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Altered small intestinal absorptive enzyme activities in leptin-deficient obese mice: influence of bowel resection.

机译:瘦素缺陷型肥胖小鼠小肠吸收酶活性的改变:肠切除的影响。

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BACKGROUND: Residual bowel increases absorption after massive small bowel resection. Leptin affects intestinal adaptation, carbohydrate, peptide, and lipid handling. Sucrase, peptidase, and acyl coenzyme A:monoacylglycerol acyltransferase (MGAT) are involved in carbohydrate, protein, and lipid absorption. We hypothesized that leptin-deficient obese mice would have altered absorptive enzymes compared with controls before and after small bowel resection. METHODS: Sucrase, peptidase (aminopeptidase N [ApN], dipeptidyl peptidase IV [DPPIV]), and MGAT activities were determined from lean control (C57BL/6J, n = 16) and leptin-deficient (Lep(ob), n = 16) mice small bowel before and after 50% resection. RESULTS: Ileal sucrase activity was greater in obese mice before and after resection. Jejunal ApN and DPPIV activities were lower for obese mice before resection; ileal ApN activity was unaltered after resection for both strains. Resection increased DPPIV activity in both strains. Jejunal MGAT in obese mice decreased postresection. In both strains, ileal MGAT activity decreased after resection, and obese mice had greater activity in remnant ileum. CONCLUSIONS: After small bowel resection, leptin-deficient mice have increased sucrase activity and diminished ileal ApN, DPPIV, and MGAT activity compared with controls. Therefore, we conclude that leptin deficiency alters intestinal enzyme activity in unresected animals and after small bowel resection. Altered handling of carbohydrate, protein, and lipid may contribute to obesity and diabetes in leptin-deficient mice.
机译:背景:大肠切除术后残留肠会增加吸收。瘦素会影响肠道适应,碳水化合物,肽和脂质的处理。蔗糖酶,肽酶和酰基辅酶A:单酰基甘油酰基转移酶(MGAT)与碳水化合物,蛋白质和脂质的吸收有关。我们假设瘦素缺乏的肥胖小鼠与小肠切除前后相比,其吸收酶会发生改变。方法:从瘦肉对照(C57BL / 6J,n = 16)和瘦素缺乏(Lep(ob),n = 16)中测定蔗糖酶,肽酶(氨基肽酶N [ApN],二肽基肽酶IV [DPPIV])和MGAT活性。 )50%切除前后的小肠小鼠。结果:切除前后肥胖小鼠的回肠蔗糖酶活性较高。切除前肥胖小鼠的空肠ApN和DPPIV活性较低;两种菌株切除后回肠ApN活性均未改变。切除均增加了两种菌株的DPPIV活性。肥胖小鼠的空肠MGAT切除后减少。在这两种品系中,切除后的回肠MGAT活性均降低,肥胖小鼠的回肠残余活性更高。结论:小肠切除后,瘦素缺陷型小鼠与对照组相比,蔗糖酶活性增加,回肠ApN,DPPIV和MGAT活性降低。因此,我们得出结论,瘦素缺乏会改变未切除动物和小肠切除后的肠道酶活性。碳水化合物,蛋白质和脂质的处理不当可能会导致瘦素缺乏症小鼠肥胖和糖尿病。

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