title: Adipocyte-specific disruption of mouse Cnot3 causes lipodystrophy.
abstract: Lipodystrophy involves a loss of adipose tissue. In mice, disruption of adipose tissue Cnot3, a subunit of the CCR4-NOT deadenylase complex, causes adipose tissue anomalies. In Cnot3ad-/-mice, white adipose tissue (WAT) decreases concomitantly with enhanced inflammation, whereas brown adipose tissue increases and contains larger lipid droplets. Cnot3ad-/-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 Cnot3ad-/-WAT, achieving levels similar to those in lipodystrophic aP2-nSrebp1c and Ppargldi/+mice; thus, Cnot3ad-/-mice exhibit lipodystrophy.
authors.affiliation: Cell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Japan.
authors.forename: Xue
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Biochemistry, Goodman Cancer Research Centre, McGill University, Montreal, Canada.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Morita
authors.affiliation: Cell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Japan.|Laboratory for Immunogenetics, Center for Integrative Medical Sciences, RIKEN, Yokohama, Japan.
authors.forename: Chisato
authors.initials: C
authors.lastname: Kikuguchi
authors.affiliation: Cell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Japan.
authors.forename: Akinori
authors.initials: A
authors.lastname: Takahashi
authors.affiliation: Cell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Japan.|Laboratory for Immunogenetics, Center for Integrative Medical Sciences, RIKEN, Yokohama, Japan.
authors.forename: Toru
authors.initials: T
authors.lastname: Suzuki
authors.affiliation: Cell Signal Unit, Okinawa Institute of Science and Technology Graduate University, Japan.|Laboratory for Immunogenetics, Center for Integrative Medical Sciences, RIKEN, Yokohama, Japan.
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yamamoto
mesh_terms: D017667:Adipocytes / Q000378:metabolism*; D002001:Adipose Tissue, Brown / Q000378:metabolism; D052436:Adipose Tissue, White / Q000378:metabolism; D000818:Animals; D004195:Disease Models, Animal; D004822:Epididymis / Q000378:metabolism; D020869:Gene Expression Profiling; D018149:Glucose Intolerance / Q000150:complications / Q000378:metabolism; D006943:Hyperglycemia / Q000150:complications / Q000378:metabolism; D006946:Hyperinsulinism / Q000150:complications / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D007333:Insulin Resistance; D008060:Lipodystrophy / Q000378:metabolism*; D008066:Lipolysis; D008297:Male; D018345:Mice, Knockout; D009928:Organ Specificity; D022722:Thermogenesis; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*
chemical_list: C569362:CNOT3 protein, mouse; D014157:Transcription Factors
keywords: Cnot3; cold intolerance; lipodystrophy