Metabolic syndrome and dermatological diseases: association and treatment

Abstract

Metabolic syndrome (MetS) is a clinical syndrome associated with cardiovascular disease, diabetes, obesity, and dyslipidemia. Its primary features include dyslipidemia, hypertension, abdominal obesity, and insulin resistance (IR). Recently, research has revealed that MetS is not only a manifestation of internal metabolic disturbances but is also closely associated with various dermatological conditions, including inflammatory skin diseases, autoimmune skin diseases, and skin tumors. These studies have clarified the complex mechanisms underlying the interaction between MetS and these skin diseases, including IR, chronic inflammatory responses, and oxidative stress. This review summarizes the association between MetS and related dermatological conditions and their shared physiological mechanisms. It aims to provide clinicians with new therapeutic strategies and preventive measures to improve the treatment outcomes and quality of life of patients with skin conditions.

Keywords: Chronic inflammation; Dermatological diseases; Insulin resistance; Lipid metabolism; Metabolic syndrome; Oxidative stress.

Fig. 1

The interactions between chronic inflammatory pathways, MetS, and various skin diseases. These interactions are primarily influenced by dietary habits, immune responses, IR, and metabolic complications. High consumption of sugar, carbohydrates, and dairy activates the PI3K/AKT and mTORC1 pathways, leading to gut microbiota dysbiosis, particularly affecting Akkermansia muciniphila. Th17 and Th1 cell activation increases the secretion of pro-inflammatory cytokines (TNF-α, IL-22, IL-17, IFN-γ, and IL-2/4/6/10), worsening psoriasis through the JAK-STAT and NF-κB pathways, which inhibit apoptosis and promote angiogenesis. NF-κB activation leads to IR, higher insulin and C-peptide levels, and increased androgen levels, intensifying sebaceous gland activity and promoting acne. Obesity is associated with Th1/Th22 cell activation and elevated IL-3/4 levels, resulting in adipokine changes (abnormal adiponectin and elevated resistin) and endothelial inflammation (McP-1, VCAM-1, and ICAM-1), indicating autoimmune dysfunction. Dysregulated lipid production promotes Cutibacterium acnes colonization, exacerbating acne. Enhanced IGF-1 and increased EGF and TGF-β2 levels cause excessive cell differentiation and proliferation, contributing to psoriasis and SLE. Oxidative stress damages intracellular proteins and DNA, increasing the risk of autoimmune disorders, including vitiligo and SLE. CVD risk is elevated because of TLR4/JNK/MAPK pathway activation, increasing TNF-α, IL-1β, and IL-6 levels. Mitochondrial dysfunction leads to diabetes, with lipid ROS causing further cellular damage. This overview highlights the complex relationship between diet, immune response, MetS, and skin diseases, providing a foundation for future research and targeted therapeutic strategies

Fig. 2

Relationship between MetS and skin diseases. MetS is associated with various skin diseases through multiple pathways. These pathways include oxidative stress leading to DNA and protein damage, IR contributing to hyperinsulinemia, lipid metabolism abnormalities affecting steroid synthesis, chronic inflammation mediated by cytokines, including TNF-α and IL-1, and genetic factors influencing susceptibility to conditions such as psoriasis and vitiligo. The interconnected mechanisms highlight the complexity of managing skin diseases in patients with MetS