Unchanged mitochondrial phenotype, but accumulation of lipids in the myometrium in obese pregnant women
Autor: | Klaus Qvortrup, Lea Hüche Larsen, Ole Hartvig Mortensen, Elisabeth R. Mathiesen, Line Engelbrechtsen, Bjørn Quistorff, Steen Seier Poulsen, Peter Damm, Christiane Gam |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Pregnancy 030219 obstetrics & reproductive medicine biology Physiology Respiratory chain Myometrium Inflammation Mitochondrion medicine.disease 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Endocrinology Mitochondrial biogenesis Internal medicine medicine biology.protein Citrate synthase Myocyte medicine.symptom reproductive and urinary physiology |
Zdroj: | The Journal of Physiology. 595:7109-7122 |
ISSN: | 0022-3751 |
DOI: | 10.1113/jp274838 |
Popis: | 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. |
Databáze: | OpenAIRE |
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