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首页> 外文期刊>Current opinion in lipidology >Advanced glycation endproducts and its receptor for advanced glycation endproducts in obesity
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Advanced glycation endproducts and its receptor for advanced glycation endproducts in obesity

机译：晚期糖基化终产物及其在肥胖症中晚期糖基化终产物的受体

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PURPOSE OF REVIEW: To highlight the potential importance of advanced glycation endproducts (AGEs) and advanced-lipoxidation endproducts (ALEs) in obesity and obesity-related complications, and the contribution of the receptor for advanced glycation endproducts (RAGE) and the glyoxylase defense system therein. RECENT FINDINGS: Formation of AGEs/ALEs and its precursors, including methylglyoxal (MGO), are increased in conditions characterized by hyperglycemia, hyperlipidemia and enhanced oxidative stress. This metabolic profile is generally considered typical for obesity. Increased plasma and/or tissue levels of MGO and of specific AGEs/ALEs, such as N-(carboxymethyl)lysine (CML), in obesity have recently been described. In addition to increased formation, the suppressed defense system in obesity against AGEs/ALEs formation, that is, the glyoxylase system, will further contribute to AGEs/ALEs formation in obesity. AGEs/ALEs are not inert. In-vitro studies showed that AGEs induced the production of inflammatory mediators in adipocytes and macrophages via RAGE activation, which may subsequently contribute to the development of obesity-related complications. SUMMARY: The recognition of an enhanced AGEs/ALEs formation in adipose tissue and the biological consequences thereof may lead to a further understanding of underlying mechanisms in dysregulated production of adipokines in obesity. ? 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins.
机译：审查目的：强调晚期糖基化终产物（AGEs）和晚期脂质氧化终产物（ALEs）在肥胖和肥胖相关并发症中的潜在重要性，以及受体对晚期糖基化终产物（RAGE）和乙醛酸酶防御系统的贡献在其中。最近的发现：在以高血糖，高血脂和氧化应激为特征的疾病中，AGEs / ALE及其前体（包括甲基乙二醛（MGO））的形成增加。通常认为这种代谢特征是肥胖的典型特征。最近已经描述了肥胖中MGO和特定AGE / ALE例如N-（羧甲基）赖氨酸（CML）的血浆和/或组织水平升高。除了增加形成，肥胖中针对AGEs / ALEs形成的防御系统的抑制，即乙醛酸酶系统，将进一步促进肥胖中AGEs / ALEs的形成。 AGEs / ALEs不是惰性的。体外研究表明，AGEs通过RAGE激活诱导脂肪细胞和巨噬细胞中炎性介质的产生，这可能随后导致肥胖相关并发症的发生。摘要：认识到在脂肪组织中增强的AGEs / ALEs形成及其生物学后果可能导致人们进一步了解肥胖中脂肪因子产生失调的潜在机制。 ？ 2013威科集团健康|利平科特·威廉姆斯和威尔金斯。

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