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PPAR alpha AND betaine

Zhixian Leng, Qin Fu, Xue Yang, Liren Ding, Chao Wen, Yanmin Zhou
Two hundred and forty 1-day-old male Arbor Acres broiler chickens were randomly assigned to five dietary treatments with six replicates of eight chickens per replicate cage for a 42-day feeding trial. Broiler chickens were fed a basal diet supplemented with 0 (control), 250, 500, 750 or 1000 mg/kg betaine, respectively. Growth performance was not affected by betaine. Incremental levels of betaine decreased the absolute and relative weight of abdominal fat (linear P < 0.05, quadratic P < 0.01), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG) and total cholesterol (TC) (linear P < 0...
August 2016: Animal Science Journal, Nihon Chikusan Gakkaihō
Chen-Xu Ge, Rong Yu, Min-Xuan Xu, Pei-Qin Li, Chen-Yu Fan, Jian-Mei Li, Ling-Dong Kong
Betaine has been proven effective in treating nonalcoholic fatty liver disease (NAFLD) in animal models, however, its molecular mechanisms remain elusive. The aims of this study were to explore the mechanisms mediating the anti-inflammatory and anti-lipogenic actions of betaine in fructose-fed rats. In this study, betaine improved insulin resistance, reduced body weight gain and serum lipid levels, and prevented hepatic lipid accumulation in fructose-fed rats. It up-regulated hepatic expression of liver X receptor-alpha (LXRα) and peroxisome proliferator-activated receptor-alpha (PPARα), with the attenuation of the changes of their target genes, including hepatic carnitine palmitoyl transferase (CPT) 1α, glycosylphosphatidylinositol anchored high density lipoprotein binding protein 1, apolipoprotein B, sterol regulatory element-binding protein 1c and adipocyte differentiation-related protein, involved in fatty acid oxidation and lipid storage in these model rats...
January 5, 2016: European Journal of Pharmacology
M Raj Lakshman, Karina Reyes-Gordillo, Ravi Varatharajalu, Jaime Arellanes-Robledo, Leslie C Leckey, Mamatha Garige, Ruchi Shah
Alcoholic steatosis, instead of being innocuous, plays a critical role in liver inflammation and fibrogenesis. The severity of fatty liver is governed by the concerted balance between lipid transport, synthesis, and degradation. Whereas scavenger receptor class B, type I (SR-B1) is critical for reverse cholesterol uptake by the liver, peroxisome proliferator-activated receptor-gamma (PPARγ) coactivator-1α and -β (PGC1α and PGC1β) are critical for lipid degradation and synthesis, respectively. Because betaine is a lipotropic agent, we have evaluated its effects on alcoholic steatosis...
September 2014: Hepatology International
Li Xu, Danping Huang, Qiaolin Hu, Jing Wu, Yizhen Wang, Jie Feng
To assess the effects of betaine on hepatic lipid accumulation and investigate the underlying mechanism, thirty-two male Sprague-Dawley rats weighing 100 (sd 2·50) g were divided into four groups, and started on one of four treatments: basal diet, basal diet with betaine administration, high-fat diet and high-fat diet with betaine administration. The results showed that no significant difference of body weight was found among experimental groups. Compared with high-fat diet-fed rats, a betaine supplementation decreased (P< 0·05) hepatic TAG accumulation induced by high-fat diet, which was also supported by hepatic histology results...
June 28, 2015: British Journal of Nutrition
Valentina Medici, Diane I Schroeder, Rima Woods, Janine M LaSalle, Yongzhi Geng, Noreene M Shibata, Janet Peerson, Emir Hodzic, Sanjana Dayal, Hidekazu Tsukamoto, Kusum K Kharbanda, Brittany Tillman, Samuel W French, Charles H Halsted
BACKGROUND: Alcoholic steatohepatitis (ASH) is caused in part by the effects of ethanol (EtOH) on hepatic methionine metabolism. METHODS: To investigate the phenotypic and epigenetic consequences of altered methionine metabolism in this disease, we studied the effects of 4-week intragastric EtOH feeding with and without the methyl donor betaine in cystathionine beta synthase (CβS) heterozygous C57BL/6J mice. RESULTS: The histopathology of early ASH was induced by EtOH feeding and prevented by betaine supplementation, while EtOH feeding reduced and betaine supplementation maintained the hepatic methylation ratio of the universal methyl donor S-adenosylmethionine (SAM) to the methyltransferase inhibitor S-adenosylhomocysteine (SAH)...
