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Metabolic analysis of adipose tissues in a rodent model of pre-pregnancy maternal obesity combined with offsprings on high-carbohydrate diet.

journal contribution
posted on 2019-05-31, 09:53 authored by A Wang, T-L Han, Z Chen, X Zhou, X Yu, H Qi, PN Baker, H Zhang
Maternal obesity is associated with adverse effects on the health of offsprings. Consumption of a high-carbohydrate (HC) diet has been found to promote abnormal fatty acid metabolism in adipose tissue. Therefore, we hypothesised that maternal obesity combined with an offspring HC diet would alter the fatty acid metabolism of adipose tissue and subsequently contribute to offspring obesity. Leprdb/+ mice were used to model pre-pregnancy maternal obesity and the C57BL/6 wildtype were used as a control group. Offspring were fed either HC diet or a normal-carbohydrate (NC) diet after weaning. Brown adipose tissue (BAT) and white adipose tissue (WAT) were collected from offspring at 20 weeks of age and their fatty acid metabolome was characterized using gas chromatography-mass spectrometry. We found that HC diet increased the body weight of offspring (males increased by 14.70% and females increased by 1.05%) compared to control mothers. However, maternal obesity alone caused a 7.9% body weight increase in female offspring. Maternal obesity combined with an offspring HC diet resulted in dynamic alterations of the fatty acid profiles of adipose tissue in male offspring. Under the impact of a HC diet, the fatty acid metabolome was solely elevated in female WAT, whereas, the fatty acid metabolites in BAT showed a similar trend in the male and female offsprings. 6,9-octadecadienoic acid and 12,15-cis-octadecatrienoic acid were significantly affected in female WAT, in response to offspring consumption of a HC diet. Our study demonstrated that maternal obesity and offspring HC diet have different metabolic effects on adipose tissue in male and female offsprings.

Funding

This work was supported by the National Natural Science Foundation of China (No.81571453, 81771607, 81871185, 81701477), The 111 Project (Yuwaizhuan (2016)32), The National Key Research and Development Program of Reproductive Health & Major Birth Defects Control and Prevention (2016YFC1000407), Chongqing Health Commission (2017ZDXM008, 2018ZDXM024) and Chongqing Science & Technology Commission (cstc2017jcyjBX0062).

History

Citation

Experimental Cell Research, 2019, 381(1), pp. 29-38

Author affiliation

/Organisation/COLLEGE OF LIFE SCIENCES

Version

  • AM (Accepted Manuscript)

Published in

Experimental Cell Research

Publisher

Elsevier for Academic Press

eissn

1090-2422

Acceptance date

2019-05-01

Copyright date

2019

Publisher version

https://www.sciencedirect.com/science/article/pii/S0014482719302320?via=ihub

Notes

The file associated with this record is under embargo until 12 months after publication, in accordance with the publisher's self-archiving policy. The full text may be available through the publisher links provided above.

Language

en

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