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Endocrine Abstracts (2018) 59 P170 | DOI: 10.1530/endoabs.59.P170

1WISDEM Centre, Human Metabolism Research Unit, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK; 2Division of Translational and Experimental Medicine, Warwick Medical School, University of Warwick, Coventry, UK; 3Departments of Cardiovascular Sciences, Health Sciences and Leicester Diabetes Centre, College of Life Sciences, University of Leicester, Leicester, UK; 4Department of Obstetrics and Gynaecology, University Hospitals of Leicester NHS Trust, Leicester Royal Infirmary, Leicester, UK; 5Department of General Surgery, University Hospitals Coventry and Warwickshire, Coventry, UK; 6Division of Endocrinology and Experimental Medicine, Imperial College London, Hammersmith Campus, London, UK.

The role of brown adipose tissue (BAT) in pathological states of energy homeostasis and impaired adipocyte function, such as obesity has been a major area of research interest in recent years. Herein, we sought to determine the direct effects of adipokines, visfatin and leptin on BAT thermogenesis. The effects of mouse recombinant visfatin, nicotinamide mononucleotide (NMN) and leptin with or without FK866 were studied on differentiated T37i cells. Treated cells were analyzed for key genes and proteins regulating BAT [UCP-1, PRD1-BF1-RIZ1 homologous domain-containing 16 (PRDM-16), PPARgamma-coactivator-1alpha (PGC-1a) and receptor-interacting protein 140 (RIP-140)] using quantitative PCR and western blot analysis. Data is presented as mean P-values. Both visfatin and leptin had significant concentration dependent effects on thermogenesis in brown pre-adipocytes and at physiological levels, increased uncoupling protein-1 (UCP-1) levels in brown adipocytes. These effects of visfatin were similar to that of nicotinamide mononucleotide (NMN), further strengthening the enzymatic role of visfatin. We also showed that leptin induced UCP-1 mRNA expression and protein production appears to be mediated by visfatin. High concentrations of both visfatin and leptin led to a dramatic decrease in UCP-1 protein levels, supporting the notion that visfatin levels are raised in obesity and that obese people have reduced BAT activity, plausibly through a reduction in UCP-1 levels. Additionally, we found differential regulation of key brown adipogenic genes, specifically, PRD1-BF1-RIZ1 homologous domain-containing 16 (PRDM-16), PPARgamma-coactivator-1alpha (PGC-1a) and receptor-interacting protein 140 (RIP-140) by visfatin. Our observations provide novel insights in the potential actions of visfatin in BAT.

Volume 59

Society for Endocrinology BES 2018

Glasgow, UK
19 Nov 2018 - 21 Nov 2018

Society for Endocrinology 

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