Sitagliptin Can Prevent the Development of Hepatic Steatosis Due to Inhibiting the Expressions of Hepatic Lipogenic-genes in High-Fructose Diet-Fed Ob/ob Mice

2015 ◽  
Vol 110 ◽  
pp. S857-S858
Author(s):  
Shinya Fukunishi ◽  
Akira Asai ◽  
Yasuhiro Tsuda ◽  
Kazuhide Higuchi
Keyword(s):  
Hepatic Steatosis ◽  
High Fructose Diet ◽  
Lipogenic Genes ◽  
High Fructose

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

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

Levocetirizine ameliorates high fructose diet-induced insulin resistance, vascular dysfunction and hepatic steatosis in rats

2014 ◽  
Vol 740 ◽  
pp. 353-363 ◽  
Author(s):  
Noha M. Shawky ◽  
George S.G. Shehatou ◽  
Mona Abdel Rahim ◽  
Ghada M. Suddek ◽  
Nariman M. Gameil
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Vascular Dysfunction ◽  
High Fructose Diet ◽  
High Fructose

scholarly journals ETHANOLIC EXTRACT OF TUBTIM-CHUMPHAE RICE BRAN DECREASES INSULIN RESISTANCE AND INTRAHEPATIC FAT ACCUMULATION IN HIGH-FAT-HIGH-FRUCTOSE DIET FED RATS

2019 ◽  
Vol 12 (1) ◽  
pp. 506
Author(s):  
Jiraprapa Ponglong ◽  
Laddawan Senggunprai ◽  
Panot Tungsutjarit ◽  
Ronnachai Changsri ◽  
Tunvaraporn Proongkhong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Hepatic Steatosis ◽  
Rice Bran ◽  
High Fat Diet ◽  
High Fat ◽  
Fat Accumulation ◽  
High Fructose Diet ◽  
High Fructose

Objective: Tubtim-chumphae rice is hybrid Thai rice with a red pericarp. This study was aimed to investigate the effect of Tubtim-chumphae rice bran on insulin resistance and intrahepatic fat accumulation in high-fat-high-fructose diet (HFFD) fed rats.Methods: Ethanolic extract of rice bran (ERB) was prepared using a 50% ethanol-water. Male Sprague-Dawley rats were fed HFFD (40% lard, 20% fructose) for 10 weeks, followed by concomitant administrations of distilled water or ERB at 250 or 500 mg/kg/day or pioglitazone at 10 mg/kg/day for a further 4 weeks in treated groups. Normal control rats were fed normal chow and distilled water. At the end of all treatments, fasting blood glucose (FBG), an oral glucose tolerance test (OGTT), serum insulin levels, lipid profiles, and liver fat contents were measured. Liver histological and peroxisome proliferator-activated receptor-α (PPAR-α) gene expression examinations were performed.Results: At week 14, control HFFD rats had significantly (p<0.05) higher FBG, low-density lipoprotein cholesterol, triglycerides, and insulin secretions together with impaired OGTT as compared to normal control rats. These parameters indicated an insulin resistant and dyslipidemic condition in HFFD rats. ERB 250 and 500 mg/kg or pioglitazone 10 mg/kg significantly ameliorated all of these changes. HFFD also caused a significant increase in fat accumulation and a decrease in PPAR-α gene expression in the livers which were significantly decreased by ERB.Conclusions: ERB decreases insulin resistance and intrahepatic fat accumulation possibly through increasing PPAR-α gene expression in HFFD rats. ERB might possibly be a neutraceutical for the metabolic syndrome patients.1. Gauthier MS, Favier R, Lavoie JM. Time course of the development of non-alcoholic hepatic steatosis in response to high-fat diet-induced obesity in rats. Br J Nutr 2006;95:273-81.2. Roberts CK, Hevener AL, Barnard RJ. Metabolic syndrome and insulin resistance: Underlying causes and modification by exercise training. Compr Physiol 2013;3:1-58.3. Grundy SM. Metabolic syndrome update. Trends Cardiovasc Med 2016;26:364-73.4. Fouret G, Gaillet S, Lecomte J, Bonafos B, Djohan F, Barea B, et al. 20-week follow-up of hepatic steatosis installation and liver mitochondrial structure and activity and their interrelation in rats fed a high-fat-high-fructose diet. Br J Nutr 2018;119:368-80.5. Dekker MJ, Su Q, Baker C, Rutledge AC, Adeli K. Fructose: A highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome. Am J Physiol Endocrinol Metab 2010;299:E685-94.6. Vichit W, Saewan N. Antioxidant activities and cytotoxicity of thai pigmented rice. Int J Pharm Pharm Sci 2015;7:329-34.7. Settharaksa S, Madaka F, Charkree K, Charoenchai L. The study of anti-inflammatory and antioxidant activity in cold press rice bran oil from rice in Thailand. Int J Pharm Pharm Sci 2014;6:428-31.8. Sukrasno S, Tuty S, Fidrianny I. Antioxidant evaluation and phytochemical content of various rice bran extracts of three varieties rice from Semarang, central Java, Indonesia. Asian J Pharm Clin Res 2017;10:377-82.9. Sabir A, Rafi M, Darusman LK. Discrimination of red and white rice bran from indonesia using HPLC fingerprint analysis combined with chemometrics. Food Chem 2017;221:1717-22.10. Niu Y, Gao B, Slavin M, Zhang X, Yang F, Bao J, et al. Phytochemical compositions, and antioxidant and anti-inflammatory properties of twenty-two red rice samples grown in Zhejiang. LWT Food Sci Technol 2013;54:521-7.11. Boonloh K, Kukongviriyapan V, Kongyingyoes B, Kukongviriyapan U, Thawornchinsombut S, Pannangpetch P, et al. Rice bran protein hydrolysates improve insulin resistance and decrease pro-inflammatory cytokine gene expression in rats fed a high carbohydrate-high fat diet. Nutrients 2015;7:6313-29.12. Peñarrieta JM, Alvarado JA, Akesson B, Bergenståhl B. Total antioxidant capacity and content of flavonoids and other phenolic compounds in canihua (Chenopodium pallidicaule): An andean pseudocereal. Mol Nutr Food Res 2008;52:708-17.13. Mungkhunthod S, Senggunprai L, Tangsucharit P, Sripui J, Kukongviriyapan U, Pannangpetch P. Antidesma thwaitesianum pomace extract improves insulin sensitivity via upregulation of PPAR-γ in high fat diet/streptozotocin-induced Type 2 diabetic rats. Asia Pac J Sci Technol 2016;21:63-76.14. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC, et al. Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28:412-9.15. Naowaboot J, Wannasiri S. Anti-lipogenic effect of Senna alata leaf extract in high-fat diet-induced obese mice. Asian Pac J Trop Biomed 2016;6:232-8.16. Couturier K, Qin B, Batandier C, Awada M, Hininger-Favier I, Canini F, et al. Cinnamon increases liver glycogen in an animal model of insulin

