Méndez-Giménez Leire, Becerril Sara, Moncada Rafael, Valentí Víctor, Fernández Secundino, Ramírez Beatriz, Catalán Victoria, Gómez-Ambrosi Javier, Soveral Graça, Malagón María M, Diéguez Carlos, Rodríguez Amaia, Frühbeck Gema
Metabolic Research Laboratory, Clínica Universidad de Navarra, IdiSNA, Irunlarrea 1, 31008, Pamplona, Spain.
CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
Obes Surg. 2017 Jul;27(7):1763-1774. doi: 10.1007/s11695-016-2532-2.
Gastric plication is a minimally invasive bariatric surgical procedure, where the greater curvature is plicated inside the gastric lumen. Our aims were to analyze the effectiveness of gastric plication on the resolution of obesity, impaired glucose tolerance, and fatty liver in an experimental model of diet-induced obesity (DIO) and to evaluate changes in glycerol metabolism, a key substrate for adiposity and gluconeogenesis, in adipose tissue and the liver.
Male Wistar DIO rats (n = 58) were subjected to surgical (sham operation and gastric plication) or dietary interventions [fed a normal diet (ND) or high-fat diet (HFD) or pair-fed to the amount of food eaten by gastric-plicated animals]. The expression of aquaglyceroporins (AQPs) in epididymal (EWAT) and subcutaneous (SCWAT) fat and the liver was analyzed by real-time PCR and Western blot.
Gastric plication did not result in a significant weight loss in DIO rats, showing a modest reduction in whole-body adiposity and hepatic steatosis. However, gastric-plicated animals exhibited an improvement in basal glycemia and glucose clearance, without changes in hepatic gluconeogenic genes. DIO was associated with an increase in glycerol, higher AQP3 and AQP7 in EWAT and SCWAT, and a decrease in hepatic AQP9. Gastric plication downregulated AQP3 in both fat depots without changes in adipose AQP7 and hepatic AQP9.
Gastric plication results in a modest reduction in adiposity and hepatosteatosis but restores glycemia by downregulating AQP3, which entails lower efflux of glycerol from fat, lower plasma glycerol availability, and a reduced use of glycerol as a substrate for hepatic gluconeogenesis.
胃折叠术是一种微创减肥手术，通过在胃腔内对胃大弯进行折叠。我们的目的是在饮食诱导肥胖（DIO）的实验模型中分析胃折叠术对肥胖、糖耐量受损和脂肪肝的改善效果，并评估脂肪组织和肝脏中甘油代谢（肥胖和糖异生的关键底物）的变化。
雄性Wistar DIO大鼠（n = 58）接受手术干预（假手术和胃折叠术）或饮食干预[喂食正常饮食（ND）、高脂饮食（HFD）或与胃折叠术动物的食量进行配对喂养]。通过实时PCR和蛋白质免疫印迹法分析附睾白色脂肪组织（EWAT）、皮下白色脂肪组织（SCWAT）和肝脏中水甘油通道蛋白（AQPs）的表达。
胃折叠术并未使DIO大鼠显著减重，全身肥胖和肝脂肪变性仅有适度减轻。然而，接受胃折叠术的动物基础血糖和葡萄糖清除率有所改善，肝糖异生基因无变化。DIO与甘油增加、EWAT和SCWAT中AQP3和AQP7升高以及肝脏中AQP9降低有关。胃折叠术下调了两个脂肪库中的AQP3，而脂肪组织中的AQP7和肝脏中的AQP9无变化。
胃折叠术可使肥胖和肝脂肪变性适度减轻，但通过下调AQP3恢复血糖水平，这意味着甘油从脂肪中的流出减少、血浆甘油可用性降低以及甘油作为肝糖异生底物的利用减少。
