Background

Poor dietary habits such as an over consumption of high fructose and high fat diet are considered as the major culprit for the induction of diabetes associated liver injury. Diabetes mellitus is a metabolic disorder that affects various vital organs of the body especially the kidney, brain, heart, and liver. The high fructose and high fat (HFHF) diet worsen the metabolic conditions by producing various pathogenic burdens such as oxidative stress, inflammation, etc. on liver. The hyperlipidemic and hyperglycemic conditions induced by HFHF diet leads to the generation of various proinflammatory mediators like TNFα, interleukin and cytokines.

Aim and methods

The systematic bibliographical literature survey was done with the help of PubMed, Google scholar and MedLine to identify all pathological and molecular concerened with HFHF induced diabetic liver injury. The consumption of HFHF diet leads to an increase in mitochondrial oxidative stress thereby decreases the liver protective antioxidants required for cell viability. HFHF diet disturbs lipid and lipoprotein clearance by elevating the level of apolipoprotein CIII and impairing the hydrolysis of triglyceride. As a result, there is an increase in free fatty acid concentration, triglycerides and diacylglycerol in the liver which further triggers the situation of insulin resistance.

Conclusion

The focus of present review is based upon the various pathological, genetic and molecular mechanism involved in the development of high-fat high fructose diet induced diabetic liver injury. However, the current review also documented few shreds of evidence related to various microRNAs (miR-31, miR-33a, miR-34a, miR-144, miR-146b, miR-150) concerned to HFHF diet which play an important role in the pathogenesis of diabetes associated liver injury Dietary life style modification may prove beneficial in the management of various metabolic disorders.

中文翻译：

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高果糖和高脂肪饮食诱发的糖尿病相关非酒精性脂肪肝疾病的病理生物学和分子联系。

背景

不良的饮食习惯，如过量食用高果糖和高脂肪饮食，被认为是诱发糖尿病相关肝损伤的主要原因。糖尿病是一种代谢疾病，会影响身体的各个重要器官，尤其是肾脏、大脑、心脏和肝脏。高果糖和高脂肪 (HFHF) 饮食通过对肝脏产生各种致病性负担，如氧化应激、炎症等，使代谢状况恶化。HFHF 饮食引起的高脂血症和高血糖症会导致各种促炎介质如 TNFα、白细胞介素和细胞因子的产生。

目的和方法

在 PubMed、Google 学者和 MedLine 的帮助下进行了系统的书目文献调查，以识别所有与 HFHF 诱导的糖尿病肝损伤有关的病理和分子。食用 HFHF 饮食会导致线粒体氧化应激增加，从而降低细胞活力所需的肝脏保护性抗氧化剂。HF HF 饮食通过提高载脂蛋白 CIII 的水平和削弱甘油三酯的水解来干扰脂质和脂蛋白的清除。结果，肝脏中的游离脂肪酸浓度、甘油三酯和二酰基甘油增加，进一步引发胰岛素抵抗的情况。

结论

本综述的重点是基于高脂高果糖饮食诱发糖尿病肝损伤的各种病理、遗传和分子机制。然而，目前的综述还记录了与 HFHF 饮食相关的各种 microRNA（miR-31、miR-33a、miR-34a、miR-144、miR-146b、miR-150）相关的少量证据，这些 microRNA 在糖尿病相关肝损伤的发病机制 饮食生活方式的改变可能证明有益于管理各种代谢紊乱。