scholarly journals Ficus thonningii Stem Bark Extracts Prevent High Fructose Diet Induced Increased Plasma Triglyceride Concentration, Hepatic Steatosis and Inflammation in Growing Sprague-Dawley Rats

2021 ◽  
Author(s):  
Eliton Chivandi ◽  
Yvonne Mhosva ◽  
Trevor Nyakudya ◽  
Pilani Nkomozepi
Keyword(s):  
Hepatic Steatosis ◽  
Low Dose ◽  
Stem Bark ◽  
Plasma Triglyceride ◽  
Insulin Concentration ◽  
High Dose ◽  
Sprague Dawley ◽  
High Fructose Diet ◽  
High Fructose ◽  
Ficus Thonningii

BACKGROUND: Ficus thonningii extracts exhibit hypoglycaemic, hypolipidaemic and antioxidant activities. We investigated the potential of methanolic F. thonningii stem-bark extracts (MEFT) to protect growing Sprague-Dawley (SD) against high-fructose diet-induced metabolic derangements (MD) in a model mimicking children fed obesogenic diets. METHODS: Eighty (40 males; 40 females) 21-days old SD rat pups were randomly allocat-ed to and administered, for 8 weeks, five treatment regimens: 1 - standard rat chow (SC) + water (PW), 2 - SC + 20% (w/v) fructose solution (FS), 3 - SC + FS + fenofibrate at 100 mg/kg bwt/day, 4 - SC + FS + low dose MEFT (LD; 50 mg/kg bwt/day) and 5 - SC + FS + high dose MEFT (HD; 500 mg/kg bwt/day). Body weight, glucose load tolerance, fasting blood glucose and triglyceride, plasma insulin concentration, sensitivity to insulin, liver mass and fat content, steatosis and inflammation were determined. RESULTS: Fructose had no effect on the rats&rsquo; growth, glucose and insulin concentration, glucose tolerance and insulin sensitivity (P&gt;0.05) but increased triglycerides in females; in-duced hepatic microsteatosis and inflammation in both sexes but macrosteatosis in females (P&lt;0.05). In females, MEFT prevented fructose-induced plasma triglyceride increase. Low dose MEFT increased liver lipid content in females (P&lt;0.05). The MEFT protected the rats against hepatic steatosis and inflammation but fenofibrate protected against hepatic mi-crosteatosis. CONCLUSION: MEFT can be used as prophylaxis against dietary fructose-induced ele-ments of MD but caution must be taken as low dose MEFT increases hepatic lipid accretion in females predisposing to fatty liver disease.

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