Insulin Resistance and Skin Diseases

Abstract

In medical practice, almost every clinician may encounter patients with skin disease. However, it is not always easy for physicians of all specialties to face the daily task of determining the nature and clinical implication of dermatologic manifestations. Are they confined to the skin, representing a pure dermatologic event? Or are they also markers of internal conditions relating to the patient's overall health? In this review, we will discuss the principal cutaneous conditions which have been linked to metabolic alterations. Particularly, since insulin has an important role in homeostasis and physiology of the skin, we will focus on the relationships between insulin resistance (IR) and skin diseases, analyzing strongly IR-associated conditions such as acanthosis nigricans, acne, and psoriasis, without neglecting emerging and potential scenarios as the ones represented by hidradenitis suppurativa, androgenetic alopecia, and hirsutism.

Acanthosis Nigricans during an HAIR-AN syndrome: "The Tree That Hides the Forest"

“…It may be indicative of either a paraneoplastic syndrome or an insulin resistance. In the latter case we will conclude that it is a benign AN [1][2][3][4]. The benign AN is an important indicator of hyperinsulinemia due to insulin resistance.…”

“…The benign AN is an important indicator of hyperinsulinemia due to insulin resistance. It may be associated with genetic syndromes or developed after taking certain drugs or on obesity grounds [1,2,[4][5][6]. We report a case of benign AN that reveals a genetic insulin resistance syndrome.…”

“…Hyperinsulinemia and associated hyperandrogenism will cause other metabolic, gynecological and psychiatric comorbidities. [1,2,4,5,9,10].…”

Influência do Índice de Massa Corporal e da Dieta na Fisiopatologia da Acne Vulgaris

“…14 Tasli et al mostraram também que os polimorfismos do IGF-1 podem contribuir para um aumento da Figura 1 -Mecanismos pelos quais a IGF-1 potencia a ação andró-gena. [8][9][10] DHT -dihidrotestosterona; DHEA -dehidroepiandrosterona; FoxO1 -proteína forkhead box 01; AR -receptor do androgénio.…”

“…8 A IGF-1 atua no recetor da IGF-1 (IGF1R), provocando uma hiperatividade da cascata de sinalização fosfatidilinositol 3 quinase (PI3K)-proteina B quinase (AKT), potenciando a ação androgénica por 3 mecanismos: i) Hiperactividade da enzima 5-alpha reductase, aumentando assim a conversão intracutânea de testosterona em dihidrotestosterona (DHT); ii) Estimulação da produção de dehidroepiandrosterona (DHEA) na glândula suprarrenal e da testosterona na gónada; iii) Translocação para o citoplasma e inibição da proteína nuclear forkhead box 01 (FoxO1), responsável por inibir o recetor celular dos androgénios. [8][9][10] ( Fig. 1) A ação da IGF-1 varia também com a atividade da proteína de ligação à IGF-3 (IGFBP-3), estando a sua bioatividade aumentada quando diminui a IGFBP-3.…”