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Abstract Acne vulgaris is one of the most common skin diseases all over the world. Adolescent and young adults are frequently involved but older individuals are not spared. It is characterized by an inflammatory reaction in the pilosbeceous follicles of the face and trunk. It is associated with androgen-mediated seborrhea, ductal hypercornification and the production of inflammatory mediators by P. acne and P. granulosum trapped within the duct by the cornified plug. Acne vulgaris pathogenesis is multifactorial. The interplay between the PSU, microbial agents, and hormonal factors have been proposed as major elements in the pathogenesis of AV. Although acne is considered an androgen-dependent disease, the occurrence of acne doesn’t correlate with plasma androgen levels. Physiologic IR during puberty leads to hyperinsulinemia, which leads to increased androgen synthesis; both hyperinsulinemia and hyperandrogenemia lead to acne formation. There is a positive relationship between circulating irisin and IR that is mediated by several possible pathophysiological mechanisms. Elevated irisin levels are associated with increased levels of inflammatory markers that lead to IR. Despite there is a transient increase in response to acute bouts of exercise, irisin decreases following chronic exercise training, along with ameliorated IR. And so, non-diabetic patients with PCOs, obesity, or metabolic syndrome are more likely to be physically inactive and show severe IR. Hence it seems plausible to assume that circulating irisin is positively associated with IR. In addition to that more carbohydrate intake will result in higher irisin levels since high-carbohydrate and/or high-fat diets induce inflammation and oxidative stress, leading to IR consequently. This observation provides further support for the positive association between circulating irisin and IR. |