Chon Su-Hyoun, Zhou Yin Xiu, Dixon Joseph L, Storch Judith
Department of Nutritional Sciences and the Rutgers Center for Lipid Research, Rutgers University, New Brunswick, New Jersey 08901.
Department of Nutritional Sciences and the Rutgers Center for Lipid Research, Rutgers University, New Brunswick, New Jersey 08901.
J Biol Chem. 2007 Nov 16;282(46):33346-33357. doi: 10.1074/jbc.M706994200. Epub 2007 Sep 11.
Intestinal monoacylglycerol (MG) metabolism is well known to involve its anabolic reesterification to triacylglycerol (TG). We recently provided evidence for enterocyte MG hydrolysis and demonstrated expression of the monoacylglycerol lipase (MGL) gene in human intestinal Caco-2 cells and rodent small intestinal mucosa. Despite the large quantities of MG derived from dietary TG, the regulation of MG metabolism in the intestine has not been previously explored. In the present studies, we examined the mRNA expression, protein expression, and activities of the two known MG-metabolizing enzymes, MGL and MGAT2, in C57BL/6 mouse small intestine, as well as liver and adipose tissues, during development and under nutritional modifications. Results demonstrate that MG metabolism undergoes tissue-specific changes during development. Marked induction of small intestinal MGAT2 protein expression and activity were found during suckling. Moreover, while substantial levels of MGL protein and activity were detected in adult intestine, its regulation during ontogeny was complex, suggesting post-transcriptional regulation of expression. In addition, during the suckling period MG hydrolytic activity is likely to derive from carboxyl ester lipase rather than MGL. In contrast to intestinal MGL, liver MGL mRNA, protein and activity all increased 5-10-fold during development, suggesting that transcriptional regulation is the primary mechanism for hepatic MGL expression. Three weeks of high fat feeding (40% kcal) significantly induced MGL expression and activity in small intestine relative to low fat feeding (10% kcal), but little change was observed upon starvation, suggesting a role for MGL in dietary lipid assimilation following a high fat intake.
肠道单酰甘油（MG）代谢涉及将其合成代谢重新酯化为三酰甘油（TG），这一点广为人知。我们最近提供了肠细胞MG水解的证据，并证明了单酰甘油脂肪酶（MGL）基因在人肠道Caco-2细胞和啮齿动物小肠黏膜中的表达。尽管膳食TG可产生大量MG，但此前尚未探索肠道中MG代谢的调控机制。在本研究中，我们检测了C57BL/6小鼠小肠以及肝脏和脂肪组织在发育过程中和营养改变情况下，两种已知的MG代谢酶MGL和MGAT2的mRNA表达、蛋白质表达及活性。结果表明，MG代谢在发育过程中会发生组织特异性变化。在哺乳期间发现小肠MGAT2蛋白质表达和活性显著诱导。此外，虽然在成年肠道中检测到大量的MGL蛋白质和活性，但其在个体发育过程中的调控较为复杂，提示存在转录后表达调控。另外，在哺乳期间，MG水解活性可能来源于羧基酯酶而非MGL。与肠道MGL不同，肝脏MGL的mRNA、蛋白质和活性在发育过程中均增加了5至10倍，表明转录调控是肝脏MGL表达的主要机制。相对于低脂喂养（10%千卡），高脂喂养（40%千卡）三周显著诱导了小肠中MGL的表达和活性，但饥饿时未见明显变化，提示MGL在高脂摄入后膳食脂质同化中发挥作用。
