Differential mitochondrial adaptation and FNDC5 production in brown and white adipose tissue in response to cold and obesity
Authors' conclusion
Depot differences in FNDC5 production and mitochondrial adaptations in response to obesity and cold might indicate a self-regulatory mechanism to control thermogenesis in response to energy needs.
Study context
- Population
- Patients with normal weight and obesity; rats with diet-induced obesity after 1 week of cold exposure; human visceral adipocytes in vitroplus 61 rats
- Participants
- 159 patients
- Comparison
- Obesity vs normal weight; cold exposure; FNDC5 concentrations in vitro
- Outcome
- FNDC5 and mitochondrial homeostasis in visceral WAT and BAT
Methodological detailshuman cohort, rat diet-induced obesity model with cold exposure, in vitro human adipocytes
- Human cohort
- Rat diet-induced obesity model with cold exposure
- In vitro human adipocytes
Main finding
As reported in the abstract
- In human visceral adipocytes, FNDC5/irisin triggered mitochondrial biogenesis (TFAM) and fusion (MFN1, MFN2, OPA1) while inhibiting peripheral fission (DNM1L, FIS1) and mitophagy (PINK1, PRKN)
- Circulating and visceral WAT FNDC5 decreased in patients and animals with obesity; its receptor integrin αV upregulated
- Obesity increased mitochondrial fusion and decreased mitophagy in visceral WAT from patients and rats
- In rat BAT, obesity upregulated Fndc5 and genes of mitochondrial biogenesis and fission
- Cold exposure promoted mitochondrial biogenesis and healthy peripheral fission while repressing Fndc5 expression and mitophagy in rat BAT
Original publication
Differential mitochondrial adaptation and FNDC5 production in brown and white adipose tissue in response to cold and obesity. Obesity (Silver Spring). Published 26 September 2024. doi:10.
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