Research

Energy balance

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.

This research suggests that targeting CIDE proteins (specifically Fsp27, Cideb, or Cidea) could be a viable therapeutic strategy for treating obesity and type 2 diabetes. While you cannot directly 'knock out' these genes, understanding their role highlights that inhibiting lipid droplet formation and promoting fatty acid oxidation are key to metabolic health. Current research points to these proteins as potential molecular targets for drug development.

GoodSupportsHIGH confidence
Animals with deficiency in Cidea, Cideb, and Fsp27 all display lean phenotypes with higher energy expenditure and are resistant to diet-induced obesity and insulin resistance.
Jingyi Gong et al. · Current Opinion in Lipidology · 2009

Why this rating

Evidence is derived from multiple knockout mouse models (Cidea, Cideb, Fsp27) showing consistent phenotypes, supported by human correlation studies.

Source

CIDE proteins and metabolic disorders

Jingyi Gong et al. · Current Opinion in Lipidology · 2009

DOI 10.1097/mol.0b013e328328d0bb

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DOI resolved against Crossref · corpus check 2026-06-10

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