scholarly journals Allopurinol ameliorates high fructose diet induced hepatic steatosis in diabetic rats through modulation of lipid metabolism, inflammation, and ER stress pathway

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
In-Jin Cho ◽  
Da-Hee Oh ◽  
Jin Yoo ◽  
You-Cheol Hwang ◽  
Kyu Jeung Ahn ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Er Stress ◽  
Hepatic Steatosis ◽  
Direct Role ◽  
Nonalcoholic Fatty Liver ◽  
High Fructose Diet ◽  
Epididymal Fat ◽  
High Fructose ◽  
Long Evans ◽  
Stress Pathway

AbstractExcess fructose consumption contributes to development obesity, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD). Uric acid (UA), a metabolite of fructose metabolism, may have a direct role in development of NAFLD, with unclear mechanism. This study aimed to evaluate role of fructose and UA in NAFLD and explore mechanisms of allopurinol (Allo, a UA lowering medication) on NAFLD in Otsuka Long-Evans Tokushima Fatty (OLETF) rats fed a high fructose diet (HFrD), with Long-Evans Tokushima Otsuka (LETO) rats used as a control. There were six groups: LETO, LETO-Allo, OLETF, OLETF-Allo, OLETF-HFrD, and OLETF-HFrD-Allo. HFrD significantly increased body weight, epididymal fat weight, and serum concentrations of UA, cholesterol, triglyceride, HbA1c, hepatic enzymes, HOMA-IR, fasting insulin, and two hour-glucose after intraperitoneal glucose tolerance tests, as well as NAFLD activity score of liver, compared to the OLETF group. Allopurinol treatment significantly reduced hepatic steatosis, epididymal fat, serum UA, HOMA-IR, hepatic enzyme levels, and cholesterol in the OLETF-HFrD-Allo group. Additionally, allopurinol significantly downregulated expression of lipogenic genes, upregulated lipid oxidation genes, downregulated hepatic pro-inflammatory cytokine genes, and decreased ER-stress induced protein expression, in comparison with the OLETF-HFrD group. In conclusion, allopurinol ameliorates HFrD-induced hepatic steatosis through modulation of hepatic lipid metabolism, inflammation, and ER stress pathway. UA may have a direct role in development of fructose-induced hepatic steatosis, and allopurinol could be a candidate for prevention or treatment of NAFLD.

Kombuchas from green and black teas reduce oxidative stress, liver steatosis and inflammation, and improve glucose metabolism in Wistar rats fed a high-fat high-fructose diet

2021 ◽  
Author(s):  
Rodrigo Cardoso ◽  
Luiza Dias Moreira ◽  
Mirian Costa ◽  
Renata Celi Lopes Toledo ◽  
Mariana Grancieri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Glucose Metabolism ◽  
Wistar Rats ◽  
Liver Steatosis ◽  
Black Tea ◽  
High Fat ◽  
High Fructose Diet ◽  
High Fructose ◽  
Green And Black Tea

The aim of this study was to evaluate the effect of green and black tea kombuchas consumption on adiposity, lipid metabolism, liver steatosis, oxidative stress, and inflammation in Wistar rats...

Ezetimibe prevents hepatic steatosis induced by a high-fat but not a high-fructose diet

2013 ◽  
Vol 305 (2) ◽  
pp. E293-E304 ◽  
Author(s):  
Masateru Ushio ◽  
Yoshihiko Nishio ◽  
Osamu Sekine ◽  
Yoshio Nagai ◽  
Yasuhiro Maeno ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Fatty Acid Synthase ◽  
Binding Protein ◽  
High Fat ◽  
High Fructose Diet ◽  
High Fructose ◽  
Element Binding Protein

Nonalcoholic fatty liver disease is the most frequent liver disease. Ezetimibe, an inhibitor of intestinal cholesterol absorption, has been reported to ameliorate hepatic steatosis in human and animal models. To explore how ezetimibe reduces hepatic steatosis, we investigated the effects of ezetimibe on the expression of lipogenic enzymes and intestinal lipid metabolism in mice fed a high-fat or a high-fructose diet. CBA/JN mice were fed a high-fat diet or a high-fructose diet for 8 wk with or without ezetimibe. High-fat diet induced hepatic steatosis accompanied by hyperinsulinemia. Treatment with ezetimibe reduced hepatic steatosis, insulin levels, and glucose production from pyruvate in mice fed the high-fat diet, suggesting a reduction of insulin resistance in the liver. In the intestinal analysis, ezetimibe reduced the expression of fatty acid transfer protein-4 and apoB-48 in mice fed the high-fat diet. However, treatment with ezetimibe did not prevent hepatic steatosis, hyperinsulinemia, and intestinal apoB-48 expression in mice fed the high-fructose diet. Ezetimibe decreased liver X receptor-α binding to the sterol regulatory element-binding protein-1c promoter but not expression of carbohydrate response element-binding protein and fatty acid synthase in mice fed the high-fructose diet, suggesting that ezetimibe did not reduce hepatic lipogenesis induced by the high-fructose diet. Elevation of hepatic and intestinal lipogenesis in mice fed a high-fructose diet may partly explain the differences in the effect of ezetimibe.

