Metabolic syndrome (MetS) has been associated with osteoarthritis (OA). Leptin, which is one of the markers of MetS, has been associated with OA pathophysiology. This study aimed to provide an update on the association between MetS and OA and on the potential role of leptin in OA. In this review, we summarized the current knowledge of the association between MetS and OA and updated the evidence on the potential role of leptin in OA. Clinical studies have investigated the epidemiologic association between MetS or its components and OA. Results suggested strong epidemiologic associations between MetS and OA, especially in the Asian population. Animal studies also indicated that metabolic dysregulation may lead to OA pathogenesis. The systemic role of MetS in OA pathophysiology is associated with obesity-related inflammation, the beneficial role of n-3 polyunsaturated fatty acids and deleterious role of cholesterol, physical inactivity, hypertension-induced subchondral ischemia, dyslipidemia-induced ectopic lipid deposition in chondrocytes, hyperglycemia-induced local effects of oxidative stress and advanced glycation end-products, low-grade systemic inflammation, and obesity-related adipokines by inducing the expression of proinflammtory factors. Leptin levels in serum/plasma and synovial fluid were associated with joint pain, radiographic progression, bone formation biomarkers, cartilage volume, knee OA incidence, and total joint arthroplasty in OA patients. Elevated leptin expression and increased effect of leptin on infrapatellar fat pad, synovium, articular cartilage, and bone were also involved in the pathogenesis of OA. Current knowledge indicates a convincing epidemiologic association between MetS and OA, especially in the Asian population. Animal studies have also shown that metabolic dysregulation may lead to OA pathogenesis. Accumulating evidence suggests that leptin may play a potential role in OA pathogenesis. Therefore, leptin and its receptor may be an emerging target for intervention in metabolic-associated OA.

中文翻译：

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代谢综合征与骨关节炎之间关系的最新进展以及瘦素在骨关节炎中的潜在作用

代谢综合征 (MetS) 与骨关节炎 (OA) 相关。瘦素是 MetS 的标志物之一，与 OA 病理生理学有关。本研究旨在提供有关 MetS 与 OA 之间关联以及瘦素在 OA 中的潜在作用的最新信息。在这篇综述中，我们总结了目前关于 MetS 和 OA 之间关联的知识，并更新了关于瘦素在 OA 中潜在作用的证据。临床研究调查了 MetS 或其组成部分与 OA 之间的流行病学关联。结果表明 MetS 和 OA 之间存在很强的流行病学关联，尤其是在亚洲人群中。动物研究还表明，代谢失调可能导致 OA 发病机制。MetS 在 OA 病理生理学中的全身作用与肥胖相关炎症有关，n-3 多不饱和脂肪酸的有益作用和胆固醇的有害作用、缺乏身体活动、高血压引起的软骨下缺血、血脂异常引起的软骨细胞异位脂质沉积、高血糖引起的氧化应激和晚期糖基化终产物的局部影响、低通过诱导促炎因子的表达来调节全身性炎症和肥胖相关脂肪因子。血清/血浆和滑液中的瘦素水平与 OA 患者的关节疼痛、放射学进展、骨形成生物标志物、软骨体积、膝关节 OA 发病率和全关节置换术有关。瘦素表达升高和瘦素对髌下脂肪垫、滑膜、关节软骨和骨骼的影响增加也参与了 OA 的发病机制。目前的知识表明 MetS 和 OA 之间存在令人信服的流行病学关联，尤其是在亚洲人群中。动物研究还表明，代谢失调可能导致 OA 发病机制。越来越多的证据表明瘦素可能在 OA 发病机制中发挥潜在作用。因此，瘦素及其受体可能是干预代谢相关 OA 的新兴靶点。