Obesity has now reached pandemic proportions, resulting in dramatic increases in the occurrence of its associated disorders including diabetes and cardiovascular disease. Understanding the processes and metabolic perturbations that contribute to the expansion of adipose depots accompanying obesity is critical for the development of appropriate therapeutics. Expansion of white adipose (WAT) tissue depots particularly the intra-abdominal depots contribute to insulin resistance and inflammation that lead to type 2 diabetes, whereas brown adipose (BAT) resists expansion because it oxidizes lipids and, consequently, it is associated with an healthier phenotype. Our studies are focused on identifying the mechanisms regulating the formation and function of white and brown adipocytes (fat cells) using a variety of experimental approaches including overexpression and knock down of specific nuclear factors that we consider to be likely regulators of these processes in cells in culture as well as in mice. At present our focus is on nuclear factors that modulate the activity of the two principal regulators of adipogenesis (fat cell differentiation) peroxisome proliferator-activated receptor gamma (PPARg) and CCAAT/enhancer binding proteins alpha, beta and delta (C/EBPs). We are particularly interested in identifying the factors regulating commitment of mesenchymal progenitors to the adipogenic lineage and are adopting a variety of approaches to achieve this goal, which includes gene profiling to discover novel regulators as well as investigating the role of selected candidate genes.
- Graduate Faculty (Primary Mentor of Grad Students), Boston University School of Medicine, Graduate Medical Sciences
- Boston Medical Center
- National Institute for Medical Research (NIMR), PhD
- University of Liverpool, BSc
- Published on 5/29/2019
Rabhi N, Farmer SR. Adipose Progenitor Cells Contribute to Lipid Spillover during Obesity. Trends Endocrinol Metab. 2019 May 29. PMID: 31153731.
- Published on 4/11/2019
Farmer SR. Boning Up on Irisin. N Engl J Med. 2019 04 11; 380(15):1480-1482. PMID: 30970196.
- Published on 12/21/2018
Henriques F, Lopes MA, Franco FO, Knobl P, Santos KB, Bueno LL, Correa VA, Bedard AH, Guilherme A, Birbrair A, Peres SB, Farmer SR, Batista ML. Toll-Like Receptor-4 Disruption Suppresses Adipose Tissue Remodeling and Increases Survival in Cancer Cachexia Syndrome. Sci Rep. 2018 Dec 21; 8(1):18024. PMID: 30575787.
- Published on 5/25/2018
Jager M, Lee MJ, Li C, Farmer SR, Fried SK, Layne MD. Aortic carboxypeptidase-like protein enhances adipose tissue stromal progenitor differentiation into myofibroblasts and is upregulated in fibrotic white adipose tissue. PLoS One. 2018; 13(5):e0197777. PMID: 29799877.
- Published on 5/15/2018
Lin JZ, Rabhi N, Farmer SR. Myocardin-Related Transcription Factor A Promotes Recruitment of ITGA5+ Profibrotic Progenitors during Obesity-Induced Adipose Tissue Fibrosis. Cell Rep. 2018 May 15; 23(7):1977-1987. PMID: 29768198.
- Published on 3/9/2018
Hou X, Zhang Y, Li W, Hu AJ, Luo C, Zhou W, Hu JK, Daniele SG, Wang J, Sheng J, Fan Y, Greenberg AS, Farmer SR, Hu MG. CDK6 inhibits white to beige fat transition by suppressing RUNX1. Nat Commun. 2018 03 09; 9(1):1023. PMID: 29523786.
- Published on 12/13/2016
Wang H, Liu L, Lin JZ, Aprahamian TR, Farmer SR. Browning of White Adipose Tissue with Roscovitine Induces a Distinct Population of UCP1+ Adipocytes. Cell Metab. 2016 Dec 13; 24(6):835-847. PMID: 27974179.
- Published on 8/26/2016
Bian H, Lin JZ, Li C, Farmer SR. Myocardin-related transcription factor A (MRTFA) regulates the fate of bone marrow mesenchymal stem cells and its absence in mice leads to osteopenia. Mol Metab. 2016 Oct; 5(10):970-9. PMID: 27689009.
- Published on 8/15/2016
Lin JZ, Farmer SR. LSD1-a pivotal epigenetic regulator of brown and beige fat differentiation and homeostasis. Genes Dev. 2016 Aug 15; 30(16):1793-5. PMID: 27601528.
- Published on 2/18/2016
Lin JZ, Farmer SR. Morphogenetics in brown, beige and white fat development. Adipocyte. 2016 Apr-Jun; 5(2):130-5. PMID: 27386157.
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