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Etiopathogenesis of acanthosis nigricans: Insulin has been demonstrated to cross dermoepidermal junction (DEJ) to reach keratinocytes. At low concentrations, insulin regulates carbohydrate, lipid and protein metabolism and can weakly promote growth by binding to “classic” insulin receptors. At higher concentrations, however, insulin can exert more potent growth-promoting effects through binding to insulin-like growth factor 1 receptors (IGF-1Rs) that are similar in size and subunit structure to insulin receptors, but bind IGF-1 with 100- to 1000-fold greater affinity than insulin. The binding stimulates proliferation of keratinocytes and fibroblasts, leading to AN | Jeong KH, Oh SJ, Chon S, Lee MH. Generalized acanthosis nigricans related to type B insulin resistance syndrome: A case report. Cutis. 2010;86:299–302. (Image courtesy of Dr. Ashwin Kosambia, Consultant Dermatologist, Mumbai, India)

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