Binds to lipid droplets and regulates their enlargement, thereby restricting lipolysis and favoring storage. At focal contact sites between lipid droplets, promotes directional net neutral lipid transfer from the smaller to larger lipid droplets. The transfer direction may be driven by the internal pressure difference between the contacting lipid droplet pair. Its role in neutral lipid transfer and lipid droplet enlargement is activated by the interaction with PLIN1. May act as a CEBPB coactivator in the white adipose tissue to control the expression of a subset of CEBPB downstream target genes, including SOCS1, SOCS3, TGFB1, TGFBR1, ID2 and XDH. When overexpressed in preadipocytes, induces apoptosis or increases cell susceptibility to apoptosis induced by serum deprivation or TGFB treatment. As mature adipocytes, that express high CIDEC levels, are quite resistant to apoptotic stimuli, the physiological significance of its role in apoptosis is unclear. May play a role in the modulation of the response to osmotic stress by preventing NFAT5 to translocate into the nucleus and activate its target genes expression. a triacyl-sn-glycerol(in) = a triacyl-sn-glycerol(out) Homodimer (By similarity). Interacts with CEBPB. Interacts with NFAT5; this interaction is direct and retains NFAT5 in the cytoplasm (By similarity). Interacts with CIDEA. Interacts with PLIN1. Diffuses quickly on lipid droplet surface, but becomes trapped and clustered at lipid droplet contact sites, thereby enabling its rapid enrichment at lipid droplet contact sites. Expressed mainly in adipose tissue, small intestine, heart, colon and stomach and, at lower levels, in brain, kidney and liver. The CIDE-N domain is involved in homodimerization which is crucial for its function in promoting lipid exchange and transfer. Ubiquitinated and targeted to proteasomal degradation, resulting in a short half-life. Protein stability depends on triaclyglycerol synthesis, fatty acid availability and lipid droplet formation (By similarity). In omental adipose tissue of obese patients matched for BMI, expression levels tend to correlate with insulin sensitivity. Expression is increased 2-3 fold in the group of patients with high insulin sensitivity, compared to the insulin-resistant group. This observation is consistent with the idea that triglyceride storage in adipocytes plays an important role in sequestering triglycerides and fatty acids away from the circulation and peripheral tissues, thus enhancing insulin sensitivity in liver and muscle. This effect is not significant in subcutaneous adipose tissue (PubMed:18509062). In subcutaneous adipose tissue of diabetic patients, tends to negatively correlate with body mass index and total fat mass, independently of insulin sensitivity (PubMed:18334488). The disease is caused by variants affecting the gene represented in this entry.