Impact of high-fat diet and antioxidant supplement on mitochondrial functions and gene transcripts in rat muscle

2002 ◽  
Vol 282 (5) ◽  
pp. E1055-E1061 ◽  
Author(s):  
R. Sreekumar ◽  
J. Unnikrishnan ◽  
A. Fu ◽  
J. Nygren ◽  
K. R. Short ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Free Radical ◽  
Stress Response ◽  
High Fat Diet ◽  
Male Rats ◽  
High Fat ◽  
Antioxidant Supplementation ◽  
Transcript Levels ◽  
Atp Production ◽  
Mitochondrial Functions

High-fat diets are reported to increase oxidative stress in a variety of tissues, whereas antioxidant supplementation prevents many diseases attributed to high-fat diet. Rodent skeletal muscle mitochondrial DNA has been shown to be a potential site of oxidative damage. We hypothesized that the effects of a high-fat diet on skeletal muscle DNA functions would be attenuated or partially reversed by antioxidant supplementation. Gene expression profiling and measurement of mitochondrial ATP production capacity were performed in skeletal muscle from male rats after feeding one of three diets (control, high-fat diet with or without antioxidants) for 36 wk. The high-fat diet altered transcript levels of 18 genes of 800 surveyed compared with the control-fed rats. Alterations included reduced expression of genes involved in free-radical scavenging and tissue development and increased expression of stress response and signal transduction genes. The magnitude of these alterations due to high-fat diet was reduced by antioxidant supplementation. Real-time PCR measurements confirmed the changes in transcript levels of cytochrome c oxidase subunit III and superoxide dismutase-1 and -2 noted by microarray approach. Mitochondrial ATP production was unaltered by dietary changes or antioxidant supplemention. It is concluded that the high-fat diet increases the transcription of genes involved in stress response but reduces those of free-radical scavenger enzymes, resulting in reduced DNA repair/metabolism (increased DNA damage). Antioxidants partially prevent these changes. Mitochondrial functions in skeletal muscle remain unaltered by the dietary intervention due to many adaptive changes in gene transcription.

Caloric restriction following early-life high fat-diet feeding represses skeletal muscle TNF in male rats

2021 ◽  
Vol 91 ◽  
pp. 108598
Author(s):  
Diego Hernández-Saavedra ◽  
Laura Moody ◽  
Xinyu Tang ◽  
Zachary J. Goldberg ◽  
Alex P. Wang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Caloric Restriction ◽  
High Fat Diet ◽  
Early Life ◽  
Male Rats ◽  
High Fat

Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance

2007 ◽  
Vol 293 (1) ◽  
pp. E31-E41 ◽  
Author(s):  
Robert C. Noland ◽  
John P. Thyfault ◽  
Sarah T. Henes ◽  
Brian R. Whitfield ◽  
Tracey L. Woodlief ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Weight Gain ◽  
High Fat Diet ◽  
Oxidative Capacity ◽  
Male Rats ◽  
High Fat ◽  
Endurance Running ◽  
Muscle Oxidative Capacity ◽  
Obesity And Diabetes

Elevated oxidative capacity, such as occurs via endurance exercise training, is believed to protect against the development of obesity and diabetes. Rats bred both for low (LCR)- and high (HCR)-capacity endurance running provide a genetic model with inherent differences in aerobic capacity that allows for the testing of this supposition without the confounding effects of a training stimulus. The purpose of this investigation was to determine the effects of a high-fat diet (HFD) on weight gain patterns, insulin sensitivity, and fatty acid oxidative capacity in LCR and HCR male rats in the untrained state. Results indicate chow-fed LCR rats were heavier, hypertriglyceridemic, less insulin sensitive, and had lower skeletal muscle oxidative capacity compared with HCR rats. Upon exposure to an HFD, LCR rats gained more weight and fat mass, and their insulin resistant condition was exacerbated, despite consuming similar amounts of metabolizable energy as chow-fed controls. These metabolic variables remained unaltered in HCR rats. The HFD increased skeletal muscle oxidative capacity similarly in both strains, whereas hepatic oxidative capacity was diminished only in LCR rats. These results suggest that LCR rats are predisposed to obesity and that expansion of skeletal muscle oxidative capacity does not prevent excess weight gain or the exacerbation of insulin resistance on an HFD. Elevated basal skeletal muscle oxidative capacity and the ability to preserve liver oxidative capacity may protect HCR rats from HFD-induced obesity and insulin resistance.

