Stromal vascular cells from rabbit perirenal adipose tissue differentiated at a high frequency in a chemically-defined serum-free medium containing insulin, transferrin, tri-iodothyronine and dexamethasone. The omission from the culture medium of dexamethasone resulted in a lack of adipose conversion. Addition of IGF-I increased glycerol-3-phosphate dehydrogenase (GPDH) activity. The conditioned media from adipocyte precursor cells contained measurable quantities of immunoreactive IGF-I as determined by RIA after neutralization of IGF binding proteins interference. Dexamethasone increased IGF-I secretion during the first seven days after plating and decreased IGF-I binding to conditioned media. Three molecular forms of IGF binding proteins (IGFBPs) were identified by Western ligand blots in conditioned media, with M(r) = 40,000, 29,000 and 25,000. The major form (M(r) = 29,000) was decreased by dexamethasone. In contrast, the M(r) = 24,000 form was increased. Specific binding of 125I-labelled IGF-I to rabbit adipocyte precursor cells was more effectively inhibited by unlabelled IGF-I than by unlabelled IGF-II or insulin. The electrophoretic migration of cross linked 125I-IGF-I to microsomal membranes revealed a complex with M(r) = 130,000 under reducing conditions corresponding to the alpha-subunit of the IGF-I receptor. The addition of IGF-I monoclonal antibody to rabbit adipocyte precursor cells cultured in serum-free medium significantly inhibited [3H]-thymidine incorporation and significantly decreased (50%) GPDH specific activities. This inhibitory effect was overcome by the addition of exogenous IGF-I. Thus stromal vascular cells isolated from perirenal adipose tissue secrete IGF-I and IGFBPs, possess IGF-I receptors and respond to exogenous and endogenous IGF-I.(ABSTRACT TRUNCATED AT 250 WORDS)