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 and occurs at a lower rate than that promoted by CIDEC. Acts as a CEBPB coactivator in mammary epithelial cells to control the expression of a subset of CEBPB downstream target genes, including ID2, IGF1, PRLR, SOCS1, SOCS3, XDH, but not casein. By interacting with CEBPB, strengthens the association of CEBPB with the XDH promoter, increases histone acetylation and dissociates HDAC1 from the promoter. When overexpressed, induces apoptosis. The physiological significance of its role in apoptosis is unclear. Interacts with CIDEC (By similarity). Directly interacts with CEBPB. Enriched at lipid droplet contact sites. Using a GFP-tagged construct, has been shown to localize to mitochondria, where it could interact with UCP1 and hence inhibit UCP1 uncoupling activity (PubMed:12910269). These data could not be confirmed (PubMed:22245780, PubMed:18509062). Highly expressed in brown adipose tissue and, at lower levels, in white adipose tissue (at protein level). Expressed in mammary gland during pregnancy and lactation, in epithelial cells, but not in the surrounding adipose tissue. Secreted into milk via milk fat globules. Undetectable in undifferentiated preadipocytes. Expressed at 15 dpc in the interscapular region of the embryo, that could correspond to the developing brown adipose tissue. Expression continues in the interscapular region at 18 dpc and postnatally. In mammary glands, begins to be highly expressed at day 14.5 of pregnancy. Expression is maintained at high levels throughout lactation and declines during post-lactational involution. Up-regulated under conditions that enhance triacylglycerol deposition, including rosiglitazone treatment and high-fat diet. This up-regulation is mediated by PPARG. Mutant animals appear normal and fertile and produce the expected Mendelian ratio of heterozygous and homozygous descendents. They are lean and resistant to diet-induced obesity and diabetes. They exhibit higher metabolic rate, lipolysis in brown adipose tissue and core body temperature when subjected to cold treatment. Mutant females are unable to properly feed their pups who die within 3 days postpartum due to severely reduced milk lipids.