Dominguez-Uscanga Astrid, Loarca-Piña Guadalupe, Gonzalez de Mejia Elvira
Programa de Posgrado en Alimentos del Centro de la República (PROPAC), Food Science, School of Chemistry, Universidad Autónoma de Querétaro, Querétaro, Qro 76010, Mexico.
Department of Food Science and Human Nutrition, University of Illinois at Urbana-Champaign, 228ERML, 1201W Gregory Drive, Urbana, IL 61801, USA.
J Nutr Biochem. 2017 Dec;50:1-15. doi: 10.1016/j.jnutbio.2017.08.011. Epub 2017 Sep 4.
The aim was to determine the effect of consuming a baked white corn/bean snack (70/30% blend) on improving diet-induced dyslipidemia and liver differential gene expression in mice fed a high-fat diet (HFD). C57BL/6 mice were randomized into six groups and different doses of the snack (0.5-2.0 g/d) supplemented to a basal HFD for 12 weeks. Unsupplemented HFD and a standard diet were used as positive and negative controls, respectively. Groups receiving HFD1.0, HFD1.5 and HFD2.0 showed attenuation in body weight gain (20%). Serum cholesterol and triglycerides were reduced (P<.05), 29% and 31%, respectively. Blood glucose was also reduced (P<.05) in all groups receiving the snack. Histological analysis showed a reduction in adipocyte diameters (P<.05) suggesting an attenuation of lipid accumulation. Snack consumption induced differential expression of 529 genes in the liver; RGS16 was the highest up-regulated molecule (+15-fold change). Increased expression of this gene could have improved glucose metabolism in HFD2.0. Ingenuity Pathway Analysis downstream analysis showed a predicted inhibition of target genes of peroxisome PPARγ and key regulators of lipogenic genes in the liver. The results suggest that consumption of a white corn/bean snack (70%/30% blend) attenuates weight gain, fat mass accumulation, adipocyte size and nonalcoholic fatty liver disease in HFD-fed mice by inhibiting PPARγ and SREBF2. The study proposes that this type of product might be beneficial by preventing dyslipidemia, obesity and hepatic steatosis.
本研究旨在确定食用烘焙白玉米/豆类零食(70/30%混合)对改善高脂饮食(HFD)喂养小鼠的饮食诱导性血脂异常和肝脏差异基因表达的影响。将C57BL/6小鼠随机分为六组,在基础高脂饮食中补充不同剂量的零食(0.5 - 2.0 g/d),持续12周。未补充零食的高脂饮食和标准饮食分别用作阳性和阴性对照。接受HFD1.0、HFD1.5和HFD2.0的组体重增加有所减轻(20%)。血清胆固醇和甘油三酯分别降低(P<0.05),降低了29%和31%。所有接受零食的组血糖也有所降低(P<0.05)。组织学分析显示脂肪细胞直径减小(P<0.05),表明脂质积累有所减轻。食用零食诱导肝脏中529个基因的差异表达;RGS16是上调幅度最大的分子(变化15倍)。该基因表达增加可能改善了HFD2.0组的葡萄糖代谢。下游的 Ingenuity Pathway Analysis分析显示,肝脏中过氧化物酶体PPARγ的靶基因和脂肪生成基因的关键调节因子受到预测性抑制。结果表明,食用白玉米/豆类零食(70%/30%混合)通过抑制PPARγ和SREBF2,减轻了高脂饮食喂养小鼠的体重增加、脂肪量积累、脂肪细胞大小和非酒精性脂肪性肝病。该研究提出,这类产品可能通过预防血脂异常、肥胖和肝脂肪变性而有益。