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In particular, the reduction of insulin levels would first of all inhibit the activity of IGF- 1, blocking a series of events involved in the pathogenesis of acne, such as hyperproliferation of keratinocytes in the pilosebaceous ducts, androgen-mediated hyperproduction of sebum, altered desquamation of the follicular epithelium, and proliferation of Propionibacterium acnes in the stratum corneum [66, 67]
Studies of cultured human vascular endothelial cells (HUVECs) have demonstrated that competitive inhibition of G6PD in the HUVECs using 6-aminonicotinamide (6-AN) or G6PD knockdown downregulate eNOS activity and nitrate levels
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