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In mice, disruption of adipose tissue <jats:italic>Cnot3<\/jats:italic>, a subunit of the <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>4\u2010<jats:styled-content style=\"fixed-case\">NOT<\/jats:styled-content> deadenylase complex, causes adipose tissue anomalies. In <jats:italic>Cnot3<\/jats:italic><jats:sup>ad\u2212\/\u2212<\/jats:sup> mice, white adipose tissue (<jats:styled-content style=\"fixed-case\">WAT<\/jats:styled-content>) decreases concomitantly with enhanced inflammation, whereas brown adipose tissue increases and contains larger lipid droplets. <jats:italic>Cnot3<\/jats:italic><jats:sup>ad\u2212\/\u2212<\/jats:sup> mice show hyperinsulinemia, hyperglycemia, insulin resistance, and glucose intolerance, and cannot maintain body temperature during cold exposure. Increased expression of inflammatory genes and decreased leptin expression also occur in <jats:italic>Cnot3<\/jats:italic><jats:sup>ad\u2212\/\u2212<\/jats:sup> <jats:styled-content style=\"fixed-case\">WAT<\/jats:styled-content>, achieving levels similar to those in lipodystrophic <jats:italic>aP2\u2010nSrebp1c<\/jats:italic> and <jats:italic>Pparg<\/jats:italic><jats:sup><jats:italic>ldi\/+<\/jats:italic><\/jats:sup> mice; thus, <jats:italic>Cnot3<\/jats:italic><jats:sup>ad\u2212\/\u2212<\/jats:sup> mice exhibit lipodystrophy.<\/jats:p>","DOI":"10.1002\/1873-3468.12550","type":"journal-article","created":{"date-parts":[[2016,12,29]],"date-time":"2016-12-29T15:06:50Z","timestamp":1483024010000},"page":"358-368","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Adipocyte\u2010specific disruption of mouse <i>Cnot3<\/i> causes 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