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 language | English (US) |
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Pages (from-to) | 358-368 |
Number of pages | 11 |
Journal | FEBS Letters |
Volume | 591 |
Issue number | 2 |
DOIs | |
State | Published - Jan 1 2017 |
Externally published | Yes |
Keywords
- Cnot3
- cold intolerance
- lipodystrophy
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology