Pathobiological and molecular connections involved in the high fructose and high fat diet induced diabetes associated nonalcoholic fatty liver disease

被引:19
|
作者
Ekta [1 ]
Gupta, Manisha [1 ]
Kaur, Amarjot [1 ]
Singh, Thakur Gurjeet [1 ]
Bedi, Onkar [1 ]
机构
[1] Chitkara Univ, Chitkara Coll Pharm, Rajpura, Punjab, India
关键词
Diabetes mellitus; High fat high fructose; Proinflammatory mediators; Apolipoprotein; Diabetic liver injury; Thioredoxin; 2; Metabolic disorders; ENDOPLASMIC-RETICULUM STRESS; INSULIN-RESISTANCE; GUT MICROBIOTA; HEPATIC STEATOSIS; METABOLIC SYNDROME; KAPPA-B; LIPOPROTEIN-LIPASE; OXIDATIVE STRESS; LIPID-METABOLISM; SKELETAL-MUSCLE;
D O I
10.1007/s00011-020-01373-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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 TNF alpha, 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.
引用
收藏
页码:851 / 867
页数:17
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