Brown adipose tissue (BAT), an organ specialized in the conversion of chemical energy from nutrients into heat through a process denominated as nonshivering thermogenesis, plays an important role in defence of body weight and homoeothermy in mammals. BAT nonshivering thermogenesis relies on the activity of the uncoupling protein 1 (UCP-1), a mitochondrial protein that, on demand, deviates proton gradient from ATP synthesis to heat generation. Energetically, this process is supported by BAT-elevated mitochondrial density and outstanding capacity to oxidize fatty acids and glucose. These unique features place BAT as an important determinant of whole-body energy, lipid and glucose homoeostases. In the present issue of Clinical Science, Poekes et al. have gathered supporting evidence indicating that, along with hyperphagia, impaired BAT diet-induced thermogenesis is an important factor driving the exacerbated diet-induced obesity, glucose intolerance and hepatic steatosis featured by foz/foz, a mouse strain that carries mutations in Alström syndrome protein 1 (ALMS1) gene mimicking human Alström syndrome. They also show that restoration of BAT nonshivering thermogenesis by intermittent cold exposure attenuated foz/foz mice obesity, glucose intolerance and liver steatosis. Altogether, these findings highlight the important contribution of BAT nonshivering thermogenesis to whole-body energy expenditure, lipid and glucose homoeostases and further support its potential utilization as a therapeutic strategy to treat metabolic diseases.
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February 2017
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Density-dependent scanning electron microscopy of calcifying vascular tissue (orange - calcification; green - collagen). Please see pp. 181-195 for more information. Image provided by Sergio Bertazzo.
Commentary|
January 30 2017
Turning up the heat against metabolic syndrome and non-alcoholic fatty liver disease
William T. Festuccia
*Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508000, Brazil
Correspondence: William T. Festuccia (email william.festuccia@usp.br or william.festuccia@gmail.com)
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Clin Sci (Lond) (2017) 131 (4): 327–328.
Article history
Received:
December 12 2016
Revision Received:
December 20 2016
Accepted:
December 20 2016
Connected Content
This is a commentary on:
Defective adaptive thermogenesis contributes to metabolic syndrome and liver steatosis in obese mice
Citation
William T. Festuccia; Turning up the heat against metabolic syndrome and non-alcoholic fatty liver disease. Clin Sci (Lond) 1 February 2017; 131 (4): 327–328. doi: https://doi.org/10.1042/CS20160855
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