scholarly journals Synbiotic kefir lowered peroxisome proliferator activated receptor gamma (PPARγ) gene expression in rat fed high-fat and high-fructose diet

2020 ◽  
Author(s):  
Nurliyani ◽  
Eni Harmayani ◽  
Sunarti
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Blood Glucose ◽  
Peroxisome Proliferator ◽  
Milk Product ◽  
High Fat ◽  
Necrosis Factor Alpha ◽  
Peroxisome Proliferator Activated Receptor ◽  
High Fructose Diet ◽  
High Fructose

Abstract Kefir is fermented milk product containing bacteria and yeast, whereas glucomannan from porang (Amorphophallus oncophyllus) tuber has known as prebiotic in vivo. Diets with a high fat and high sugar will stimulate metabolic syndrome. The objective of this study were to determine the effect of synbiotic kefir (goat milk kefir enriched with porang glucomannan) on blood glucose, hemoglobin A1c (HbA1c), free fatty acid (FFA), tumor necrosis factor alpha (TNF-α), gene expression of peroxisome proliferator activated receptor gamma (PPARγ), and insulin producing cells in rat fed high- fat and high- fructose (HFHF) diet. Rats were divided into 5 groups: normal; high fat high fructose (HFHF); HFHF + probiotic kefir; HFHF + synbiotic kefir; and HFHF + simvastatin. There was no significantly differences in plasma blood glucose in HFHF rat after treated with synbiotic kefir. However, synbiotic kefir could decrease HbA1c and plasma TNFα, and inhibit the increasing FFA in HFHF rats. Probiotic and synbiotic kefir could decrease gene expression of PPARγ2 in both of adipose and liver tissue in HFHF rats, but had no effect on total number of Langerhans islet and insulin producing cell. In conclusion, synbiotic kefir could ameliorate the health of rats in condition of high-fat and high-fructose diet, through decreasing in HbA1c, TNFα, and gene expression of PPARγ2 and also prevent the increasing of FFA. Therefore, synbiotic kefir containing porang glucomannan is expected to be a suggestion for the food industry to develop synbiotic-based functional foods which has the potential to improve metabolic syndrome

scholarly journals Synbiotic Goat Milk Kefir Lowered Peroxisome Proliferator Activated Receptor Gamma (PPARγ) Gene Expression in Rat Adipose and Liver Tissue

2021 ◽  
Author(s):  
Nurliyani Nurliyani ◽  
Eni Harmayani ◽  
Sunarti Sunarti
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Blood Glucose ◽  
Liver Tissue ◽  
Goat Milk ◽  
Peroxisome Proliferator ◽  
Milk Product ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Insulin Producing Cells

Abstract Background Kefir is a fermented milk product containing bacteria and yeast, whereas glucomannan from porang (Amorphophallus oncophyllus) tuber is known as a prebiotic in vivo. Diets with a high fat and high sugar will stimulate metabolic syndrome associated with changes in gene expression including peroxisome proliferator activated receptor gamma (PPARγ). The purpose of this study was to determine the effect of goat milk kefir enriched with porang glucomannan (synbiotic kefir) and goat milk kefir without glucomannan (probiotic kefir) on blood glucose, hemoglobin A1c (HbA1c), free fatty acid (FFA), tumor necrosis factor alpha (TNF-α), gene expression of peroxisome proliferator activated receptor gamma (PPARγ), and insulin-producing cells in rats fed a high-fat and high-fructose (HFHF) diet. Methods Male Sprague Dawley rats 8–12 weeks old (n = 30) treated with HFHF diets for two weeks, and then divided into five dietary groups (each group consisted of 6 rats): 1) normal control (received a standard diet only); 2) rats fed HFHF; 3) rats fed HFHF + probiotic kefir; 4) rats fed HFHF + synbiotic kefir; and 5) rats fed HFHF + simvastatin. The dose of kefir was 3.6 mL/200 g body weight/day and simvastatin was 0.72 mg/day. All of these treatments were carried out for 4 weeks. Results There were no significant differences in plasma blood glucose in HFHF rats after and before treatment, but decreased in plasma HbA1c and TNFα (p < 0.05) and inhibited the increase of FFA in rats after synbiotic kefir treatment (paired-samples t-test). Probiotic and synbiotic kefir decreased the gene expression of PPARγ2 (p < 0.05) in both of adipose and liver tissue in HFHF rats but had no effect on the total number of Langerhans islets and insulin-producing cells (one way ANOVA). Conclusions Synbiotic kefir could ameliorate the health of rats fed HFHF diet through decreasing HbA1c, TNFα, and PPARγ2 gene expression and preventing an increase in FFA. The results indicate that goat milk synbiotic kefir potentially improve metabolic syndrome.

