Effects of dietary omega-3 on dystrophic cardiac and diaphragm muscles as evaluated by 1H magnetic resonance spectroscopy: Metabolic profile and calcium-related proteins

Maurício, Adriana Fogagnolo; Carvalho, Samara Camaçarí de; Neto, Humberto Santo; Marques, Maria Júlia

doi:10.1016/j.clnesp.2017.03.005

Cited by 8 publications

(10 citation statements)

References 55 publications

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“…Many researchers have investigated various dietary supplements to inhibit muscle pathology or strengthen non-diseased muscles, whether it be for athletes or against aging, type 2 diabetes, or MD [ 83 , 84 , 85 , 86 , 87 , 110 , 128 , 129 , 130 , 131 , 132 , 133 ]. In MD, increasing the percentage of slow fibers is often the goal, but not necessarily the only goal.…”

Section: Dietary Supplementsmentioning

confidence: 99%

“…Feeding MD hamsters flaxseed-derived omega-3 from birth until death significantly improved skeletal muscle histopathology [ 129 ]. Additional studies in mdx mice, both young [ 130 ] and old [ 131 ], benefitted from omega-3 treatment. The benefits include reduced ROS, increased grip strength, decreased fibrosis, and improved echo parameters.…”

Section: Fatty Acid Supplementsmentioning

confidence: 99%

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Skeletal Muscle Metabolism in Duchenne and Becker Muscular Dystrophy—Implications for Therapies

Heydemann

2018

Nutrients

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The interactions between nutrition and metabolism and skeletal muscle have long been known. Muscle is the major metabolic organ—it consumes more calories than other organs—and therefore, there is a clear need to discuss these interactions and provide some direction for future research areas regarding muscle pathologies. In addition, new experiments and manuscripts continually reveal additional highly intricate, reciprocal interactions between metabolism and muscle. These reciprocal interactions include exercise, age, sex, diet, and pathologies including atrophy, hypoxia, obesity, diabetes, and muscle myopathies. Central to this review are the metabolic changes that occur in the skeletal muscle cells of muscular dystrophy patients and mouse models. Many of these metabolic changes are pathogenic (inappropriate body mass changes, mitochondrial dysfunction, reduced adenosine triphosphate (ATP) levels, and increased Ca2+) and others are compensatory (increased phosphorylated AMP activated protein kinase (pAMPK), increased slow fiber numbers, and increased utrophin). Therefore, reversing or enhancing these changes with therapies will aid the patients. The multiple therapeutic targets to reverse or enhance the metabolic pathways will be discussed. Among the therapeutic targets are increasing pAMPK, utrophin, mitochondrial number and slow fiber characteristics, and inhibiting reactive oxygen species. Because new data reveals many additional intricate levels of interactions, new questions are rapidly arising. How does muscular dystrophy alter metabolism, and are the changes compensatory or pathogenic? How does metabolism affect muscular dystrophy? Of course, the most profound question is whether clinicians can therapeutically target nutrition and metabolism for muscular dystrophy patient benefit? Obtaining the answers to these questions will greatly aid patients with muscular dystrophy.

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Section: Dietary Supplementsmentioning

confidence: 99%

Section: Fatty Acid Supplementsmentioning

confidence: 99%

Skeletal Muscle Metabolism in Duchenne and Becker Muscular Dystrophy—Implications for Therapies

Heydemann

2018

Nutrients

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“…Omega-3 fatty acid administration slows DMD progression, partly due to a reduction in TRPC1 expression [44].…”

Section: Trpc1mentioning

confidence: 99%

TRPC channels in exercise-mimetic therapy

Numaga‐Tomita

Oda

Nishiyama

et al. 2018

Pflugers Arch - Eur J Physiol

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Physical exercise yields beneficial effects on all types of muscle cells, which are essential for the maintenance of cardiovascular homeostasis and good blood circulation. Daily moderate exercise increases systemic antioxidative capacity, which can lead to the prevention of the onset and progression of oxidative stress-related diseases. Therefore, exercise is now widely accepted as one of the best therapeutic strategies for the treatment of ischemic (hypoxic) diseases. Canonical transient receptor potential (TRPC) proteins are non-selective cation channels activated by mechanical stress and/or stimulation of phospholipase C-coupled surface receptors. TRPC channels, especially diacylglycerol-activated TRPC channels (TRPC3 and TRPC6; TRPC3/6), play a key role in the development of cardiovascular remodeling. We have recently found that physical interaction between TRPC3 and NADPH oxidase (Nox) 2 under hypoxic stress promotes Nox2-dependent reactive oxygen species (ROS) production and mediates rodent cardiac plasticity, and inhibition of the TRPC3-Nox2 protein complex results in enhancement of myocardial compliance and flexibility similar to that observed in exercise-treated hearts. In this review, we describe current understanding of the roles of TRPC channels in striated muscle (patho)physiology and propose that targeting TRPC-based protein complexes could be a new strategy to imitate exercise therapy.

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“…Embora escassas, as primeiras pesquisas sobre a ação de glicocorticoides no músculo diafragma datam de 1950 e vêm aumentando com o passar dos anos (Leupin, 1950;Wool, 1960;Veldsema-Currie et al, 1976;Drakontides, 1982;Wilcox et al, 1989;Viires et al, 1990;Petrof et al, 1995;Jiang et al, 1996;Nava et al, 1996;Fletcher et al, 2000;Eason et al, 2003;Mahzabin et al, 2017;Mauricio et al, 2017;Spaulding et al, 2020), porém, não compatível com sua importância clínica, uma vez que muitos pacientes em terapia com glicocorticoides são portadores de doenças neuromusculares degenerativas, indo a óbito, principalmente por falência do sistema respiratório (Engel AG, 1994). Figura 5.…”

Section: Glicocorticoides E a Atrofia Muscular Esqueléticaunclassified

“…Mecanismos diversos durante o processo de atrofia muscular culminam no desequilíbrio entre síntese e degradação proteica, com redução da área de secção transversa (Schiaffino et al, 2013), havendo aumento da transcrição de atrogenes ligados aos FoxOs, da sinalização inflamatória ligados a via NF-kβ e seus derivados, bem como o desequilíbrio do cálcio intracelular (Mauricio et al, 2017).…”

Section: Alvos Potenciais No Tratamento Da Atrofia Muscularunclassified

Análise histológica e molecular do músculo diafragma após tratamento com diferentes glicocorticoides e sob a associação do ácido graxo ômega 3 e dexametasona em ratos

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Effects of dietary omega-3 on dystrophic cardiac and diaphragm muscles as evaluated by 1H magnetic resonance spectroscopy: Metabolic profile and calcium-related proteins

Cited by 8 publications

References 55 publications

Skeletal Muscle Metabolism in Duchenne and Becker Muscular Dystrophy—Implications for Therapies

Skeletal Muscle Metabolism in Duchenne and Becker Muscular Dystrophy—Implications for Therapies

TRPC channels in exercise-mimetic therapy

Análise histológica e molecular do músculo diafragma após tratamento com diferentes glicocorticoides e sob a associação do ácido graxo ômega 3 e dexametasona em ratos

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