Abstract

Cold-induced thermogenesis increases energy expenditure and can reduce body weight in mammals, so the genes involved in it are thought to be potential therapeutic targets for treating obesity and diabetes. In the quest for more effective therapies, a great deal of research has been conducted to elucidate the regulatory mechanism of cold-induced thermogenesis. Over the last decade, a large number of genes that can enhance or suppress cold-induced thermogenesis have been discovered, but a comprehensive list of these genes is lacking. To fill this gap, we examined all of the annotated human and mouse genes and curated those demonstrated to enhance or suppress cold-induced thermogenesis by in vivo or ex vivo experiments in mice. The results of this highly accurate and comprehensive annotation are hosted on a database called CITGeneDB, which includes a searchable web interface to facilitate broad public use. The database will be updated as new genes are found to enhance or suppress cold-induced thermogenesis. It is expected that CITGeneDB will be a valuable resource in future explorations of the molecular mechanism of cold-induced thermogenesis, helping pave the way for new obesity and diabetes treatments.Database URL: http://citgenedb.yubiolab.org

Highlights

  • Cold-induced thermogenesis (CIT) is a process by which mammals increase their resting energy expenditure in cold temperatures

  • CITGeneDB is a comprehensive resource of CIT-enhancing and -suppressive human and mouse genes

  • It should be noted that our current study focuses only on CIT, the genes that were curated may be involved in other types of thermogenesis

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Summary

Introduction

Cold-induced thermogenesis (CIT) is a process by which mammals increase their resting energy expenditure in cold temperatures. Okada et al found that knockout of Acot increased oxygen consumption rates in both primary brown adipocytes and isolated BAT from the mutant mice, and up-regulated BAT thermogenic genes after exposure to a 4C environment for 96 hours [5], indicating a suppressive role of Acot in BAT thermogenesis As another example, knockout of Zfp423 decreased oxygen consumption of mouse subcutaneous WAT and down-regulated the expression of a number of WAT browning marker genes, such as Cidea and Elovl, after exposing Zfp423-/- mice to progressively colder temperatures, suggesting that gene Zfp423 can promote the browning of WAT under cold-exposure conditions [6].

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