June 2014: Alcoholism, Clinical and Experimental Research
Lijun Wang, Li Chen, Yaozong Tan, Jun Wei, Ying Chang, Tianru Jin, Huilian Zhu
BACKGROUND: Betaine is a methyl donor and has been considered as a lipotropic effect substance. But its mechanism remains unclear. Hepatic steatosis is associated with abnormal expression of genes involved in hepatic lipid metabolism. DNA methylation contributes to the disregulation of gene expression. Here we hypothesized that betaine supplement and subsequent DNA methylation modifications alter the expression of genes that are involved in hepatic lipid metabolism and hence alleviate hepatic triglyceride accumulation...
2013: Lipids in Health and Disease
Christoph Dahlhoff, Charles Desmarchelier, Manuela Sailer, Rainer W Fürst, Alexander Haag, Susanne E Ulbrich, Björn Hummel, Rima Obeid, Jürgen Geisel, Bernhard L Bader, Hannelore Daniel
Obesity is an underlying risk factor in the development of cardiovascular disease, dyslipidemia and non-alcoholic fatty liver disease (NAFLD). Increased hepatic lipid accumulation is a hallmark in the progression of NAFLD and impairments in liver phosphatidylcholine (PC) metabolism may be central to the pathogenesis. Hepatic PC biosynthesis, which is linked to the one-carbon (C1) metabolism by phosphatidylethanolamine N-methyltransferase, is known to be important for hepatic lipid export by VLDL particles. Here, we assessed the influence of a high-fat (HF) diet and NAFLD status in mice on hepatic methyl-group expenditure and C1-metabolism by analyzing changes in gene expression, protein levels, metabolite concentrations, and nuclear epigenetic processes...
2013: PloS One
Vishnudutt Purohit, Bin Gao, Byoung-Joon Song
Alcoholic fatty liver is a potentially pathologic condition which can progress to steatohepatitis, fibrosis, and cirrhosis if alcohol consumption is continued. Alcohol exposure may induce fatty liver by increasing NADH/NAD(+) ratio, increasing sterol regulatory element-binding protein-1 (SREBP-1) activity, decreasing peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activity, and increasing complement C3 hepatic levels. Alcohol may increase SREBP-1 activity by decreasing the activities of AMP-activated protein kinase and sirtuin-1...
February 2009: Alcoholism, Clinical and Experimental Research
Alexander Koch, Bettina König, Gabriele I Stangl, Klaus Eder
We tested the hypothesis that transcription of novel organic cation transporters (OCTNs) is directly regulated by peroxisome proliferator-activated receptor (PPAR)-alpha. Therefore, wild-type mice and mice deficient in PPAR alpha (PPAR alpha-/-) were treated with the PPAR alpha agonist WY 14,643. Wild-type mice treated with WY 14,643 had a greater abundance of OCTN2 mRNA in their liver, muscle, kidney, and small intestine and a greater abundance of OCTN3 mRNA in kidney and small intestine than did untreated wild-type mice (P < 0...
March 2008: Experimental Biology and Medicine
Robert Ringseis, Sebastian Luci, Julia Spielmann, Holger Kluge, Maren Fischer, Stefanie Geissler, Gaiping Wen, Frank Hirche, Klaus Eder
Recent studies have shown that treatment of rodents with agonists of peroxisome proliferator-activated receptor (PPAR)-alpha causes an up-regulation of novel organic cation transporter (OCTN)-2, a carnitine transporter, and increases carnitine concentration in the liver. This study was performed to investigate whether such effects occur also in pigs which like humans have a lower expression of PPAR alpha and are less responsive to treatment with PPAR alpha agonists than rodents. An experiment with 18 pigs was performed which were fed a control diet or the same diet supplemented with 5 g clofibrate/kg for 28 days...
March 31, 2008: European Journal of Pharmacology
Robert Ringseis, Stefanie Pösel, Frank Hirche, Klaus Eder
Activation of PPARalpha by clofibrate has recently been shown to cause upregulation of carnitine transporter organic cation transporter (OCTN) 2 and elevated carnitine concentrations in rat liver. The present study has been conducted to further explore the effect of clofibrate on OCTN expression, carnitine biosynthesis, and carnitine accumulation in different rat tissues, and thus two groups of rats were fed diets containing 0.5% clofibrate or 0% clofibrate (control group). PPARalpha-responsive genes were markedly upregulated in the liver (P<0...
August 2007: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
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