PDF(Pubmed)
Abstract：
While a definitive mechanism-of-action remains to be identified, recent findings indicate that ghrelin, particularly the unacylated form (UnAG), stimulates skeletal muscle fatty acid oxidation. The biological importance of UnAG-mediated increases in fat oxidation remains unclear, as UnAG peaks in the circulation before mealtimes, and decreases rapidly during the postprandial situation before increases in postabsorptive circulating lipids. Therefore, we aimed to determine if the UnAG-mediated stimulation of fat oxidation would persist long enough to affect the oxidation of meal-derived fatty acids, and if UnAG stimulated the translocation of fatty acid transporters to the sarcolemma as a mechanism-of-action. In isolated soleus muscle strips from male rats, short-term pre-treatment with UnAG elicited a persisting stimulus on fatty acid oxidation 2 h after the removal of UnAG. UnAG also caused an immediate phosphorylation of AMPK, but not an increase in plasma membrane FAT/CD36 or FABPpm. There was also no increase in AMPK signaling or increased FAT/CD36 or FABPpm content at the plasma membrane at 2 h which might explain the sustained increase in fatty acid oxidation. These findings confirm UnAG as a stimulator of fatty acid oxidation and provide evidence that UnAG may influence the handling of postprandial lipids. The underlying mechanisms are not known.
摘要：
虽然确定的作用机制尚待确定，最近的研究结果表明ghrelin,特别是未酰化形式(UnAG)，刺激骨骼肌脂肪酸氧化。UnAG介导的脂肪氧化增加的生物学重要性尚不清楚。因为UnAG在进餐时间前的循环中达到峰值，并且在餐后情况下迅速减少，然后吸收后循环脂质增加。因此,我们的目的是确定UnAG介导的脂肪氧化刺激是否会持续足够长的时间来影响膳食衍生脂肪酸的氧化，如果UnAG刺激脂肪酸转运蛋白向肌膜的转运作为一种作用机制。在雄性大鼠的孤立比目鱼肌条中，去除UnAG后2小时，用UnAG进行短期预处理会对脂肪酸氧化产生持续的刺激。UnAG也引起AMPK的立即磷酸化,但质膜FAT/CD36或FABPpm不增加。在2小时时，AMPK信号传导也没有增加，质膜上的FAT/CD36或FABPpm含量也没有增加，这可能解释了脂肪酸氧化的持续增加。这些发现证实了UnAG是脂肪酸氧化的刺激物，并提供了UnAG可能影响餐后脂质处理的证据。潜在的机制是未知的。
