The second key feature in the pathogenesis of acne is excess sebum production from the sebaceous gland. Patients with acne produce more sebum than those without acne although the quality of sebum is the same between the two groups (18). One of the components of sebum, triglycerides, may play a role in acne pathogenesis. Triglycerides are broken down into free fatty acids by P. acnes, normal flora of the pilosebaceous unit. These free fatty acids promote further bacterial clumping and colonization of P. acnes, incite inflammation, and may be comedogenic (19).
Androgenic hormones also influence sebum production. Similar to their action on the follicular infundibular keratinocytes, androgen hormones bind to and influence sebocyte activity (20). Those with acne have higher average serum androgen levels (although still within normal range) than unaffected controls (21,22). 5-alpha reductase, the enzyme responsible for converting testosterone to the potent DHT, has greatest activity in areas of skin prone to acne, the face, chest, and back (23).
The role of estrogen on sebum production is not well defined. The dose of estrogen required to decrease sebum production is greater than the dose required to inhibit ovulation (24). The mechanisms by which estrogens may work include: (i) directly opposing the effects of androgens within the sebaceous gland; (ii) inhibiting the production of androgens by gonadal tissue via a negative feedback loop on pituitary gonadotrophin release; and (iii) regulating genes that suppress sebaceous gland growth or lipid production (25).