Research
Energy balance
Fsp27 (Cidec) deficiency in white adipose tissue induces a 'browning' effect, characterized by increased mitochondrial activity, smaller lipid droplets, and improved insulin sensitivity.
Fsp27 normally prevents white fat from acting like brown fat. When Fsp27 is absent, white fat starts behaving like brown fat (browning), increasing calorie burning and improving insulin sensitivity. This suggests that inhibiting Fsp27 could be a way to turn white fat into a metabolically active tissue that burns calories.
GoodSupportsHIGH confidence
Fsp27-null WAT tends to acquire properties of BAT, such as smaller lipid droplets, increased mitochondrial activity, and enhanced expression of BAT-specific genes such as Ucp1, Cidea, PPARalpha, and Dio2.
Why this rating
Supported by multiple studies on Fsp27 knockout mice showing consistent browning phenotypes.
Source
CIDE proteins and metabolic disorders
Jingyi Gong et al. · Current Opinion in Lipidology · 2009
DOI 10.1097/mol.0b013e328328d0bb
narrative_reviewCited 167×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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- Genetic deficiency or knockdown of CIDE family proteins (Cidea, Cideb, Fsp27) induces a lean phenotype, increases energy expenditure, and confers resistance to diet-induced obesity and insulin resistance.Good
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