Acne, a disorder of pilosebaceous units, is one of the common skin disorders worldwide and is seen primarily in adolescents. Androgens have been recognized to increase the size of sebaceous glands, increase sebum production, and stimulate keratinocyte proliferation, thereby causing acne. Physiologic insulin resistance during puberty leads to hyperinsulinemia, which in turn leads to increased androgen synthesis
1; both hyperinsulinemia and hyperandrogenemia lead to acne formation. Hyperinsulinemia increases the level of free insulin-like growth factor 1 (IGF-1) and decreases the level of insulin-like growth factor binding protein 3.
2 Insulin-like growth factor 1 increases the mean facial sebum excretion rate, increases serum levels of dihydrotestosterone and dehydroepiandrosterone sulfate, and causes sebocyte proliferation.
3 Hyperinsulinemia also increases levels of epidermal growth factors and transforming growth factor β, which elevate levels of plasma nonesterified fatty acids, thus causing inflammation and acne.
4 Insulin resistance plays a pivotal role in the cluster of metabolic abnormalities that are components of the metabolic syndrome.