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 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 Beta-sitosterol upregulated paraoxonase-1 via peroxisome proliferator-activated receptor-γ in irradiated rats

2017 ◽  
Vol 95 (6) ◽  
pp. 661-666 ◽  
Author(s):  
Enas Mahmoud Moustafa ◽  
Noura Magdy Thabet
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Enzyme Activities ◽  
Liver Tissue ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Oxidative Stress Marker ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ

This study was designed to evaluate the effect of beta-sitosterol (BS) on the peroxisome proliferator-activated receptor gamma (PPAR-γ) gene expression role in the activity of paraoxonase (PON-1) enzyme in oxidative stress status of irradiated rats. Animals were exposed to whole body γ-radiation single dose 6 Gy and received BS dose (40 mg·(kg body mass)−1·day−1, orally). In liver tissue, gene expression of PPAR-γ ligand was determined. Oxidative stress marker (malondialdehyde, MDA) and antioxidant enzyme activities (superoxide dismutase (SOD), catalase (CAT), PON-1, and arylesterase (ARE)) were assayed in serum and liver tissue. Also, serum lipid profile (cholesterol, triglycerides (TG), low-density lipoprotein cholesterol (LDL-c), and high-density lipoprotein cholesterol (HDL-c)) was measured. In irradiated animals that received BS, expression of PPAR-γ ligand increase significantly associated with increase in PON-1 and ARE enzyme activities. Also, the activities of SOD, CAT enzymes, and HDL-c levels display elevation. By contrast, significant decrease in MDA content, cholesterol, TG, and LDL-c levels were revealed after BS administration. Our findings in this study provide the evidence that BS has radio-protective effect via regulating the gene expression of PPAR-γ, causing an increase in PON-1 and ARE enzyme activities. This action of BS is due to its free radical scavenging properties, antioxidant effect, lowering of cholesterol, and PPAR-γ agonist properties.

scholarly journals Gene expressions of de novo hepatic lipogenesis in feline hepatic lipidosis

2019 ◽  
Vol 22 (6) ◽  
pp. 500-505
Author(s):  
Chiara Valtolina ◽  
Joris H Robben ◽  
Monique E van Wolferen ◽  
Hedwig S Kruitwagen ◽  
Ronald J Corbee ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Liver Tissue ◽  
Fatty Acid Synthase ◽  
De Novo ◽  
Control Group ◽  
Peroxisome Proliferator ◽  
Hepatic Lipidosis ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ

Objectives The aim of this study was to evaluate if de novo hepatic lipid synthesis contributes to fatty acid overload in the liver of cats with feline hepatic lipidosis (FHL). Methods Lipogenic gene expression of peroxisome proliferator-activated receptor-alpha ( PPAR-α), peroxisome proliferator-activated receptor-gamma ( PPAR-γ), fatty acid synthase ( FASN) and sterol regulatory element-binding factor ( SREBF1) were evaluated using quantitative RT-PCR in liver tissue of six cats with FHL and compared with the liver tissue of eight healthy cats. Results In liver tissue, PPAR-α, PPAR-γ and FASN mRNA expression levels were not significantly different ( P >0.12, P >0.89 and P >0.5, respectively) in the FHL group compared with the control group. SREBF1 gene expression was downregulated around 10-fold in the FHL group vs the control group ( P = 0.039). Conclusions and relevance The downregulation of SREBF1 in the liver tissue of cats with FHL does not support the hypothesis that de novo lipogenesis in the liver is an important pathway of fatty acid accumulation in FHL.

scholarly journals Deoxyribonucleic Acid Methylation and Gene Expression of PPARGC1A in Human Muscle Is Influenced by High-Fat Overfeeding in a Birth-Weight-Dependent Manner

2010 ◽  
Vol 95 (6) ◽  
pp. 3048-3056 ◽  
Author(s):  
Charlotte Brøns ◽  
Stine Jacobsen ◽  
Emma Nilsson ◽  
Tina Rönn ◽  
Christine B. Jensen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Dna Methylation ◽  
Birth Weight ◽  
Control Diet ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Peripheral Insulin Resistance

