Thus, the present study suggests that PCB-138-induced LD enlargement endows adipocytes with resistance to TNF-α-induced cell death and that Fsp27, perilipin, and survivin, at least in part, help adipocytes to sustain enlarged LDs, contributing to the induction of obesity.
Data show that ASO-Fsp27 and fenofibrate synergize to promote resistance to diet-induced obesity and hypertriglyceridemia and to reverse hepatic steatosis, inflammation, oxidative stress, and fibrosis.
These data suggest that partial reduction of FSP27 activity (e.g., using ASOs) might be exploited therapeutically in insulin-resistant obese or overweight patients.
Here, we aimed to investigate lipid droplet protein (CIDEC/FSP27 and perilipinA (PLIN1)) gene expression in human adipose tissue in association with obesity, insulin resistance and mitochondrial gene expression.
The mRNA expressions and protein levels of PPAR-γ and CIDEC genes started to increase in HFD mice as compared to ND mice and decreased gradually during the late phase of obesity in VAT.
In both sc and visceral adipose tissue, FNDC5 gene expression decreased significantly in association with obesity and was positively associated with brown adipose tissue markers, lipogenic, insulin pathway-related, mitochondrial, and alternative macrophage gene markers and negatively associated with LEP, TNFα, and FSP27 (a known repressor of brown genes).
An FSP27 knockout mouse demonstrated lean phenotypes with atrophic adipose tissue as a result of high-energy expenditure; this mouse line was also resistant to diet-induced obesity and insulin resistance.
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.