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UCP1: its involvement and utility in obesity

Abstract

Energy balance to prevent the development of obesity is dependent on energy expenditure. Although physical activity is the dominant mechanism for dissipating excess energy, a system of thermogenesis that evolved to protect the body from hypothermia is based upon the uncoupling of oxidative phosphorylation in brown adipocytes by the mitochondrial uncoupling protein (UCP1). It has been shown that upregulation of UCP1 by genetic manipulations or pharmacological agents can reduce obesity and improve insulin sensitivity. Recent evidence has shown the existence of two sources for brown adipocytes, one appearing as discrete brown fat depots during fetal development and the other appears during post-natal development as diffuse populations in traditional white fat depots. The latter can be induced by adrenergic stimulation depending on the genetic background of the animals and the nutritional environment. Understanding the biological and environmental factors controlling the expression of these two brown adipocyte populations promises to provide new strategies by which enhanced thermogenesis can be used to reduce obesity.

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Acknowledgements

Starting with Anders Jacobsson, a graduate student from the Wenner-Gren Institute in Stockholm, who came to my laboratory in 1983 with an antibody against UCP1 to work on cloning of Ucp1 cDNA, I wish to thank the large number of post-doctoral associates and collaborators who have worked with me defining the structure and function of the Ucp1 gene and its role in thermogenesis and body weight regulation. I also acknowledge the financial support through R01 HD08431 from the NIH throughout this period.

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Correspondence to L P Kozak.

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Kozak, L., Anunciado-Koza, R. UCP1: its involvement and utility in obesity. Int J Obes 32 (Suppl 7), S32–S38 (2008). https://doi.org/10.1038/ijo.2008.236

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