysiological mechanisms remain unclear and insufficient uterine contractility has been suggested. This study examined whether reduced myometrial mitochondrial capacity or quantity could contribute as a pathophysiological mechanism to labour dystocia. Data did not support reduced myometrial mitochondrial capacity or quantity in the myometrium at term in obese women, but a reduced myocyte density with increased triglyceride content was demonstrated, which could lead to poorer uterine contractility. These results add to the understanding of systemic effects of obesity, placing also the myometrium at term as an affected non‐adipose tissue.