Metabolic Syndrome and Skin Diseases

Abstract

The increasing prevalence of Metabolic syndrome (MetS) is a worldwide health problem, and the association between MetS and skin diseases has recently attracted growing attention. In this review, we summarize the associations between MetS and skin diseases, such as psoriasis, acne vulgaris, hidradenitis suppurativa, androgenetic alopecia, acanthosis nigricans, and atopic dermatitis. To discuss the potential common mechanisms underlying MetS and skin diseases, we focus on insulin signaling and insulin resistance, as well as chronic inflammation including adipokines and proinflammatory cytokines related to molecular mechanisms. A better understanding of the relationship between MetS and skin diseases contributes to early diagnosis and prevention, as well as providing clues for developing novel therapeutic strategies.

Transcriptome-Wide m6A Methylation in Skin Lesions From Patients With Psoriasis Vulgaris

“…For example, in PP vs. NN, hypermethylated DMRs in PP were specifically associated with the G-protein-coupled receptor signaling pathway ( Figure 2B and Supplementary Data 3), including cannabinoid receptors that are involved in the proliferation/differentiation and immune activity of keratinocytes, indicating that these hypermethylated DMRs may participate in critical processes of psoriasis vulgaris (Tóth et al, 2019). Meanwhile, hypomethylated DMRs in PP were specifically associated with the polyol metabolic process (Figure 2C and Supplementary Data 3), which may be related to the previous epidemiological finding that psoriasis patients tended to suffer from metabolic diseases (Hu et al, 2019). When compared with PN, hypermethylated DMRs in PP were specifically associated with cell cycle-related items (e.g., mitotic cell cycle process, mitotic cell cycle, cell cycle, and mitotic nuclear division) ( Supplementary Figure 5A and Supplementary Data 3), while hypomethylated DMRs in PP were specifically associated with negative regulation of cellular component movement, locomotion, and learning (Supplementary Figure 5B and Supplementary Data 3).…”

What causes hidradenitis suppurativa ?—15 years after

“…128 As a result, reduced adiponectin and increased resistin serum levels have been identified as surrogate biomarkers for insulin resistance in patients with HS. 129 Resistin and visfatin were proposed to be involved in HS pathogenesis. 130 Moreover, nutritional excess in metabolic syndrome can lead to adipose tissue expansion and adipocyte hypertrophy associated with increased release of inflammatory mediators.…”

“…In subcutaneous adipose tissue, this can cause cutaneous inflammatory responses but also spill-over of inflammatory mediators into the systemic circulation contributing to progression of the metabolic syndrome. 129,131 Among the inflammatory mediators produced by adipocytes are arachidonic acid-derived polyunsaturated fatty acids (PUFAs) of the ω6 class, the so-called eicosanoids. High-fat diet and in particular western diet containing a high ω-6/ω-3 ratio can further enhance the release of arachidonic acid-derived lipid mediators by adipocytes.…”

Adipokines as Biomarkers of Atopic Dermatitis in Adults

“…The main target of this polypeptide are receptors located in the ventromedial nucleus of the hypothalamus, whose activation reduces satiety and raises energy consumption. Leptin is also synthesized by keratinocytes and endothelial cells and its receptors are present in numerous peripheral tissues [44,45]. Leptin was originally thought to polarize Th lymphocytes into Th1.…”

“…Leptin was originally thought to polarize Th lymphocytes into Th1. The immunogenic effects of leptin include the formation of proinflammatory cytokines such as TNF-α, IL-1, IL-6, and IL-8 [46], and the promotion of monocyte diapedesis through the endothelial wall involving the activation of adhesion molecules [44]. Recent studies on human leukocytes show that leptin exerts no effect on neutrophil chemotaxis; instead, leptin is a potent activator of peripheral B lymphocytes and IL-4 and IL-13 secretion by eosinophils and basophils [46].…”