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首页> 外文期刊>Nutrients >The Addition of Liquid Fructose to a Western-Type Diet in LDL-R ?/? Mice Induces Liver Inflammation and Fibrogenesis Markers without Disrupting Insulin Receptor Signalling after an Insulin Challenge
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The Addition of Liquid Fructose to a Western-Type Diet in LDL-R ?/? Mice Induces Liver Inflammation and Fibrogenesis Markers without Disrupting Insulin Receptor Signalling after an Insulin Challenge

机译：在LDL-Rα/β的西式饮食中添加液态果糖小鼠在胰岛素挑战后诱导肝炎症反应和纤维生成标记而不破坏胰岛素受体信号传导

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A high consumption of fat and simple sugars, especially fructose, has been related to the development of insulin resistance, but the mechanisms involved in the effects of these nutrients are not fully understood. This study investigates the effects of a Western-type diet and liquid fructose supplementation, alone and combined, on insulin signalling and inflammation in low-density lipoprotein (LDL) receptor-deficient mice (LDL-R ?/? ). LDL-R ?/? mice were fed chow or Western diet ±15% fructose solution for 12 weeks. Plasma glucose and insulin, and the expression of genes related to inflammation in the liver and visceral white adipose tissue (vWAT), were analysed. V-akt murine thymoma viral oncogene homolog-2 (Akt) activation was measured in the liver of the mice after a single injection of saline or insulin. None of the dietary interventions caused inflammation in vWAT, whereas the Western diet induced hepatic inflammation, which was further enhanced by liquid fructose, leading also to a significant increase in fibrogenesis markers. However, there was no change in plasma glucose or insulin, or insulin-induced Akt phosphorylation. In conclusion, hepatic inflammation and fibrogenesis markers induced by a Western diet supplemented with liquid fructose in LDL-R ?/? mice are not associated with a significant impairment of hepatic insulin signalling.
机译：大量摄入脂肪和单糖，尤其是果糖与胰岛素抵抗的发展有关，但尚未完全了解这些营养素的作用机理。这项研究调查了西式饮食和果糖液体补充剂单独或组合对低密度脂蛋白（LDL）受体缺陷型小鼠（LDL-Rα/β）的胰岛素信号传导和炎症的影响。 LDL-R？/？给小鼠喂食物或西式饮食±15％果糖溶液12周。分析了血浆葡萄糖和胰岛素，以及与肝脏和内脏白色脂肪组织（vWAT）中炎症相关的基因的表达。单次注射盐水或胰岛素后，在小鼠肝脏中测量了V-akt鼠胸腺瘤病毒致癌基因同源物2（Akt）的激活。饮食干预均未引起vWAT炎症，而西方饮食引起肝炎症，液体果糖进一步加剧了肝炎症，还导致纤维生成标记物显着增加。但是，血浆葡萄糖或胰岛素或胰岛素诱导的Akt磷酸化没有改变。总之，西餐饮食补充液态果糖可降低LDL-Rα/β引起的肝炎症反应和肝纤维化标记。小鼠与肝胰岛素信号明显受损无关。

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