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肥胖、炎症与胰岛素抵抗的相关性:信号通路与治疗干预的新视角。

Association between obesity, inflammation and insulin resistance: Insights into signaling pathways and therapeutic interventions.

机构信息

Department of Biochemistry, School of Bioengineering and Biosciences, Lovely Professional University, Phagwara, Punjab, India

Department of Biotechnology, School of Bioengineering and Biosciences, Lovely Professional University, Phagwara, Punjab, India

出版信息

Diabetes Res Clin Pract. 2023 Jun;200:110691. doi: 10.1016/j.diabres.2023.110691. Epub 2023 May 6.

Abstract

Obesity, a metabolic disorder, is becoming a worldwide epidemic that predominantly increases the risk for various diseases including metabolic inflammation, insulin resistance, and cardiovascular diseases. However, the mechanisms that link obesity with other metabolic diseases are not completely understood. In obesity, various inflammatory pathways that cause inflammation in adipose tissue of an obese individual become activated and exacerbate the disease. Obesity-induced low-grade metabolic inflammation perturbates the insulin signaling pathway and leads to insulin resistance. Researchers have identified several pathways that link the impairment of insulin resistance through obesity-induced inflammation like activation of Nuclear factor kappa B (NF-κB), suppressor of cytokine signaling (SOCS) proteins, cJun-N-terminal Kinase (JNK), Wingless-related integration site (Wnt), and Toll-like receptor (TLR) signaling pathways. In this review article, the published studies have been reviewed to identify the potential and influential role of different signaling pathways in the pathogenesis of obesity-induced metabolic inflammation and insulin resistance along with the discussion on potential therapeutic strategies. Therapies targeting these signaling pathways show improvements in metabolic diseases associated with obesity, but require further testing and confirmation through clinical trials.

摘要

肥胖是一种代谢紊乱,正在成为一种全球性的流行疾病,主要增加了各种疾病的风险,包括代谢性炎症、胰岛素抵抗和心血管疾病。然而,将肥胖与其他代谢疾病联系起来的机制尚不完全清楚。在肥胖中,导致肥胖个体脂肪组织炎症的各种炎症途径被激活并使疾病恶化。肥胖引起的低度代谢性炎症扰乱了胰岛素信号通路,导致胰岛素抵抗。研究人员已经确定了几种途径,通过肥胖引起的炎症来联系胰岛素抵抗的损害,如核因子 kappa B(NF-κB)的激活、细胞因子信号抑制物(SOCS)蛋白、cJun-N-末端激酶(JNK)、无翅相关整合位点(Wnt)和 Toll 样受体(TLR)信号通路。在这篇综述文章中,回顾了已发表的研究,以确定不同信号通路在肥胖引起的代谢性炎症和胰岛素抵抗发病机制中的潜在和重要作用,并讨论了潜在的治疗策略。针对这些信号通路的治疗方法显示出对与肥胖相关的代谢性疾病的改善,但需要通过临床试验进一步测试和确认。

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