Effects of fenofibrate and its combination with lovastatin on the expression of genes involved in skeletal muscle atrophy, including FoxO1 and its targets

Ajima, Haruka; Kai, Yuko; Fujimaki, Junya; Akashi, Shiori; Morita, Akihito; Ezaki, Osamu; Kamei, Yasutomi; Miura, Shinji

doi:10.2131/jts.46.11

Cited by 4 publications

(3 citation statements)

References 44 publications

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“…Also, studies have reported that exposures of weeks to several years of PPARα agonists treatment may induce hepatocellular chronic active and cholestatic hepatitis, as well as increase the level of serum transaminase, which may be dose related (132). Besides, fibrates have a risk of muscle astrophy, and the combination of fibrates and stains may also increase the risk of rhabdomyolysis (133). Other adverse effects include renal damage that fibrates may impair the generation of vasodilatory prostaglandins, leading to a reversible decrease in glomerular filtration rate and a elevation of serum creatinine (134,135), and gallbladder disease such as gall stone, but the incidence varies remarkably between compounds (132).…”

Section: Discussionmentioning

confidence: 99%

PPAR-α Modulators as Current and Potential Cancer Treatments

et al. 2021

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Cancer is one of the leading causes of mortality worldwide. PPAR modulators may hold great potential for the management of cancer patients. Indeed, PPARs are critical sensors and regulators of lipid, and they are able to promote eNOS activation, regulate immunity and inflammation response, and affect proliferation and differentiation of cancer cells. Cancer, a name given to a group of diseases, is characterized by multiple distinctive biological behaviors, including angiogenesis, abnormal cell proliferation, aerobic glycolysis, inflammation, etc. In the last decade, emerging evidence has shown that PPAR-α, a nuclear hormone receptor, can modulate carcinogenesis via exerting effects on one or several characteristic pathological behaviors of cancer. Therefore, the multi-functional PPAR modulators have substantial promise in various types of cancer therapies. This review aims to consolidate the functions of PPAR-α, as well as discuss the current and potential applications of PPAR-α agonists and antagonists in tackling cancer.

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Section: Discussionmentioning

confidence: 99%

PPAR-α Modulators as Current and Potential Cancer Treatments

et al. 2021

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“…It may range from an asymptomatic increase in plasma CK level or simple myalgia to life-threatening rhabdomyolysis. These side effects should be considered and must be early recognized and properly managed to prevent drugrelated morbidity and mortality (Ajima et al, 2021) .…”

Section: Discussionmentioning

confidence: 99%

Can Coenzyme Q10 alleviate the toxic effect of fenofibrate on skeletal muscle?

El-Bassouny

Mansour

EL-Lakany

et al. 2023

Preprint

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Fenofibrate is an antilipidemic drug that increases the activity of the lipoprotein lipase enzyme thus enhancing lipolysis, however, it may cause myopathy and rhabdomyolysis in humans. Coenzyme Q10 (CoQ10) is an endogenously synthesized compound that is found in most living cells and plays an important role in cellular metabolism. It acts as the electron carrier in the mitochondrial respiratory chain. This study aimed to elucidate FEN-induced skeletal muscle changes in rats and to evaluate CoQ10 efficacy in preventing or alleviating these changes. Forty adult male rats were divided equally into four groups: the negative control group that received saline, the positive control group that received CoQ10, the FEN-treated group received FEN, and the FEN+CoQ10 group, (received both FEN followed by CoQ10 daily for 4 weeks. Animals were sacrificed and blood samples were collected to assess creatine kinase (CK). Soleus muscle samples were taken and processed for light and electron microscopic studies. This study showed that FEN increased CK levels and induced inflammatory cellular infiltration and disorganization of muscular architecture with lost striations. FEN increased the percentage of degenerated collagen fibers, and immune expression of caspase 3. Ultrastructurally, it caused degeneration of myofibrils with distorted cell organelles. Treatment with CoQ10 could markedly ameliorate these FEN-induced structural changes and mostly regain the normal architecture of muscle fibers due to its antifibrotic and antiapoptotic effects. In conclusion, treatment with CoQ10 improved muscular structure by suppressing oxidative stress, attenuating inflammation, and inhibiting apoptosis.

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“…These side effects should be considered and must be recognized early and properly managed to prevent drug-related morbidity and mortality (Ajima et al. 2021 ) .…”

Section: Discussionmentioning

confidence: 99%

Can coenzyme Q10 alleviate the toxic effect of fenofibrate on skeletal muscle?

El-Bassouny

Mansour

Ellakkany

et al. 2023

Histochem Cell Biol

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Fenofibrate (FEN) is an antilipidemic drug that increases the activity of the lipoprotein lipase enzyme, thus enhancing lipolysis; however, it may cause myopathy and rhabdomyolysis in humans. Coenzyme Q10 (CoQ10) is an endogenously synthesized compound that is found in most living cells and plays an important role in cellular metabolism. It acts as the electron carrier in the mitochondrial respiratory chain. This study aimed to elucidate FEN-induced skeletal muscle changes in rats and to evaluate CoQ10 efficacy in preventing or alleviating these changes. Forty adult male rats were divided equally into four groups: the negative control group that received saline, the positive control group that received CoQ10, the FEN-treated group that received FEN, and the FEN + CoQ10 group that received both FEN followed by CoQ10 daily for 4 weeks. Animals were sacrificed and blood samples were collected to assess creatine kinase (CK). Soleus muscle samples were taken and processed for light and electron microscopic studies. This study showed that FEN increased CK levels and induced inflammatory cellular infiltration and disorganization of muscular architecture with lost striations. FEN increased the percentage of degenerated collagen fibers and immune expression of caspase-3. Ultrastructurally, FEN caused degeneration of myofibrils with distorted cell organelles. Treatment with CoQ10 could markedly ameliorate these FEN-induced structural changes and mostly regain the normal architecture of muscle fibers due to its antifibrotic and antiapoptotic effects. In conclusion, treatment with CoQ10 improved muscular structure by suppressing oxidative stress, attenuating inflammation, and inhibiting apoptosis.

show abstract

Effects of fenofibrate and its combination with lovastatin on the expression of genes involved in skeletal muscle atrophy, including FoxO1 and its targets

Cited by 4 publications

References 44 publications

PPAR-α Modulators as Current and Potential Cancer Treatments

PPAR-α Modulators as Current and Potential Cancer Treatments

Can Coenzyme Q10 alleviate the toxic effect of fenofibrate on skeletal muscle?

Can coenzyme Q10 alleviate the toxic effect of fenofibrate on skeletal muscle?

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