Center for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute, Orlando, FL 32827, USA.
Department of Pharmacology & Experimental Therapeutics, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
Prostaglandins Leukot Essent Fatty Acids. 2018 Sep;136:161-169. doi: 10.1016/j.plefa.2017.01.002. Epub 2017 Jan 11.
To further understand the role of lipogenesis and lipotoxicity in the development of obesity and diabetes, lipidomes of various organs from ob/ob mice and their wild type controls were analyzed by shotgun lipidomics at 10, 12, and 16 weeks of age. We observed that the amounts of fatty acyl (FA) chains corresponding to those from de novo synthesis (e.g., 16:0, 16:1, and 18:1 FA) were substantially elevated in ob/ob mice, consistent with increased expression of genes and proteins involved in biosynthesis. Polyunsaturated fatty acid species were moderately increased in the examined tissues of ob/ob mice, since they can only be absorbed from diets or elongated from the ingested n-3 or n-6 FA. Different profiles of FA chains between ob/ob mouse liver and skeletal muscle reflect diverging lipogenesis pathways in these organs. Amounts of vaccenic acids (i.e., 18:1(n-7) FA) in 12- and 16-week ob/ob mouse liver were significantly increased compared to their controls, indicating enhanced de novo synthesis of this acid through 16:1(n-7) FA in the liver starting at 12 weeks of age. Coincidentally, synthesis of triacylglycerol from monoacylglycerol in the liver was also increased in ob/ob mice starting at 12 weeks of age, as revealed by simulation of triacylglycerol synthesis. Moreover, levels of lipotoxic lipid classes were significantly higher in ob/ob mice than their age-matched controls, supporting the notion that elevated lipotoxic components are tightly associated with insulin resistance in ob/ob mice. Taken together, the current study revealed that lipogenesis and lipotoxicity in ob/ob mice likely contribute to insulin resistance and provides great insights into the underlying mechanisms of diabetes and obesity.
为了进一步了解脂肪生成和脂肪毒性在肥胖和糖尿病发展中的作用,我们通过 shotgun 脂质组学技术分析了 10、12 和 16 周龄 ob/ob 小鼠及其野生型对照的各种器官的脂质组。我们观察到,从头合成(例如,16:0、16:1 和 18:1 FA)的脂肪酸(FA)链的量在 ob/ob 小鼠中显著升高,这与参与生物合成的基因和蛋白质的表达增加一致。多不饱和脂肪酸在 ob/ob 小鼠的检查组织中适度增加,因为它们只能从饮食中吸收或从摄入的 n-3 或 n-6 FA 中延长。ob/ob 小鼠肝脏和骨骼肌中 FA 链的不同图谱反映了这些器官中不同的脂肪生成途径。与对照相比,12 和 16 周龄 ob/ob 小鼠肝脏中的壬酸(即 18:1(n-7) FA)的量显著增加,表明这种酸通过 16:1(n-7) FA 在肝脏中的从头合成从 12 周龄开始增强。巧合的是,从单酰甘油合成三酰甘油的肝脏合成在 12 周龄的 ob/ob 小鼠中也增加了,这是通过模拟三酰甘油合成揭示的。此外,与年龄匹配的对照相比,ob/ob 小鼠中的脂毒性脂质类别的水平显著更高,支持这样的观点,即升高的脂毒性成分与 ob/ob 小鼠中的胰岛素抵抗密切相关。总之,本研究揭示了 ob/ob 小鼠中的脂肪生成和脂肪毒性可能导致胰岛素抵抗,并为糖尿病和肥胖症的潜在机制提供了重要的见解。