The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, Karolinska University Hospital L1, SE-171 76 Stockholm, Sweden.
Department of Molecular Medicine and Surgery, Integrative Physiology, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
Sci Adv. 2021 Mar 12;7(11). doi: 10.1126/sciadv.abc2931. Print 2021 Mar.
Increased levels of apolipoprotein CIII (apoCIII), a key regulator of lipid metabolism, result in obesity-related metabolic derangements. We investigated mechanistically whether lowering or preventing high-fat diet (HFD)-induced increase in apoCIII protects against the detrimental metabolic consequences. Mice, first fed HFD for 10 weeks and thereafter also given an antisense (ASO) to lower apoCIII, already showed reduced levels of apoCIII and metabolic improvements after 4 weeks, despite maintained obesity. Prolonged ASO treatment reversed the metabolic phenotype due to increased lipase activity and receptor-mediated hepatic uptake of lipids. Fatty acids were transferred to the ketogenic pathway, and ketones were used in brown adipose tissue (BAT). This resulted in no fat accumulation and preserved morphology and function of liver and BAT. If ASO treatment started simultaneously with the HFD, mice remained lean and metabolically healthy. Thus, lowering apoCIII protects against and reverses the HFD-induced metabolic phenotype by promoting physiological insulin sensitivity.
载脂蛋白 CIII(apoCIII)水平升高是脂质代谢的关键调节因子,可导致肥胖相关的代谢紊乱。我们通过机制研究探讨了降低或预防高脂肪饮食(HFD)诱导的 apoCIII 增加是否可以预防有害的代谢后果。首先用 HFD 喂养小鼠 10 周,然后给予反义寡核苷酸(ASO)以降低 apoCIII,即使保持肥胖,4 周后也已显示出 apoCIII 水平降低和代谢改善。延长 ASO 治疗由于脂肪酶活性增加和受体介导的肝脏脂质摄取而逆转代谢表型。脂肪酸被转移到生酮途径,酮体被用于棕色脂肪组织(BAT)。这导致没有脂肪积累,并保留肝脏和 BAT 的形态和功能。如果 ASO 治疗与 HFD 同时开始,小鼠保持苗条和代谢健康。因此,降低 apoCIII 通过促进生理性胰岛素敏感性来预防和逆转 HFD 诱导的代谢表型。