High-fat diet induces skeletal muscle oxidative stress in a fiber type-dependent manner in rats

Pinho, Ricardo A.; Sepa-Kishi, Diane M.; Bikopoulos, George; Wu, Michelle Victoria; Uthayakumar, Abinas; Mohasses, Arta; Hughes, Maria Celia; Perry, Christopher G. R.; Ceddia, Rolando B.

doi:10.1016/j.freeradbiomed.2017.07.005

Cited by 63 publications

(72 citation statements)

References 39 publications

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Section: Discussionsupporting

confidence: 65%

“…Those muscles present a distinct fibre composition, which could partly explain the different results. Additionally, muscle with a different composition seems to respond in a different manner to a HFD in relationship to redox homeostasis (Pinho et al., ). In the present study, mitochondria from soleus muscle demonstrated a reduction in H 2 O 2 emission in state 2 after 7 and 14 days of HFD.…”

Section: Discussionmentioning

confidence: 99%

“…It is important to highlight that our findings are based on respiration driven by pyruvate and succinate, and these findings cannot be extended to other substrates, such as fatty acids. Mitochondrial respiration driven by fatty acid seems to increase in some DIO models (Pinho et al., ) along with the expression and activity of fatty acid oxidation machinery (fatty acid translocase [CD36], fatty acid binding protein [FABP], Carnitine palmitoyltransferase I [CPT‐1]; Bonen et al., ). These metabolic adaptations during feeding with a HFD raise a question about mitochondrial plasticity according to the fuel supply.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, it could be speculated that mitochondria from DIO mice might not be able to generate an appropriate membrane potential. Recently, Pinho et al (2017) showed that during lipid overload, mitochondria from soleus muscle showed a 100% increase in the expression of uncoupling proteins 2 and 3. These data suggest that the reduction in ROS emission in the early stages of obesity, similar to the ones detected in the present study, could be linked to mitochondrial uncoupling.…”

Section: Discussionmentioning

confidence: 99%

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Decrement in resting and insulin‐stimulated soleus muscle mitochondrial respiration is an early event in diet‐induced obesity in mice

Brunetta

Paula

Oliveira

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?What are the temporal responses of mitochondrial respiration and mitochondrial responsivity to insulin in soleus muscle fibres from mice during the development of obesity and insulin resistance? What is the main finding and its importance?Short‐ and long‐term feeding with a high‐fat diet markedly reduced soleus mitochondrial respiration and mitochondrial responsivity to insulin before any change in glycogen synthesis. Muscle glycogen synthesis and whole‐body insulin resistance were present after 14 and 28 days, respectively. Our findings highlight the plasticity of mitochondria during the development of obesity and insulin resistance. Abstract Recently, significant attention has been given to the role of muscle mitochondrial function in the development of insulin resistance associated with obesity. Our aim was to investigate temporal alterations in mitochondrial respiration, H2O2 emission and mitochondrial responsivity to insulin in permeabilized skeletal muscle fibres during the development of obesity in mice. Male Swiss mice (5–6 weeks old) were fed with a high‐fat diet (60% calories from fat) or standard diet for 7, 14 or 28 days to induce obesity and insulin resistance. Diet‐induced obese (DIO) mice presented with reduced glucose tolerance and hyperinsulinaemia after 7 days of high‐fat diet. After 14 days, the expected increase in muscle glycogen content after systemic injection of glucose and insulin was not observed in DIO mice. At 28 days, blood glucose decay after insulin injection was significantly impaired. Complex I (pyruvate + malate) and II (succinate)‐linked respiration and oxidative phosphorylation (ADP) were decreased after 7 days of high‐fat diet and remained low in DIO mice after 14 and 28 days of treatment. Moreover, mitochondria from DIO mice were incapable of increasing respiratory coupling and ADP responsivity after insulin stimulation in all observed periods. Markers of mitochondrial content were reduced only after 28 days of treatment. The mitochondrial H2O2 emission profile varied during the time course of DIO, with a reduction of H2O2 emission in the early stages of DIO and an increased emission after 28 days of treatment. Our data demonstrate that DIO promotes transitory alterations in mitochondrial physiology during the early and late stages of insulin resistance related to obesity.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Decrement in resting and insulin‐stimulated soleus muscle mitochondrial respiration is an early event in diet‐induced obesity in mice

Brunetta

Paula

Oliveira

et al. 2019

Experimental Physiology

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“…In the context of obesity and high fat diet (HFD) feeding, the excessive consumption of nutrients is thought to drive mitochondrial dysfunction. One pathway which may be responsible for this is oxidative stress, by which an increase in reactive oxygen species (ROS) compromises mitochondrial function through reductions in mitochondrial biogenesis and impaired oxidation efficiency [8][9][10]. Mitochondria play a central role in oxidative metabolisms which involves the catabolism of fuel (lipids, proteins, and carbohydrates) to produce adenosine triphosphate (ATP), the main form of cellular energy.…”

