4.6 Article

Adipochemokines induced by ultraviolet irradiation contribute to impaired fat metabolism in subcutaneous fat cells

期刊

BRITISH JOURNAL OF DERMATOLOGY
卷 178, 期 2, 页码 492-501

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WILEY
DOI: 10.1111/bjd.15907

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资金

  1. Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science, ICT & Future Planning [NRF-2013R1A1A1065100, NRF-2015R1D1A1A01059179]
  2. Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI) - Ministry of Health & Welfare, Republic of Korea [HI14C1277]

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BackgroundAdipose tissue is now appreciated as the pivotal regulator of metabolic and endocrine functions. Subcutaneous (SC) fat, in contrast to visceral fat, may protect against metabolic syndrome and systemic inflammation. We demonstrated that chronic as well as acute ultraviolet (UV) irradiation to the skin induces loss of underlying SC fat. UV-irradiated SC fat may produce chemokines or cytokines that modulate lipid homeostasis and secretion of adipokines. ObjectivesTo elucidate UV-induced specific adipochemokines implicated in UV-induced modulation of SC fat. MethodsPrimary cultured adipocytes were treated with conditioned medium from UV- or sham-irradiated skin cells. Young and older healthy participants provided SC fat from sun-exposed and sun-protected skin. Sun-protected skin from other participants was irradiated with UV. Differentially expressed adipochemokines were screened by cytokine array, and confirmed invitro and invivo. The functions of select adipochemokines involved in lipid metabolism were examined via short interfering RNA-mediated knockdown of cognate receptors. ResultsSpecific adipochemokines, including C-X-C motif chemokine (CXCL) family members such as CXCL5/ENA-78, and C-C motif chemokine (CCL) family members such as CCL20/MIP-3 and CCL5/RANTES, were greatly induced in SC fat by UV exposure. They could impair triglyceride synthesis via downregulation of lipogenic enzymes and sterol regulatory element-binding protein-1 through their respective cognate receptors, CXC chemokine receptor type (CXC-R)2, C-C chemokine receptor type (CCR)-6, and CCR-5. In addition, UV irradiation induced infiltration of adipose tissue macrophages responsible for the secretion of several chemokines into SC fat. ConclusionsThese UV-induced adipochemokines may be implicated in the reduction of lipogenesis in SC fat, leading to impairment of fat homeostasis and associated comorbidities such as obesity. What's already known about this topic? Acute and chronic ultraviolet (UV) exposure induces loss of underlying subcutaneous fat. What does this study add? UV-induced adipochemokines such as C-X-C motif chemokine 5, C-C motif chemokine (CCL)5 and CCL20 reduce lipogenesis. What is the translational message? UV-induced adipochemokines lead to fat homeostasis impairment and related comorbidities. Linked Comment:Balato and Raimondo. Br J Dermatol 2018; 178:327-328. Respond to this article

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