Effect of dietary advanced glycation end products on mouse liver.
Effect of dietary advanced glycation end products on mouse liver.
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DOI：
10.1371/journal.pone.0035143
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Zhu L
中科院分区：
文献类型：
--
作者：
Patel R;Baker SS;Liu W;Desai S;Alkhouri R;Kozielski R;Mastrandrea L;Sarfraz A;Cai W;Vlassara H;Patel MS;Baker RD;Zhu L
非酒精性脂肪性肝炎（NASH）的确切病理生理学尚不清楚。以往的研究表明，饮食中的晚期糖基化终末产物（AGEs）可引起肝脏氧化应激。我们的目的是研究饮食AGEs对肝脏健康的影响及其在NASH发病机制中的可能作用。方法：两组小鼠饲料相同，但AGE含量不同。一组喂食高AGE饮食，第二组喂食常规AGE饮食。评估肝组织学、丙氨酸氨基转移酶、天冬氨酸氨基转移酶、空腹血糖、空腹胰岛素、胰岛素抵抗和糖耐量。研究结果：组织学检查显示，在第26周时，高AGE组的肝脏中发生了中性粒细胞浸润;脂肪变性没有伴随肝脏炎症。在第39周，两组的肝脏均表现出大或小脂肪变性，但未检测到炎症。与高AGE组相比，常规AGE组在第26周检测到更高的胰岛素水平（P =0.034）。 第39周时，常规AGE组的丙氨酸氨基转移酶（P<0.01）和天冬氨酸氨基转移酶（P = 0.02）水平高于高AGE组。 结论：我们证明了高AGE饮食可以在没有脂肪变性的情况下引起肝脏炎症。我们的研究结果表明，饮食AGEs可能在启动肝脏炎症中发挥作用，从而促进NASH的疾病进展。我们的观察表明，高AGE单独引起的炎症并没有持续下去，这表明了有趣的未来方向，以研究AGEs如何促进肝脏中的促氧化和抗氧化途径。
The exact pathophysiology of non-alcoholic steatohepatitis (NASH) is not known. Previous studies suggest that dietary advanced glycation end products (AGEs) can cause oxidative stress in liver. We aim to study the effects of dietary AGEs on liver health and their possible role in the pathogenesis of NASH. METHODS: Two groups of mice were fed the same diet except the AGE content varied. One group was fed a high AGE diet and the second group was fed a regular AGE diet. Liver histology, alanine aminotransferase, aspartate aminotransferase, fasting glucose, fasting insulin, insulin resistance and glucose tolerance were assessed. RESULTS: Histology revealed that neutrophil infiltration occurred in the livers of the high AGE group at week 26; steatosis did not accompany liver inflammation. At week 39 livers from both groups exhibited macro- or micro-steatosis, yet no inflammation was detected. Higher insulin levels were detected in the regular AGE group at week 26 (P = 0.034), compared to the high AGE group. At week 39, the regular AGE group showed higher levels of alanine aminotransferase (P<0.01) and aspartate aminotransferase (P = 0.02) than those of the high AGE group. CONCLUSIONS: We demonstrate that a high AGE diet can cause liver inflammation in the absence of steatosis. Our results show that dietary AGEs could play a role in initiating liver inflammation contributing to the disease progression of NASH. Our observation that the inflammation caused by high AGE alone did not persist suggests interesting future directions to investigate how AGEs contribute to pro-oxidative and anti-oxidative pathways in the liver.
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影响因子：
3.7
作者：
Baker SS;Baker RD;Liu W;Nowak NJ;Zhu L
通讯作者：
Zhu L
DOI：
10.1111/j.1530-0277.2006.00288.x
发表时间：
2007-01-01
影响因子：
3.2
作者：
Kojima, Hideyuki;Sakurai, Shinya;Tamagawa, Yasuhiro
通讯作者：
Tamagawa, Yasuhiro
DOI：
10.1111/j.1440-1746.2007.04943.x
发表时间：
2007-07-01
影响因子：
4.1
作者：
Hyogo, Hideyuki;Yamagishi, Sho-ichi;Tazuma, Susumu
通讯作者：
Tazuma, Susumu
影响因子：
13.5
作者：
Browning, JD;Szczepaniak, LS;Hobbs, HH
通讯作者：
Hobbs, HH
影响因子：
82.9
作者：
Lin, HZ;Yang, SQ;Diehl, AM
通讯作者：
Diehl, AM