Protective Mechanism of Common Buckwheat (Fagopyrum esculentum Moench.) against Nonalcoholic Fatty Liver Disease Associated with Dyslipidemia in Mice Fed a High-Fat and High-Cholesterol Diet

2020 ◽  
Vol 68 (24) ◽  
pp. 6530-6543
Author(s):  
Zi-Rui Huang ◽  
Jia-Cong Deng ◽  
Qiu-Yi Li ◽  
Ying-Jia Cao ◽  
Yi-Chen Lin ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver Disease ◽  
High Cholesterol Diet ◽  
Protective Mechanism ◽  
Cholesterol Diet ◽  
Common Buckwheat ◽  
High Cholesterol ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Fagopyrum Esculentum Moench

scholarly journals Perilla Oil Supplementation Ameliorates High-Fat/High-Cholesterol Diet Induced Nonalcoholic Fatty Liver Disease in Rats via Enhanced Fecal Cholesterol and Bile Acid Excretion

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Ting Chen ◽  
Fahu Yuan ◽  
Hualin Wang ◽  
Yu Tian ◽  
Lei He ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver Disease ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Perilla Oil ◽  
Cholesterol Excretion ◽  
Fecal Cholesterol

Recent experimental studies and clinical trials have shown that hepatic cholesterol metabolic disorders are closely related to the development of nonalcoholic fatty liver disease (NAFLD). The main goal of this study was to investigate the efficacy of the perilla oil rich in alpha-linolenic acid (ALA) against NASH and gain a deep insight into its potential mechanisms. Rats were fed a high-fat/high-cholesterol diet (HFD) supplement with perilla oil (POH) for 16 weeks. Routine blood biochemical tests and histological staining illustrated that the perilla oil administration improved HFD-induced hyperlipidemia, reduced hepatic steatosis, and inhibited hepatic inflammatory infiltration and fibrosis. Perilla oil also increased fecal bile acid and cholesterol excretion. Hepatic RNA-Seq analysis found that the long time perilla oil supplement notably modified the gene expression involved in cholesterol metabolism. Our results implicate that, after long-term high level dietary cholesterol feeding, rat liver endogenous synthesis of cholesterol and cholesterol-rich low density lipoprotein uptake was significantly inhibited, and perilla oil did not modulate expression of genes responsible for cholesterol synthesis but did increase cholesterol removed from hepatocytes by conversion to bile acids and increased fecal cholesterol excretion.

scholarly journals Osteocalcin Protects Against Nonalcoholic Steatohepatitis in a Mouse Model of Metabolic Syndrome

Endocrinology ◽  
2014 ◽  
Vol 155 (12) ◽  
pp. 4697-4705 ◽  
Author(s):  
Anisha A. Gupte ◽  
Omaima M. Sabek ◽  
Daniel Fraga ◽  
Laurie J. Minze ◽  
Satoru K. Nishimoto ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Nonalcoholic Steatohepatitis ◽  
Fatty Liver Disease ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease, particularly its more aggressive form, nonalcoholic steatohepatitis (NASH), is associated with hepatic insulin resistance. Osteocalcin, a protein secreted by osteoblast cells in bone, has recently emerged as an important metabolic regulator with insulin-sensitizing properties. In humans, osteocalcin levels are inversely associated with liver disease. We thus hypothesized that osteocalcin may attenuate NASH and examined the effects of osteocalcin treatment in middle-aged (12-mo-old) male Ldlr−/− mice, which were fed a Western-style high-fat, high-cholesterol diet for 12 weeks to induce metabolic syndrome and NASH. Mice were treated with osteocalcin (4.5 ng/h) or vehicle for the diet duration. Osteocalcin treatment not only protected against Western-style high-fat, high-cholesterol diet-induced insulin resistance but substantially reduced multiple NASH components, including steatosis, ballooning degeneration, and fibrosis, with an overall reduction in nonalcoholic fatty liver disease activity scores. Further, osteocalcin robustly reduced expression of proinflammatory and profibrotic genes (Cd68, Mcp1, Spp1, and Col1a2) in liver and suppressed inflammatory gene expression in white adipose tissue. In conclusion, these results suggest osteocalcin inhibits NASH development by targeting inflammatory and fibrotic processes.

scholarly journals Temporal Development of Dyslipidemia and Nonalcoholic Fatty Liver Disease (NAFLD) in Syrian Hamsters Fed a High-Fat, High-Fructose, High-Cholesterol Diet

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 604
Author(s):  
Victoria Svop Jensen ◽  
Christian Fledelius ◽  
Erik Max Wulff ◽  
Jens Lykkesfeldt ◽  
Henning Hvid
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
High Fructose

The use of translationally relevant animal models is essential, also within the field of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Compared to frequently used mouse and rat models, the hamster may provide a higher degree of physiological similarity to humans in terms of lipid profile and lipoprotein metabolism. However, the effects in hamsters after long-term exposure to a NASH diet are not known. Male Syrian hamsters were fed either a high-fat, high-fructose, high-cholesterol diet (NASH diet) or control diets for up to 12 months. Plasma parameters were assessed at two weeks, one, four, eight and 12 months and liver histopathology and biochemistry was characterized after four, eight and 12 months on the experimental diets. After two weeks, hamsters on NASH diet had developed marked dyslipidemia, which persisted for the remainder of the study. Hepatic steatosis was present in NASH-fed hamsters after four months, and hepatic stellate cell activation and fibrosis was observed within four to eight months, respectively, in agreement with progression towards NASH. In summary, we demonstrate that hamsters rapidly develop dyslipidemia when fed a high-fat, high-fructose, high-cholesterol diet. Moreover, within four to eight months, the NASH-diet induced hepatic changes with resemblance to human NAFLD.

Bifidobacterium adolescentis and Lactobacillus rhamnosus alleviate non-alcoholic fatty liver disease induced by a high-fat, high-cholesterol diet through modulation of different gut microbiota-dependent pathways

2020 ◽  
Vol 11 (7) ◽  
pp. 6115-6127
Author(s):  
Gang Wang ◽  
Ting Jiao ◽  
Yue Xu ◽  
Daozheng Li ◽  
Qian Si ◽  
...  
Keyword(s):  
Liver Disease ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

B. adolescentis and L. rhamnosus alleviate non-alcoholic fatty liver disease induced by a high-fat, high-cholesterol diet through modulation on different gut microbiota-dependent pathways. The SCFAs are important participants.

scholarly journals AIM-deficient mouse fed a high-trans fat, high-cholesterol diet: a new animal model for nonalcoholic fatty liver disease

2019 ◽  
Vol 68 (2) ◽  
pp. 147-158 ◽  
Author(s):  
Ginga Komatsu ◽  
Toru Nonomura ◽  
Mai Sasaki ◽  
Yuki Ishida ◽  
Satoko Arai ◽  
...  
Keyword(s):  
Animal Model ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
High Cholesterol Diet ◽  
Deficient Mouse ◽  
Trans Fat ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Nonalcoholic Fatty Liver
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