Journal article

Deletion of Trim28 in committed adipocytes promotes obesity but preserves glucose tolerance

Simon T Bond, Emily J King, Darren C Henstridge, Adrian Tran, Sarah C Moody, Christine Yang, Yingying Liu, Natalie A Mellett, Artika P Nath, Michael Inouye, Elizabeth J Tarling, Thomas Q de Aguiar Vallim, Peter J Meikle, Anna C Calkin, Brian G Drew



The effective storage of lipids in white adipose tissue (WAT) critically impacts whole body energy homeostasis. Many genes have been implicated in WAT lipid metabolism, including tripartite motif containing 28 (Trim28), a gene proposed to primarily influence adiposity via epigenetic mechanisms in embryonic development. However, in the current study we demonstrate that mice with deletion of Trim28 specifically in committed adipocytes, also develop obesity similar to global Trim28 deletion models, highlighting a post-developmental role for Trim28. These effects were exacerbated in female mice, contributing to the growing notion that Trim28 is a sex-specific regulator of obesity. Mechanisticall..

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Awarded by National Health and Medical Research Council (NHMRC) of Australia

Awarded by National Heart Foundation of Australia

Funding Acknowledgements

We acknowledge funding support from the Victorian State Government OIS program to Baker Heart and Diabetes Institute. These studies were supported by funding from the National Health and Medical Research Council (NHMRC) of Australia (to BGD APP1128060). B.G.D. and A.C.C. were supported by National Heart Foundation of Australia, Future Leader Fellowships (101789 and 100067, respectively). We thank all members of the MMA, LMCD, and Metabolomics laboratories at BHDI for their ongoing contributions. We also thank Prof. Mark Febbraio (Baker Institute) for providing us with AdipoQ-Cre mice, and are grateful for the assistance of Angela Cheng (UCLA) for help with RNA library preparation and sequence analysis.