Abstract
Common obesity and inherited lipodystrophies, rare disorders characterized by a partial (familial partial lipodystrophy; FPLD) or complete (congenital generalized lipodystrophy; CGL) lack of adipose tissue, are both associated with metabolic complications such as insulin resistance and type 2 diabetes. Mutations in the transcription factor peroxisome proliferator activated receptor (PPAR)γ and a number of its downstream target genes result in lipodystrophy. We hypothesize that signalling by another transcription factor, sterol response element binding protein (SREBP)1c, also needs to be intact to prevent lipodystrophy. The future challenge is to understand how inactivation of such central players or of their upstream regulators or downstream effectors can affect adipose tissue in a depot-specific fashion.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