Abstract Context: Low birth weight (LBW) and unhealthy diets are risk factors of metabolic disease including type 2 diabetes (T2D). Genetic, nongenetic, and epigenetic data propose a role of the key metabolic regulator peroxisome proliferator-activated receptor γ, coactivator 1α (PPARGC1A) in the development of T2D. Objective: Our objective was to investigate gene expression and DNA methylation of PPARGC1A and coregulated oxidative phosphorylation (OXPHOS) genes in LBW and normal birth weight (NBW) subjects during control and high-fat diets. Design, Subjects, and Main Outcome Measures: Twenty young healthy men with LBW and 26 matched NBW controls were studied after 5 d high-fat overfeeding (+50% calories) and after a control diet in a randomized manner. Hyperinsulinemic-euglycemic clamps were performed and skeletal muscle biopsies excised. DNA methylation and gene expression were measured using bisulfite sequencing and quantitative real-time PCR, respectively. Results: When challenged with high-fat overfeeding, LBW subjects developed peripheral insulin resistance and reduced PPARGC1A and OXPHOS (P &lt; 0.05) gene expression. PPARGC1A methylation was significantly higher in LBW subjects (P = 0.0002) during the control diet. However, PPARGC1A methylation increased in only NBW subjects after overfeeding in a reversible manner. DNA methylation of PPARGC1A did not correlate with mRNA expression. Conclusions: LBW subjects developed peripheral insulin resistance and decreased gene expression of PPARGC1A and OXPHOS genes when challenged with fat overfeeding. The extent to which our finding of a constitutively increased DNA methylation in the PPARGC1A promoter in LBW subjects may contribute needs to be determined. We provide the first experimental support in humans that DNA methylation induced by overfeeding is reversible.

scholarly journals Effect of Eight Weeks of Aerobic Progressive Training with Capsaicin on Changes in PGC-1α and UPC-1 Expression in Visceral Adipose Tissue of Obese Rats With Diet

2020 ◽  
Vol 10 (2) ◽  
pp. 106-117
Author(s):  
Maryam Mostafavian ◽  
◽  
Ahmad Abdi ◽  
Javad Mehrabani ◽  
Alireza Barari ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
High Fat Diet ◽  
Uncoupling Protein ◽  
Normal Diet ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Visceral Adipose

Objective: Decreased physical activity coupled with increased High‐Fat Diet (HFD) intake prompts obesity. Current research suggests that changing White Adipose Tissue (WAT) to brown promotes energy expenditure to counter obesity. The purpose of this study was to investigate the effects of aerobic Progressive training and Capsaicin (Cap) on Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and Uncoupling protein-1 (UPC-1) gene expression in rat fed a high-fat diet. Methods: 40 male Wistar rats aged 8-12 weeks, were fed a Normal Diet (ND) (n=8) or HFD (n=32) for 8 weeks. After 8 weeks, rats were divided into 5 groups: ND, HFD, High-Fat Diet-Training (HFDT), High-Fat Diet-Capsaicin (HFDCap), high-fat diet-training-capsaicin (HFDTCap). Training groups have performed a progressive aerobic running program on a motor-driven treadmill for eight weeks. Capsaicin (4 mg/kg/day) were administered orally, by gavage, once a day. PGC-1α and UCP-1 gene expression levels in the VAT were measured by Real-time PCR method. Results: The results of this study showed that PGC-1α and UCP-expression was decreased in HFD group compared to ND group. Also, the expression of PGC-1α and UPC-1 in HFDT, HFDCap and HFDTCap groups was significantly increased compared to HFD. The expression of PGC-1α and UPC-1 in HFDTCap was also significantly increased compared to HFDT and HFDCap groups. Conclusion: Possibly, eight weeks of progressive training combined with capsaicin administration has an effect on the browning of visceral adipose tissue in HFD rats by increasing expression of PGC-1α and UCP-1.

scholarly journals Anti-Obesity Effects of Lactobacillus fermentum CQPC05 Isolated from Sichuan Pickle in High-Fat Diet-Induced Obese Mice through PPAR-α Signaling Pathway

2019 ◽  
Vol 7 (7) ◽  
pp. 194 ◽  
Author(s):  
Kai Zhu ◽  
Fang Tan ◽  
Jianfei Mu ◽  
Ruokun Yi ◽  
Xianrong Zhou ◽  
...  
Keyword(s):  
Western Blot ◽  
High Fat Diet ◽  
Liver Tissue ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Peroxisome Proliferator ◽  
Obese Mice ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Expression Levels

