Supplementing dietary sugar promotes endoplasmic reticulum stress-independent insulin resistance and fatty liver in goose
Supplementing dietary sugar promotes endoplasmic reticulum stress-independent insulin resistance and fatty liver in goose
复制标题
补充膳食糖促进鹅内质网应激非依赖性胰岛素抵抗和脂肪肝
DOI：
10.1016/j.bbrc.2016.05.149
复制
发表时间：
2016-08-05
影响因子：
3.1
通讯作者：
Gong, Daoqing
中科院分区：
文献类型：
--
作者：
Geng, Tuoyu;Zhao, Xing;Gong, Daoqing
众所周知，内质网应激（ERS）有助于哺乳动物胰岛素抵抗（IR）和非酒精性脂肪性肝病（NAFLD）。然而，我们最近证明了传统饲粮（主要由煮熟的玉米组成）的过度喂养不会诱发鹅的ERS。细胞研究表明，高糖和棕榈酸盐可触发哺乳动物细胞的ERS，我们假设在传统饮食中添加糖可诱导ERS，从而促进胰岛素抵抗和脂肪肝。为了验证这一假设，我们首先用高糖（25 mM和50 mM）和棕榈酸盐（0.5 mM）处理鹅原代肝细胞，并添加或不添加0.25 mM油酸盐。数据表明，与哺乳动物细胞一样，高糖和棕榈酸盐确实诱导了鹅原代肝细胞的ERS，添加0.25 mM油酸盐可以抑制棕榈酸盐诱导的ERS。然后，我们通过体内研究验证了这一假设，将过量饲喂传统或新型饲粮（即传统饲粮中添加糖）的朗德鹅与正常饲喂熟玉米的对照组鹅进行了ERS、IR和脂肪肝的比较。传统饲粮和新型饲粮对鹅的糖耐量、胰岛素耐量和餐后血糖的影响表明，饲粮中添加糖可促进IR。这种促进伴随着肝脏重量和腹部脂肪重量相对于体重的增加趋势。令人惊讶的是，与传统饲粮相比，新型饲粮的过量喂养没有引起鹅脂肪肝的ERS，甚至进一步抑制了ERS。综上所述，我们的研究结果表明，添加糖可促进鹅的ERS-independent IR和脂肪肝。这是有趣的发现因素(s)保护鹅肝从ERS以及非ERS机制下的IR。(C) 2016 Elsevier Inc.版权所有。
It is known that endoplasmic reticulum stress (ERS) contributes to insulin resistance (IR) and nonalcoholic fatty liver disease (NAFLD) in mammals. However, we recently demonstrated that overfeeding with a traditional diet (mainly consisting of cooked maize) does not induce ERS in goose. As cellular studies show that high glucose and palmitate can trigger ERS in mammalian cells, we hypothesized that supplementing sugar to the traditional diet could induce ERS, thus promoting insulin resistance and fatty liver. To test the hypothesis, we first treated goose primary hepatocytes with high glucose (25 mM and 50 mM) and palmitate (0.5 mM) supplemented with or without 0.25 mM oleate. Data indicated that, as in mammalian cells, high glucose and palmitate indeed induced ERS in goose primary hepatocytes, and palmitate-induced ERS was suppressed by supplemental 0.25 mM oleate. We then tested the hypothesis with an in vivo study, in which Landes geese overfed with traditional or novel diets (i.e., the traditional diet supplemented with sugar) were compared with control geese (normally fed with cooked maize) for ERS, IR and fatty liver. The differences in glucose tolerance, insulin tolerance and postprandial blood glucose between the geese overfed with traditional and novel diets suggested that supplementing dietary sugar promoted IR. This promotion was accompanied with an increasing trend of liver weight and abdominal fat weight relative to body weight. Surprisingly, compared to overfeeding with the traditional diet, overfeeding with the novel diet did not induce ERS, even further suppressed ERS in goose fatty liver. Together, our findings suggest that supplementing dietary sugar promotes ERS-independent IR and fatty liver in goose. It is intriguing to discover the factor(s) protecting goose liver from ERS as well as the non-ERS mechanism underlying IR. (C) 2016 Elsevier Inc. All rights reserved.