Cholesterol is an obligate intermediate in steroidogenesis. It may be synthesized by steroidogenic cells or taken up from circulating lipoproteins. In the adrenal, ovary, placenta, and possibly the testes of many species, including man, lipoprotein cholesterol is the major source of steroidogenic substrate. Lipoprotein cholesterol uptake is hormonally regulated in these tissues, with the exception of the placenta, and coordinated with intracellular cholesterol synthesis and mobilization of cholesteryl esters to ensure a continuous supply of free cholesterol for steroid synthesis. When the rate of cholesterol uptake exceeds the rate of steroidogenesis, intracellular cholesterol synthesis is suppressed and cholesterol in excess of cellular needs is esterified and stored for future use. During the last decade the mechanisms and regulation of lipoprotein cholesterol uptake by steroidogenic tissues have been elucidated. Two distinct lipoprotein-specific, hormonally regulated mechanisms for taking up extracellular cholesterol have been found in steroidogenic cells. Not all steroidogenic tissues possess both mechanisms. It is our purpose to review these findings.