The Protective Effects of Probiotics on High Fat Diet-Induced Oxidative Damage Using a Comet Assay in Rats

2014 ◽  
Vol 998-999 ◽  
pp. 350-353
Author(s):  
Xiao Lian Chen ◽  
Lin Zhi Gong ◽  
Jian Xiong Xu
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Comet Assay ◽  
Oxidative Damage ◽  
Dna Fragmentation ◽  
High Fat Diet ◽  
Male Rats ◽  
Control Group ◽  
High Fat ◽  
Significant Difference

The objective of this study was to investigate the antioxidant capability and preventive effect of probiotics on high fat diet induced oxidative damage. Thirty male rats were randomly divided into three groups.The control group consumed a normal standard diet (5% fat, w:w), the high fat diet group received a high fat diet (20% fat, w:w), and probiotics group received a high fat diet supplemented with 2% probiotics. After 6 weeks, antioxidant capability of liver was determined and DNA fragmentation of liver cell was determined using a comet assay. The results showed that high fat diet could induce oxidative stress, shown as significant increases in lipid peroxidation and nitric oxide free radical, significant decrease in activities of superoxide dismutase and glutathione peroxidase, the percentage of DNA fragmentation was markedly increased, compared with control group. These alterations were significantly reversed in probiotics supplemented group and had no significant difference in antioxidant capability, lipid peroxidation and DNA damage compared with control group. Present observation indicated the probiotics had antioxidant property, which could scavenge free radical and enhance antioxidant defense system, and had the positive protective function on oxidative damage.

Chronic high-fat diet increases acute neuroendocrine stress response independently of prenatal dexamethasone treatment in male rats

2013 ◽  
Vol 26 (1) ◽  
pp. 8-18 ◽  
Author(s):  
Anders Abildgaard ◽  
Sten Lund ◽  
Karin S Hougaard
Keyword(s):  
Stress Response ◽  
Hpa Axis ◽  
High Fat Diet ◽  
Forced Swim Test ◽  
Male Rats ◽  
Adolescent Male ◽  
Late Adolescent ◽  
High Fat ◽  
Obesity And Diabetes ◽  
Increased Risk

ObjectiveIntrauterine growth restriction (IUGR) has been associated with metabolic disorders later in life such as obesity and diabetes as well as psychiatric disorders such as depression and schizophrenia. Therefore, we wanted to investigate whether behavioural, metabolic or neuroendocrine abnormalities could be provoked or exacerbated by a high-fat diet (HFD) in an experimental model of IUGR.MethodsPregnant dams were exposed to dexamethasone (DEX) in the third gestational week to induce IUGR. Late adolescent male offspring of DEX- and vehicle-treated dams were then fed a HFD or standard chow for 8 weeks and subjected to a variety of assessments.ResultsOnly diet affected the hypothalamus-pituitary-adrenal (HPA) axis stress response, as HFD doubled the observed corticosterone levels following acute restraint. HFD and prenatal DEX exposure concomitantly exacerbated depressive-like behaviour in the forced swim test, even though no interaction was seen. Prenatal DEX treatment tended to increase the basal acoustic startle response (ASR), while an interaction between HFD and DEX was present in the ASR pre-pulse inhibition suggestive of fundamental changes in neuronal gating mechanisms. Metabolic parameters were only affected by diet, as HFD increased fasting glucose and insulin levels.ConclusionWe conclude that chronic HFD may be more important in programming of the HPA axis stress responsiveness than an adverse foetal environment and therefore potentially implies an increased risk for developing psychiatric and metabolic disease.

Effects of caloric restriction on mitochondrial function and gene transcripts in rat muscle

2002 ◽  
Vol 283 (1) ◽  
pp. E38-E43 ◽  
Author(s):  
R. Sreekumar ◽  
J. Unnikrishnan ◽  
A. Fu ◽  
J. Nygren ◽  
K. R. Short ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Caloric Restriction ◽  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Control Diet ◽  
Radical Scavenging ◽  
Reactive Oxygen ◽  
Male Rats ◽  
Transcript Levels ◽  
Atp Production

Rodent skeletal muscle mitochondrial DNA has been shown to be a potential site of oxidative damage during aging. Caloric restriction (CR) is reported to reduce oxidative stress and prolong life expectancy in rodents. Gene expression profiling and measurement of mitochondrial ATP production capacity were performed in skeletal muscle of male rats after feeding them either a control diet or calorie-restricted diet (60% of control diet) for 36 wk to determine the potential mechanism of the beneficial effects of CR. CR enhanced the transcripts of genes involved in reactive oxygen free radical scavenging function, tissue development, and energy metabolism while decreasing expression of those genes involved in signal transduction, stress response, and structural and contractile proteins. Real-time PCR measurments confirmed the changes in transcript levels of cytochrome- c oxidase III, superoxide dismutase (SOD)1, and SOD2 that were noted by the microarray approach. Mitochondrial ATP production and citrate synthase were unaltered by the dietary changes. We conclude that CR alters transcript levels of several genes in skeletal muscle and that mitochondrial function in skeletal muscle remains unaltered by the dietary intervention. Alterations in transcripts of many genes involved in reactive oxygen scavenging function may contribute to the increase in longevity reported with CR.

