Abstract：
BACKGROUND: In normal circumstances, AT secretes anti-inflammatory adipokines (AAKs) which regulates lipid metabolism, insulin sensitivity, vascular hemostasis, and angiogenesis. However, during obesity AT dysfunction occurs and leads to microvascular imbalance and secretes several pro-inflammatory adipokines (PAKs), thereby favoring atherogenic dyslipidemia and insulin resistance. Literature suggests decreased levels of circulating AAKs and increased levels of PAKs in obesity-linked disorders. Importantly, AAKs have been reported to play a vital role in obesity-linked metabolic disorders mainly insulin resistance, type-2 diabetes mellitus and coronary heart diseases. Interestingly, AAKs counteract the microvascular imbalance in AT and exert cardioprotection via several signaling pathways such as PI3-AKT/PKB pathway. Although literature reviews have presented a number of investigations detailing specific pathways involved in obesity-linked disorders, literature concerning AT dysfunction and AAKs remains sketchy. In view of the above, in the present contribution an effort has been made to provide an insight on the AT dysfunction and role of AAKs in modulating the obesity and obesity-linked atherogenesis and insulin resistance.
METHODS: \"Obesity-linked insulin resistance\", \"obesity-linked cardiometabolic disease\", \"anti-inflammatory adipokines\", \"pro-inflammatory adipokines\", \"adipose tissue dysfunction\" and \"obesity-linked microvascular dysfunction\" are the keywords used for searching article. Google scholar, Google, Pubmed and Scopus were used as search engines for the articles.
CONCLUSIONS: This review offers an overview on the pathophysiology of obesity, management of obesity-linked disorders, and areas in need of attention such as novel therapeutic adipokines and their possible future perspectives as therapeutic agents.
METHODS: \"Obesity-linked insulin resistance\", \"obesity-linked cardiometabolic disease\", \"anti-inflammatory adipokines\", \"pro-inflammatory adipokines\", \"adipose tissue dysfunction\" and \"obesity-linked microvascular dysfunction\" are the keywords used for searching article. Google scholar, Google, Pubmed and Scopus were used as search engines for the articles.
CONCLUSIONS: This review offers an overview on the pathophysiology of obesity, management of obesity-linked disorders, and areas in need of attention such as novel therapeutic adipokines and their possible future perspectives as therapeutic agents.
摘要：
背景：在正常情况下，AT分泌抗炎脂肪因子（AAKs），调节脂质代谢，胰岛素敏感性，血管止血,和血管生成。然而,在肥胖期间，AT功能障碍发生并导致微血管失衡并分泌几种促炎脂肪因子（PAKs），从而有利于致动脉粥样硬化的血脂异常和胰岛素抵抗。文献表明，肥胖相关疾病中循环AAK水平降低，PAK水平升高。重要的是,据报道，AAKs在肥胖相关的代谢紊乱中起着至关重要的作用，主要是胰岛素抵抗。2型糖尿病和冠心病。有趣的是,AAKs通过PI3-AKT/PKB途径等几种信号通路抵消AT中的微血管失衡并发挥心脏保护作用。尽管文献综述已经提出了许多研究，详细介绍了与肥胖相关的疾病有关的特定途径，关于AT功能障碍和AAKs的文献仍然是粗略的。鉴于上述情况,在目前的贡献中，已经努力提供关于AT功能障碍和AAK在调节肥胖和肥胖相关的动脉粥样硬化和胰岛素抵抗中的作用的见解。
方法：“肥胖相关的胰岛素抵抗”，“肥胖相关的心脏代谢疾病”，“抗炎脂肪因子”，“促炎性脂肪因子”，“脂肪组织功能障碍”和“肥胖相关的微血管功能障碍”是用于搜索文章的关键词。谷歌学者，Google,Pubmed和Scopus被用作文章的搜索引擎。
结论：这篇综述概述了肥胖的病理生理学，肥胖相关疾病的管理，以及需要关注的领域，例如新型治疗性脂肪因子及其作为治疗剂的未来前景。
方法：“肥胖相关的胰岛素抵抗”，“肥胖相关的心脏代谢疾病”，“抗炎脂肪因子”，“促炎性脂肪因子”，“脂肪组织功能障碍”和“肥胖相关的微血管功能障碍”是用于搜索文章的关键词。谷歌学者，Google,Pubmed和Scopus被用作文章的搜索引擎。
结论：这篇综述概述了肥胖的病理生理学，肥胖相关疾病的管理，以及需要关注的领域，例如新型治疗性脂肪因子及其作为治疗剂的未来前景。
