胰岛素抵抗，即对胰岛素生物反应的降低，是许多疾病（如肥胖、2型糖尿病、心血管疾病、多囊卵巢综合征、某些癌症和神经退行性疾病）的风险因素之一。其主要原因之一是慢性低度炎症，通过促炎性通路（如c-Jun N端激酶（JNK）通路和核因子kappa B（NFκB）通路）介导。白细胞介素(IL)-38是一种新发现的细胞因子，属于IL-1家族。通过IL-38可能通过三条假设途径与特定受体结合并抑制其促炎活性。这些通路与白细胞介素36受体(IL-36R)、IL-1受体辅助蛋白样1（IL1RAPL1）和IL-1受体1(IL1R1)有关。有研究表明IL-38与改善胰岛素敏感性有关，可能通过测量胰岛素抵抗患者的血清IL-38浓度或与胰岛素抵抗指数相关。然而，关于IL-38本身的生物活性及其在胰岛素抵抗发病机制中的作用仍有许多问题有待解答。本研究的目标是展示IL-38及其生物活性、假定的信号通路、与胰岛素抵抗的联系以及对IL-38研究的未来展望。我们提出，与IL-38相关的信号传导可能是治疗胰岛素抵抗及相关疾病的潜在靶点。版权所有© Bentham Science Publishers；如有任何疑问，请发送电子邮件至epub@benthamscience.net。

Insulin resistance, i.e., decreased biological response to insulin, is a risk factor for many diseases, such as obesity, type 2 diabetes (T2DM), cardiovascular disease, polycystic ovary syndrome, some forms of cancer and neurodegenerative diseases. One of its main causes is chronic low-grade inflammation, mediated by the proinflammatory pathways, such as the c-Jun N-terminal kinase (JNK) pathway and the nuclear factor kappa B (NFκB) pathway. Interleukin (IL)-38 (IL-38) is a newly discovered cytokine that belongs to the IL-1 family. There are three hypothetical pathways through which IL-38 may bind to the specific receptors and inhibit their proinflammatory activity. Those pathways are associated with IL-36 receptor (IL-36R), IL-1 receptor accessory protein-like 1 (IL1RAPL1) and IL-1 receptor 1 (IL1R1). There are studies linking IL-38 to improve insulin sensitivity through the difference in serum IL-38 in patients with insulin resistance or the correlation of IL-38 concentrations with insulin resistance indexes. However, many questions still remain regarding the biological activity of IL-38 itself and its role in the pathogenesis of insulin resistance. The goal of this study is to showcase IL-38, its biological activity, hypothesized signaling pathways, connection with insulin resistance and future perspectives of research on IL-38. We present that IL-38 associated signaling can be a potential target for the treatment of insulin resistance and associated diseases.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.