scholarly journals Trimetazidine and exercise provide comparable improvements to high fat diet-induced muscle dysfunction through enhancement of mitochondrial quality control

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Wenliang Zhang ◽  
Baiyang You ◽  
Dake Qi ◽  
Ling Qiu ◽  
Jeffrey W. Ripley-Gonzalez ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Quality Control ◽  
Mitochondrial Dysfunction ◽  
Muscle Atrophy ◽  
High Fat Diet ◽  
C2c12 Cells ◽  
Muscle Dysfunction ◽  
High Fat ◽  
Mitochondrial Quality Control ◽  
Mitochondrial Functions

AbstractObesity induces skeletal muscle dysfunction. The pathogenesis of which appears to substantially involve mitochondrial dysfunction, arising from impaired quality control. Exercise is a major therapeutic strategy against muscle dysfunction. Trimetazidine, a partial inhibitor of lipid oxidation, has been proposed as a metabolic modulator for several cardiovascular pathologies. However, the effects of Trimetazidine on regulating skeletal muscle function are largely unknown. Our present study used cell culture and obese mice models to test a novel hypothesis that Trimetazidine could improve muscle atrophy with similar results to exercise. In C2C12 cells, high palmitic acid-induced atrophy and mitochondrial dysfunction, which could be reversed by the treatment of Trimetazidine. In our animal models, with high-fat diet-induced obesity associated with skeletal muscle atrophy, Trimetazidine prevented muscle dysfunction, corrected metabolic abnormalities, and improved mitochondrial quality control and mitochondrial functions similarly to exercise. Thus, our study suggests that Trimetazidine successfully mimics exercise to enhance mitochondrial quality control leading to improved high-fat diet-induced muscle dysfunction.

scholarly journals Chronic AMP-activated protein kinase activation and a high-fat diet have an additive effect on mitochondria in rat skeletal muscle

2010 ◽  
Vol 109 (2) ◽  
pp. 511-520 ◽  
Author(s):  
Natasha Fillmore ◽  
Daniel L. Jacobs ◽  
David B. Mills ◽  
William W. Winder ◽  
Chad R. Hancock
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
High Fat Diet ◽  
Chemical Activation ◽  
Additive Effect ◽  
Male Rats ◽  
Fiber Types ◽  
High Fat ◽  
Rat Skeletal Muscle ◽  
Amp Activated Protein Kinase

Factors that stimulate mitochondrial biogenesis in skeletal muscle include AMP-activated protein kinase (AMPK), calcium, and circulating free fatty acids (FFAs). Chronic treatment with either 5-aminoimidazole-4-carboxamide riboside (AICAR), a chemical activator of AMPK, or increasing circulating FFAs with a high-fat diet increases mitochondria in rat skeletal muscle. The purpose of this study was to determine whether the combination of chronic chemical activation of AMPK and high-fat feeding would have an additive effect on skeletal muscle mitochondria levels. We treated Wistar male rats with a high-fat diet (HF), AICAR injections (AICAR), or a high-fat diet and AICAR injections (HF + AICAR) for 6 wk. At the end of the treatment period, markers of mitochondrial content were examined in white quadriceps, red quadriceps, and soleus muscles, predominantly composed of unique muscle-fiber types. In white quadriceps, there was a cumulative effect of treatments on long-chain acyl-CoA dehydrogenase, cytochrome c, and peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) protein, as well as on citrate synthase and β-hydroxyacyl-CoA dehydrogenase (β-HAD) activity. In contrast, no additive effect was noted in the soleus, and in the red quadriceps only β-HAD activity increased additively. The additive increase of mitochondrial markers observed in the white quadriceps may be explained by a combined effect of two separate mechanisms: high-fat diet-induced posttranscriptional increase in PGC-1α protein and AMPK-mediated increase in PGC-1α protein via a transcriptional mechanism. These data show that chronic chemical activation of AMPK and a high-fat diet have a muscle type specific additive effect on markers of fatty acid oxidation, the citric acid cycle, the electron transport chain, and transcriptional regulation.

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