Assessment of Serum Apelin Levels and its Relation to Insulin Resistance in Acne Vulgaris Patients

Abstract

cne vulgaris is a chronic inflammatory disease of the pilosebaceous unit, and it is one of the most common dermatological conditions worldwide. Some of the key mechanisms of pathogenesis are the disturbed sebaceous gland activity associated with excess sebum production and alterations in sebum fatty acid composition, dysregulation of the hormone microenvironment, interaction with neuropeptides, follicular hyperkeratinization, and induction of inflammation and dysfunction of the innate and adaptive immunity. Apelin is a new peptide identified as the endogenous ligand of the G protein-coupled receptor, APJ. Apelin is secreted from brain, placenta, lungs, heart, kidneys also from the veins of coronary artery, saphenous vein, kidneys and adrenal gland. Apelin is secreted as preproapelin, that has the sequence of 77 amino acids, preproapelin is then fragmented by protease and apelin will be named as Apelin-13, Apelin-17 and Apelin-36, depending on the number of amino acids it contains. Apelin-36 and apelin-13 represent the predominant and most active isoforms. The increase in blood glucose stimulates insulin secretion which decreases the availability of binding protein for insulin-like growth factor 1 (IGF-1) which facilitates its effects on basal keratinocyte proliferation. Also, insulin induces the synthesis of androgens which in turn cause acne, and this explains the relation between acne vulgaris and insulin resistance.