scholarly journals Role of swimming on muscle PGC-1α, FNDC5 mRNA, and assessment of serum omentin, adropin, and irisin in high carbohydrate high fat (HCHF) diet induced obesity in rats

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Ehsan Badawy ◽  
Nabila A. El-laithy ◽  
Safaa M. Morsy ◽  
Magdi N. Ashour ◽  
Tahany R. Elias ◽  
...  
Keyword(s):  
Swimming Exercise ◽  
Control Group ◽  
Standard Diet ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
High Carbohydrate ◽  
Diet Induced Obesity ◽  
Organ Systems

Abstract Background Exercise benefits a variety of organ systems in mammals, and some of the best recognized effects of exercise on muscle are mediated by the transcriptional peroxisome proliferator-activated receptor gamma co-activator 1-α (PGC-1α). The regulatory effect of swimming on muscle PGC-1α, FNDC5 mRNA expression, and subsequently irisin levels is more controversial. This study aimed to investigate the role of swimming as an exercise on the expression of peroxisome proliferator-activated receptor-gamma coactivator1 alpha (PGC-1α) and Fibronectin type III domain containing 5 (FNDC5) mRNA in skeletal muscle and assessment of serum omentin, adropin, irisin, and PGC-1α levels in high carbohydrate high fat (HCHF) diet induced obesity in rats. Sixty male albino rats are randomly divided into 4 groups (15 rats/group). In the first group (control), rats are fed with standard diet. The 2nd group (cont + swim) is fed on standard diet and made swimming exercise. The 3rd group of rats is fed on HCHF, whereas in the 4th group (HCHF + swim) is also fed on HCHF diet and made swimming exercise for 20 weeks. Blood glucose, insulin, HOMA-IR, lipid profile, omentin, irisin, adropin, and PGC-1α were measured. Also, FNDC5 and PGC-1α are extracted and purified from muscle tissue samples measured by PCR test. Results Our results showed significant increase in glucose, insulin, insulin resistance, cholesterol, and triglycerides with significant decrease in omentin, irisin, adropin, PGC-1α, and HDL in HCHF group as compared to the control group. These results improved after exercise in all parameter in HCHF + swim group compare to HCHF group. Also, there was inverse correlation between omentin and fasting glucose and HOMA-IR in HCHF + swim group. Conclusions It concluded that swimming exercise improved all the above measured parameters in serum and tissues which might have been promising for the prevention of metabolic diseases.

scholarly journals Citrus ichangensisPeel Extract Exhibits Anti-Metabolic Disorder Effects by the Inhibition of PPARγand LXR Signaling in High-Fat Diet-Induced C57BL/6 Mouse

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Xiaobo Ding ◽  
Shengjie Fan ◽  
Yan Lu ◽  
Yu Zhang ◽  
Ming Gu ◽  
...  
Keyword(s):  
Fatty Acid Synthase ◽  
Target Genes ◽  
Body Weight Gain ◽  
Density Lipoprotein ◽  
Chow Diet ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Nutritional Disorder ◽  
Peroxisome Proliferator Activated Receptor ◽  
Diet Induced Obesity

Obesity is a common nutritional disorder associated with type 2 diabetes, cardiovascular diseases, dyslipidemia, and certain cancers. In this study, we investigated the effects ofCitrus ichangensispeel extract (CIE) in high-fat (HF) diet-induced obesity mice. Female C57BL/6 mice were fed a chow diet or an HF diet alone or supplemented with 1% w/w CIE for 8 weeks. We found that CIE treatment could lower blood glucose level and improve glucose tolerance. In the HF+CIE group, body weight gain, serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-c) levels, and liver triglyceride (TG) and TC concentrations were significantly (P<0.05) decreased relative to those in the HF group. To elucidate the mechanism of CIE on the metabolism of glucose and lipid, related genes expression in liver were examined. In liver tissue, CIE significantly decreased the mRNA expression levels of peroxisome proliferator-activated receptorγ(PPARγ) and its target genes, such as fatty acid synthase (FAS) and acyl-CoA oxidase (ACO). Moreover, CIE also decreased the expression of liver X receptor (LXR)αandβwhich are involved in lipid and glucose metabolism. These results suggest that CIE administration could alleviate obesity and related metabolic disorders in HF diet-induced obesity mice through the inhibition of PPARγand LXR signaling.

scholarly journals Evaluation of the role of peroxisome-proliferator-activated receptor α in the regulation of cardiac pyruvate dehydrogenase kinase 4 protein expression in response to starvation, high-fat feeding and hyperthyroidism

2002 ◽  
Vol 364 (3) ◽  
pp. 687-694 ◽  
Author(s):  
Mark J. HOLNESS ◽  
Nicholas D. SMITH ◽  
Karen BULMER ◽  
Teresa HOPKINS ◽  
Geoffrey F. GIBBONS ◽  
...  
Keyword(s):  
Protein Expression ◽  
Pyruvate Dehydrogenase ◽  
Fold Increase ◽  
Pyruvate Dehydrogenase Kinase ◽  
Peroxisome Proliferator ◽  
Wild Type ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor

Inactivation of cardiac pyruvate dehydrogenase complex (PDC) after prolonged starvation and in response to hyperthyroidism is associated with enhanced protein expression of pyruvate dehydrogenase kinase (PDK) isoform 4. The present study examined the potential role of peroxisome-proliferator-activated receptor α (PPARα) in adaptive modification of cardiac PDK4 protein expression after starvation and in hyperthyroidism. PDK4 protein expression was analysed by immunoblotting in homogenates of hearts from fed or 48h-starved rats, rats rendered hyperthyroid by subcutaneous injection of tri-iodothyronine and a subgroup of euthyroid rats maintained on a high-fat/low-carbohydrate diet, with or without treatment with the PPARα agonist WY14,643. In addition, PDK4 protein expression was analysed in hearts from fed, 24h-starved or 6h-refed wild-type or PPARα-null mice. PPARα activation by WY14,643 in vivo over the timescale of the response to starvation failed to up-regulate cardiac PDK4 protein expression in rats maintained on standard diet (WY14,643, 1.1-fold increase; starvation, 1.8-fold increase) or influence the cardiac PDK4 response to starvation. By contrast, PPARα activation by WY14,643 in vivo significantly enhanced cardiac PDK4 protein expression in rats maintained on a high-fat diet, which itself increased cardiac PDK4 protein expression. PPARα deficiency did not abolish up-regulation of cardiac PDK4 protein expression in response to starvation (2.9-fold increases in both wild-type and PPARα-null mice). Starvation and hyperthyroidism exerted additive effects on cardiac PDK4 protein expression, but PPARα activation by WY14,643 did not influence the response of cardiac PDK4 protein expression to hyperthyroidism in either the fed or starved state. Our data support the hypothesis that cardiac PDK4 protein expression is regulated, at least in part, by a fatty acid-dependent, PPARα-independent mechanism and strongly implicate a fall in insulin in either initiating or facilitating the response of cardiac PDK4 protein expression to starvation.

Antagonism of peroxisome proliferator-activated receptor γ prevents high-fat diet-induced obesity in vivo

2006 ◽  
Vol 72 (1) ◽  
pp. 42-52 ◽  
Author(s):  
Ryosuke Nakano ◽  
Eiji Kurosaki ◽  
Shigeru Yoshida ◽  
Masanori Yokono ◽  
Akiyoshi Shimaya ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Diet Induced Obesity
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