Sichuan pickle is a traditional fermented food in China which is produced by the spontaneous fermentation of Chinese cabbage. In this study, the anti-obesity effects of a new lactic acid bacterium (Lactobacillus fermentum CQPC05, LF-CQPC05) isolated from Sichuan pickles were assessed in vivo. An obese animal model was established in mice by inducing obesity with high-fat diet. Both serum and tissues were collected from the mice, and then subjected to qPCR and Western blot analyses. The results showed that LF-CQPC05 could decrease the values of hepatosomatic, epididymal fat, and perirenal fat indices that were induced by a high-fat diet in mice. Moreover, LF-CQPC05 reduced the levels of alanine aminotransferase (ALT), aspartate aminotransaminase (AST), total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C), and increased the level of high-density lipoprotein cholesterol (HDL-C) in both serum samples and liver tissues of obese mice fed with a high-fat diet. Pathological observations demonstrated that LF-CQPC05 could alleviate the obesity-induced pathological changes in the liver tissue of mice, and reduce the degree of adipocyte enlargement. The results of qPCR and Western blot analyses further indicated that LF-CQPC05 upregulated the mRNA and protein expression levels of lipoprotein lipase (LPL), PPAR-α: peroxisome proliferator-activated receptor-alpha (PPAR-α), (cholesterol 7 alpha-hydroxylase) CYP7A1, and carnitine palmitoyltransferase 1 (CPT1A), and downregulated the expression levels of peroxisome proliferator-activated receptor-gamma (PPAR-γ) and CCAAT enhancer-binding protein alpha (C/EBP-α) in both liver tissue and epididymal adipose tissue. Taken altogether, this study reveals that LF-CQPC05 can effectively inhibit high-fat diet-induced obesity. Its anti-obesity effect is comparable to that of l-carnitine, and is superior to that of Lactobacillus delbrueckii subsp. bulgaricus, a common strain used in the dairy industry. Therefore, LF-CQPC05 is a high-quality microbial strain with probiotic potential.

scholarly journals Hepatic sirtuin 1 is dispensable for fibrate-induced peroxisome proliferator-activated receptor-α function in vivo

2014 ◽  
Vol 306 (7) ◽  
pp. E824-E837 ◽  
Author(s):  
Jessica A. Bonzo ◽  
Chad Brocker ◽  
Changtao Jiang ◽  
Rui-Hong Wang ◽  
Chu-Xia Deng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Target Genes ◽  
Sirtuin 1 ◽  
Peroxisome Proliferator ◽  
Wild Type ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor

Peroxisome proliferator-activated receptor-α (PPARα) mediates metabolic remodeling, resulting in enhanced mitochondrial and peroxisomal β-oxidation of fatty acids. In addition to the physiological stimuli of fasting and high-fat diet, PPARα is activated by the fibrate class of drugs for the treatment of dyslipidemia. Sirtuin 1 (SIRT1), an important regulator of energy homeostasis, was downregulated in fibrate-treated wild-type mice, suggesting PPARα regulation of Sirt1 gene expression. The impact of SIRT1 loss on PPARα functionality in vivo was assessed in hepatocyte-specific knockout mice that lack the deacetylase domain of SIRT1 ( Sirt1 ΔLiv). Knockout mice were treated with fibrates or fasted for 24 h to activate PPARα. Basal expression of the PPARα target genes Cyp4a10 and Cyp4a14 was reduced in Sirt1 ΔLiv mice compared with wild-type mice. However, no difference was observed between wild-type and Sirt1 ΔLiv mice in either fasting- or fibrate-mediated induction of PPARα target genes. Similar to the initial results, there was no difference in fibrate-activated PPARα gene induction. To assess the relationship between SIRT1 and PPARα in a pathophysiological setting, Sirt1 ΔLiv mice were maintained on a high-fat diet for 14 wk, followed by fibrate treatment. Sirt1 ΔLiv mice exhibited increased body mass compared with control mice. In the context of a high-fat diet, Sirt1 ΔLiv mice did not respond to the cholesterol-lowering effects of the fibrate treatment. However, there were no significant differences in PPARα target gene expression. These results suggest that, in vivo, SIRT1 deacetylase activity does not significantly impact induced PPARα activity.

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