Department of Vascular Medicine, Academic Medical Center, Meibergdreef 9, Room F4-159.2, 1105 AZ, Amsterdam, The Netherlands.
Med Clin North Am. 2011 Sep;95(5):893-902. doi: 10.1016/j.mcna.2011.06.003.
Dyslipidemia associated with obesity and the metabolic syndrome is one of the central features contributing to the increased CV risk in these patients. In view of the pandemic of the metabolic syndrome, it is imperative to fully understand the mechanisms leading to the metabolic lipid phenotype before embarking upon optimal treatment strategies. The traditional concept that insulin resistance causes increased FFA flux via increased TG hydrolysis in adipose tissue is still of a central theme in the general hypothesis. The combination of increased hepatic VLDL secretion with impaired LPL-mediated TG clearance explains the hypertriglyceridemia phenotype of the metabolic syndrome. Hence, central IR may be an important factor contributing to peripheral hypertriglyceridemia. Recently recognized regulatory systems include the profound impact of the hypothalamus on TG secretion and glucose control. In addition, dysfunctional (or inflamed) intra abdominal adipose tissue has emerged as a potent regulator of dyslipidemia and IR. It will be a challenge to design novel treatment modalities that target “dysfunctional” fat or central IR to attempt to prevent the epidemic of CV disease secondary to the metabolic syndrome.
与肥胖和代谢综合征相关的血脂异常是导致这些患者心血管风险增加的核心特征之一。鉴于代谢综合征的流行，在制定最佳治疗策略之前，充分了解导致代谢性脂质表型的机制至关重要。传统观点认为，胰岛素抵抗通过增加脂肪组织中甘油三酯的水解导致游离脂肪酸通量增加，这仍然是一般假说的核心主题。肝 VLDL 分泌增加与 LPL 介导的甘油三酯清除受损相结合，解释了代谢综合征的高甘油三酯血症表型。因此，中心型胰岛素抵抗可能是导致外周型高甘油三酯血症的一个重要因素。最近发现的调节系统包括下丘脑对甘油三酯分泌和葡萄糖控制的深远影响。此外，功能失调（或炎症）的内脏脂肪组织已成为血脂异常和胰岛素抵抗的有力调节者。设计针对“功能失调”脂肪或中心型胰岛素抵抗的新型治疗方法以试图预防代谢综合征引起的心血管疾病流行将是一项挑战。