Section: Introductionmentioning

confidence: 99%

Exercise-Induced Benefits on Glucose Handling in a Model of Diet-Induced Obesity Are Reduced by Concurrent Nicotinamide Mononucleotide

Laybutt

Kim

et al. 2020

Preprint

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Highlights• NMN dampened exercise-induced benefits on glucose handling in diet-induced obesity.• NMN administration in exercise enhanced ratio of antioxidants to prooxidants.• We suggest NMN administration may not be beneficial when NAD + levels are replete. ABSTRACTObjective: Almost 40% of adults worldwide are classified as overweight or obese. Exercise is a beneficial intervention in obesity, partly due to increases in mitochondrial activity, with a potential role for the concomitant increase in nicotinamide adenine dinucleotide (NAD + ).Recent studies have shown that increasing NAD + levels through pharmacological supplementation with precursors such as nicotinamide mononucleotide (NMN) improved metabolic health in high fat diet (HFD) fed mice. We examined the combined effects of NMN and treadmill exercise on the metabolic dysregulation in HFD-induced obesity.Methods: Five-week old female C57BL/6J mice were exposed to control diet or HFD. Mice fed HFD were treated with NMN in drinking water (400mg/kg; HNMN), treadmill exercise (HEx) or combined NMN and exercise (HNEx). Results:Unexpectedly, NMN administration impaired several aspects of exercise-induced benefits in HFD mice, including glucose tolerance, glucose stimulated insulin secretion from islets and reduced hepatic triglyceride accumulation. Mechanistically, HNEx mice displayed increased antioxidant and reduced prooxidant gene expression in both islets and muscle, suggesting that altered redox status is associated with the loss of exercise-induced health benefits with NMN co-treatment. Conclusion:Our data show that NMN treatment blocks the beneficial metabolic effects of exercise in a mouse model of diet-induced obesity in association with disturbances in redox metabolism.

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Vitamin D3 mitigates myopathy and metabolic dysfunction in rats with metabolic syndrome: the potential role of dipeptidyl peptidase-4

Shoier,

Ghareib,

Kothayer

et al. 2024

Naunyn-Schmiedeberg's Arch Pharmacol

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Metabolic syndrome is associated with vitamin D3 deficiency. This work aims to examine the efficacy of vitamin D3 in inhibiting MetS-induced myopathy and to determine whether the beneficial effects of vitamin D3 are mediated by the inhibition of dipeptidyl peptidase-4 (DPP-4). An in silico study investigated the potential effectiveness of vitamin D3 on the inhibition of the DPP-4 enzyme. An in vitro assay of the DPP-4 inhibitory effect of vitamin D3 was performed. In vivo and over 12 weeks, both diet (with 3% salt) and drinking water (with 10% fructose) were utilized to induce MetS. In the seventh week, rats received either vitamin D3, vildagliptin, a combination of both, or vehicles. Serum lipids, adipokines, glycemic indices, and glucagon-like peptide-1 (GLP-1), muscular glucose transporter type-4 (GLUT-4) content, DPP-4, adenosine monophosphate kinase (AMPK) activities, and Sudan Black B-stained lipids were assessed. Muscular reactive oxygen species (ROS), caspase-3, and desmin immunostaining were used to determine myopathy. MetS-induced metabolic dysfunction was ameliorated by vitamin D3, which also reduced intramuscular glycogen and lipid accumulation. This is demonstrated by the attenuation of MetS-induced myopathy by vitamin D3, decreased oxidative stress, increased desmin immuno-expression, and caspase-3 activity. Our in silico data demonstrated that vitamin D3 is capable of inhibiting DPP-4, which is further supported by biochemical findings. Vitamin D3 increased serum GLP-1, muscular AMPK activity, and GLUT-4 content, whereas the levels of muscular ROS were decreased in MetS. Vildagliptin and its combination with vitamin D3 yielded comparable results. It is suggested that the DPP-4 inhibitory potential of vitamin D3 is responsible for the amelioration of MetS-induced metabolic changes and myopathy.

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High-fat diet induces skeletal muscle oxidative stress in a fiber type-dependent manner in rats

Cited by 63 publications

References 39 publications

Decrement in resting and insulin‐stimulated soleus muscle mitochondrial respiration is an early event in diet‐induced obesity in mice

Decrement in resting and insulin‐stimulated soleus muscle mitochondrial respiration is an early event in diet‐induced obesity in mice

Exercise-Induced Benefits on Glucose Handling in a Model of Diet-Induced Obesity Are Reduced by Concurrent Nicotinamide Mononucleotide

Vitamin D3 mitigates myopathy and metabolic dysfunction in rats with metabolic syndrome: the potential role of dipeptidyl peptidase-4

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