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Maternal Obesity in Pregnancy Developmentally Programs Adipose Tissue Inflammation in Young, Lean Male Mice Offspring.

Published version
Peer-reviewed

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Authors

Alfaradhi, Maria Z 
Kusinski, Laura C 
Fernandez-Twinn, Denise S 
Pantaleão, Lucas C 
Carr, Sarah K 

Abstract

Obesity during pregnancy has a long-term effect on the health of the offspring including risk of developing the metabolic syndrome. Using a mouse model of maternal diet-induced obesity, we employed a genome-wide approach to investigate the microRNA (miRNA) and miRNA transcription profile in adipose tissue to understand mechanisms through which this occurs. Male offspring of diet-induced obese mothers, fed a control diet from weaning, showed no differences in body weight or adiposity at 8 weeks of age. However, offspring from the obese dams had up-regulated cytokine (Tnfα; P < .05) and chemokine (Ccl2 and Ccl7; P < .05) signaling in their adipose tissue. This was accompanied by reduced expression of miR-706, which we showed can directly regulate translation of the inflammatory proteins IL-33 (41% up-regulated; P < .05) and calcium/calmodulin-dependent protein kinase 1D (30% up-regulated; P < .01). We conclude that exposure to obesity during development primes an inflammatory environment in adipose tissue that is independent of offspring adiposity. Programming of adipose tissue miRNAs that regulate expression of inflammatory signaling molecules may be a contributing mechanism.

Description

Keywords

Adipose Tissue, Adiposity, Animals, Body Weight, Chemokines, Cytokines, Female, Interleukin-33, Male, Maternal Nutritional Physiological Phenomena, Maternal-Fetal Exchange, Mice, MicroRNAs, Obesity, Pregnancy

Journal Title

Endocrinology

Conference Name

Journal ISSN

0013-7227
1945-7170

Volume Title

157

Publisher

The Endocrine Society
Sponsorship
Biotechnology and Biological Sciences Research Council (BB/M001636/1)
Medical Research Council (MC_UU_12012/4)
Biotechnology and Biological Sciences Research Council (BB/M001865/1)
Wellcome Trust (089940/Z/09/Z)
British Heart Foundation (None)
Medical Research Council (MC_PC_12012)
This work was supported by Funding sources: National Council for the Improvement of Higher Education (CAPES - Brazil - BEX 10 594/13–2); National Counsel of Technological and Scientific Development (CNPq – Brazil – PDE/204416/ 2014–0); Medical Research Council (MC UU 12012/4 and MC UU12012/5), BBSRC (BB/M001636/1) and the Wellcome Trust (089940/Z/09/Z).