scholarly journals Sitagliptin can inhibit the development of hepatic steatosis in high-fructose diet-fed ob/ob mice

2015 ◽  
Vol 57 (3) ◽  
pp. 244-253 ◽  
Author(s):  
Tetsuya Sujishi ◽  
Shinya Fukunishi ◽  
Masaaki Ii ◽  
Ken Nakamura ◽  
Keisuke Yokohama ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
High Fructose Diet ◽  
High Fructose

β-Sitosterol mitigates the development of high-fructose diet-induced nonalcoholic fatty liver disease in growing male Sprague–Dawley rats

2020 ◽  
Vol 98 (1) ◽  
pp. 44-50 ◽  
Author(s):  
Nontobeko M. Gumede ◽  
Busisani W. Lembede ◽  
Pilani Nkomozepi ◽  
Richard L. Brooksbank ◽  
Kennedy H. Erlwanger ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Liver Lipid ◽  
Male Rat ◽  
Nonalcoholic Fatty Liver ◽  
High Fructose Diet ◽  
Group I ◽  
High Fructose

Fructose contributes to the development of nonalcoholic fatty liver disease (NAFLD). β-Sitosterol (Bst), a naturally occurring phytosterol, has antihyperlipidaemic and hepatoprotective properties. This study interrogated the potential protective effect of β-sitosterol against NAFLD in growing rats fed a high-fructose diet, modelling children fed obesogenic diets. Forty-four 21 day old male rat pups were randomly allocated to and administered the following treatments for 12 weeks: group I, standard rat chow (SRC) + plain drinking water (PW) + plain gelatine cube (PC); group II, SRC + 20% w/v fructose solution (FS) as drinking fluid + PC; group III, SRC + FS + 100 mg/kg fenofibrate in a gelatine cube; group IV, SRC + FS + 20 mg/kg β-sitosterol gelatine cube (Bst); group V, SRC + PW + Bst. Terminally, the livers were dissected out, weighed, total liver lipid content determined, and histological analyses done. Harvested plasma was used to determine the surrogate biomarkers of liver function. The high-fructose diet caused increased (p < 0.05) hepatic lipid (total) accretion (>10% liver mass), micro- and macrovesicular hepatic steatosis, and hepatic inflammation. β-Sitosterol and fenofibrate prevented the high-fructose diet-induced macrovesicular steatosis and prevented the progression of NAFLD to steatohepatitis. β-Sitosterol can prospectively be used to mitigate diet-induced NAFLD.

scholarly journals Adoptive Cell Transfer of Regulatory T Cells Exacerbates Hepatic Steatosis in High-Fat High-Fructose Diet-Fed Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Mikhaïl A. Van Herck ◽  
Luisa Vonghia ◽  
Wilhelmus J. Kwanten ◽  
Thomas Vanwolleghem ◽  
Didier G. Ebo ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Hepatic Steatosis ◽  
Adoptive Cell Transfer ◽  
Cell Transfer ◽  
High Fat ◽  
High Fructose Diet ◽  
High Fructose

Dietary fish oil differentially ameliorates high-fructose diet-induced hepatic steatosis and hyperlipidemia in mice depending on time of feeding

2018 ◽  
Vol 52 ◽  
pp. 45-53 ◽  
Author(s):  
Katsutaka Oishi ◽  
Tatsuya Konishi ◽  
Chiaki Hashimoto ◽  
Saori Yamamoto ◽  
Yoshinori Takahashi ◽  
...  
Keyword(s):  
Fish Oil ◽  
Hepatic Steatosis ◽  
High Fructose Diet ◽  
High Fructose ◽  
Dietary Fish ◽  
Time Of Feeding
Sign in / Sign up

Export Citation Format

Share Document