Adipocyte-specific disruption of mouse Cnot3 causes lipodystrophy

Xue Li, Masahiro Morita, Chisato Kikuguchi, Akinori Takahashi, Toru Suzuki, Tadashi Yamamoto

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)358-368
Number of pages11
JournalFEBS Letters
Volume591
Issue number2
DOIs
StatePublished - Jan 1 2017

Keywords

  • Cnot3
  • cold intolerance
  • lipodystrophy

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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