Abstract :
Lipoprotein metabolism may be viewed as a process whereby large, triglyceride-carrying particles from the intestine and liver are broken down into smaller cholesterol-enriched lipoprotein particles. In the process, triglyceride is transported from the intestine and liver to adipose and other storage tissues. Androgen appears to affect lipoprotein metabolism in a number of ways. These include: increasing the activity of lipoprotein lipase and hepatic triglyceride lipase, resulting in higher levels of triglyceride in adipose tissue and a drop in total circulating high-density lipoprotein levels, respectively, and decreasing catabolic removal of low-density lipoproteins from circulating plasma. In pre- and postmenopausal women, androgen progestins in some oral contraceptives, especially the older 19-nortestosterone derivatives such as norgestrel, lower high-density lipoprotein and raise low-density lipoprotein levels. Newer 19-nortestosterone derivatives, such as desogestrel and norgestimate, have a lesser effect on circulating lipoproteins. Nonoral androgenic progestins (e.g., subcutaneous norgestrel) have little effect on circulating lipids, however, which indicates the significance of the “first pass” through the liver for oral agents. The effects of androgens on atherogenesis are largely unexplored, although preliminary studies indicate that they may promote the atherogenic process.