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 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

Impact of high-fat and high-fat-high-fructose diet on vessels and heart in rats with metabolic syndrome

2017 ◽  
Vol 280 ◽  
pp. S274
Author(s):  
Barbara Kaprinay ◽  
Boris Lipták ◽  
Ružena Sotníková ◽  
Vladimír Knezl ◽  
Zdenka Gáspárová
Keyword(s):  
Metabolic Syndrome ◽  
High Fat ◽  
High Fructose Diet ◽  
High Fructose

scholarly journals Effects of Ferulic Acid and γ-Oryzanol on High-Fat and High-Fructose Diet-Induced Metabolic Syndrome in Rats

PLoS ONE ◽  
2015 ◽  
Vol 10 (2) ◽  
pp. e0118135 ◽  
Author(s):  
Ou Wang ◽  
Jia Liu ◽  
Qian Cheng ◽  
Xiaoxuan Guo ◽  
Yong Wang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Ferulic Acid ◽  
High Fat ◽  
High Fructose Diet ◽  
High Fructose

scholarly journals Comparative Effects and Mechanisms of Chitosan and Its Derivatives on Hypercholesterolemia in High-Fat Diet-Fed Rats

2019 ◽  
Vol 21 (1) ◽  
pp. 92 ◽  
Author(s):  
Chen-Yuan Chiu ◽  
Tsai-En Yen ◽  
Shing-Hwa Liu ◽  
Meng-Tsan Chiang
Keyword(s):  
Molecular Weight ◽  
Protein Expression ◽  
Density Lipoprotein ◽  
Cholesterol Homeostasis ◽  
Chitosan Oligosaccharide ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Gene Expressions ◽  
Necrosis Factor Alpha ◽  
Peroxisome Proliferator Activated Receptor

The present study investigated and compared the effects of different molecular weights of chitosan (high molecular weight chitosan (HC) and low molecular weight chitosan (LC)) and its derivatives (chitosan oligosaccharide (CO)) on cholesterol regulation in high-fat (HF) diet-fed rats. A diet supplementation of 5% HC, 5% LC, or 5% CO for 8 weeks showed hypocholesterolemic potential in HF diet-fed rats. Unexpectedly, a 5% CO-supplemented diet exerted hepatic damage, producing increased levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and tumor necrosis factor-alpha (TNF-α). The supplementation of HC and LC, unlike CO, significantly decreased the hepatic total cholesterol (TC) levels and increased the fecal TC levels in HF diet-fed rats. The hepatic protein expression of the peroxisome proliferator-activated receptor-α (PPARα) in the HF diet-fed rats was markedly decreased, which could be significantly reversed by both HC and LC, but not CO, supplementation. Unlike the supplementation of CO, both HC and LC supplementation could effectively reverse the HF-inhibited/induced gene expressions of the low-density lipoprotein receptor (LDLR) and cholesterol 7α-hydroxylase (CYP7A1), respectively. The upregulated intestinal acyl-CoA cholesterol acyltransferase 2 (ACAT2) protein expression in HF diet-fed rats could be reversed by HC and LC, but not CO, supplementation. Taken together, a supplementation of 5% CO in HF diet-fed rats may exert liver damage via a higher hepatic cholesterol accumulation and a higher intestinal cholesterol uptake. Both HC and LC effectively ameliorated the hypercholesterolemia and regulated cholesterol homeostasis via the activation and inhibition of hepatic (AMPKα and PPARα) and intestinal (ACAT2) cholesterol-modulators, respectively, as well as the modulation of downstream signals (LDLR and CYP7A1).

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