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脂肪组织功能障碍与高三酰甘油血症:机制与治疗。

Adipose tissue dysfunction and hypertriglyceridemia: mechanisms and management.

机构信息

Department of Vascular Medicine, University Medical Center, Utrecht, the Netherlands Department of Metabolic and Endocrine Diseases, University Medical Center, Utrecht, the Netherlands.

出版信息

Obes Rev. 2011 Oct;12(10):829-40. doi: 10.1111/j.1467-789X.2011.00900.x. Epub 2011 Jul 12.

DOI:10.1111/j.1467-789X.2011.00900.x
PMID:21749607
Abstract

Elevated plasma triglyceride levels, as often seen in obese subjects, are independently associated with an increased risk of cardiovascular diseases. By secreting adipokines (such as adiponectin and leptin) and other proteins (such as lipoprotein lipase and cholesteryl ester transferase protein), adipose tissue affects triglyceride metabolism. In obesity, adipocyte hypertrophy leads to many changes in adipocyte function and production of anti- and pro-inflammatory cytokines. Furthermore, free fatty acids are released into the circulation contributing to insulin resistance. Adipose tissue dysfunction will eventually lead to abnormalities in lipid metabolism, such as hypertriglyceridemia (due to increased hepatic very-low-density lipoprotein production and decreased triglyceride hydrolysis), small dense low-density lipoprotein particles, remnant lipoproteins and low high-density lipoprotein cholesterol levels, all associated with a higher risk for the development of cardiovascular diseases. The clinical implications of elevated plasma triglycerides are still a matter of debate. Understanding the pathophysiology of adipose tissue dysfunction in obesity, which is becoming a pandemic condition, is essential for designing appropriate therapeutic interventions. Lifestyle changes are important to improve adipose tissue function in obese patients. Pharmacological interventions to improve adipose tissue function need further evaluation. Although statins are not very potent in reducing plasma triglycerides, they remain the mainstay of therapy for cardiovascular risk reduction in high-risk patients.

摘要

血浆甘油三酯水平升高,如肥胖患者常见的情况,与心血管疾病风险增加独立相关。脂肪组织通过分泌脂联素和瘦素等脂肪因子和脂蛋白脂肪酶和胆固醇酯转移蛋白等其他蛋白质,影响甘油三酯代谢。在肥胖中,脂肪细胞肥大导致脂肪细胞功能和产生抗炎和促炎细胞因子的许多变化。此外,游离脂肪酸被释放到循环中,导致胰岛素抵抗。脂肪组织功能障碍最终将导致脂质代谢异常,如高甘油三酯血症(由于肝脏极低密度脂蛋白产生增加和甘油三酯水解减少)、小而密的低密度脂蛋白颗粒、残粒脂蛋白和低高密度脂蛋白胆固醇水平,所有这些都与心血管疾病发展的风险增加相关。血浆甘油三酯升高的临床意义仍存在争议。了解肥胖中脂肪组织功能障碍的病理生理学,这在全球范围内已经成为一种流行疾病,对于设计适当的治疗干预措施至关重要。生活方式的改变对于改善肥胖患者的脂肪组织功能很重要。改善脂肪组织功能的药物干预需要进一步评估。尽管他汀类药物在降低血浆甘油三酯方面效果并不十分显著,但它们仍然是高危患者降低心血管风险的主要治疗方法。

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