Final Report Summary - FUEGO (Global Network of Excellence for Research on Adipose Tissue Plasticity and Human Thermogenesis)
Our joint exchange programme significantly contributed to strengthen the cooperative potential for health-related RTD between EU/AC and EECA countries through staff exchanges and networking activities. This is exemplified by the total of six papers published by the consortium partners in reputable journals. In our first paper by Svensson et al. (2014), we for the first time characterized the human perirenal adipose tissue depot on molecular, protein and cellular levels. Our results report the presence of BAT in this depot as confirmed by the presence of both multi- and unilocular UCP1-positive adipocytes-albeit a large inter-individual variation within the samples collected-, and a higher expression of BAT-related genes that were highly correlated to UCP1 gene compared to the ones expressed specifically to WAT. We also identified gene RXRγ as a new transcription factor that could be involved in the development of BAT. In our second paper by Valente et al. (2015), we found that a single L-menthol skin administration increased thermogenesis and metabolic rate in humans. These effects are minor following L-menthol oral administration probably due to faster glucuronidation and greater blood menthol glucuronide levels. Based on the aforementioned findings, and emerging evidence on the beneficial cooling effects of L-menthol on UCP1-mediated thermogenesis and BAT-like activity in classical WAT depots, in our third paper by Sakellariou et al. (2016), we proposed a L-Menthol-induced browning of WAT hypothesis model, whereby chronic L-menthol dietary treatment could putatively activate cold-sensitive TRPM8 and TRPA1 receptors located on the cell membrane of human white adipocytes, thus inducing an intracellular [Ca2+] increased and browning of WAT. In our fourth paper by de França et al. (2016), we demonstrated that a higher sympathetic flux to inguinal BAT as a consequence of the administration of a low-protein high-carbohydrate diet to rats activates thermogenesis and UCP1 content in the tissue. Finally, in our fifth paper by Pereira et al. (2017), we reported that a low-protein high-carbohydrate diet to rats led to browning in the perirenal WAT, and that higher utilization of fatty acids from blood lipoproteins acted as fuel for thermogenesis. Increased G3P generation by glyceroneogenesis increased fatty acids re-esterification from lipolysis, explaining the increased triacylglycerol storage in the inguinal WAT. In our sixth paper by Flouris et al. (2017), we conducted a systematic review to evaluate the effect of regular exercise training on UCP1 expression in BAT in experimental animal models.
Our analysis revealed that regular exercise training may possibly not represent a major stimulus of UCP1 expression in BAT. We concluded that additional research should focus on the physiological effects of exercise training on BAT thermogenic activity, especially in humans, given the remarkable inconsistency in the results from the analysed studies, and the limited available evidence.
Through the secondments, the researchers gained benefits such as new skills, personal development, career progress, exposure to a different organizational culture, opportunity to change direction, transfer of knowledge, and time for contemplation and re-evaluation of existing skills and abilities. In addition, the researchers had the chance to attend conferences through which they shared knowledge and information regarding the impact of genetics on cardiometabolic disease.