Enhanced Muscle Strength in Dyslipidemic Mice and Its Relation to Increased Capacity for Fatty Acid Oxidation

Tomczyk, Marta; Braczko, Alicja; Jabłońska, Patrycja; Mika, Adriana; Przyborowski, Kamil; Jędrzejewska, Agata; Krol, Oliwia; Kus, Filip; Śledziński, Tomasz; Chłopicki, Stefan; Słomińska, Ewa M.; Smolenski, Ryszard T.

doi:10.3390/ijms222212251

Cited by 3 publications

(3 citation statements)

References 47 publications

(69 reference statements)

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“…Forelimb grip strength was measured by a grip strength meter (GSM Grip strength meter, Ugo Basile, Gemonio VA, Italy) as described earlier [ 36 ]. Briefly, the animal was held on the apparatus so that only the forelimb paws grasped the specially designed mouse flat mesh assembly.…”

Section: Methodsmentioning

confidence: 99%

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Rosiglitazone Ameliorates Cardiac and Skeletal Muscle Dysfunction by Correction of Energetics in Huntington’s Disease

Tomczyk

Braczko

Mierzejewska

et al. 2022

Cells

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Huntington’s disease (HD) is a rare neurodegenerative disease that is accompanied by skeletal muscle atrophy and cardiomyopathy. Tissues affected by HD (central nervous system [CNS], skeletal muscle, and heart) are known to suffer from deteriorated cellular energy metabolism that manifests already at presymptomatic stages. This work aimed to test the effects of peroxisome proliferator-activated receptor (PPAR)-γ agonist—rosiglitazone on grip strength and heart function in an experimental HD model—on R6/1 mice and to address the mechanisms. We noted that rosiglitazone treatment lead to improvement of R6/1 mice grip strength and cardiac mechanical function. It was accompanied by an enhancement of the total adenine nucleotides pool, increased glucose oxidation, changes in mitochondrial number (indicated as increased citric synthase activity), and reduction in mitochondrial complex I activity. These metabolic changes were supported by increased total antioxidant status in HD mice injected with rosiglitazone. Correction of energy deficits with rosiglitazone was further indicated by decreased accumulation of nucleotide catabolites in HD mice serum. Thus, rosiglitazone treatment may not only delay neurodegeneration but also may ameliorate cardio- and myopathy linked to HD by improvement of cellular energetics.

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Section: Methodsmentioning

confidence: 99%

“…Mitochondria were isolated from the soleus muscle and heart, and prepared based on the previously described procedure [ 36 , 39 ]. Analysis was performed by Seahorse Metabolic Flux Analyzer (Agilent Technologies, Santa Clara, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

Rosiglitazone Ameliorates Cardiac and Skeletal Muscle Dysfunction by Correction of Energetics in Huntington’s Disease

Tomczyk

Braczko

Mierzejewska

et al. 2022

Cells

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“…On the other hand, forced v-ATPase disassembly might be an attractive strategy to rectify the substrate balance in heart and muscle metabolic diseases characterized by dyslipidemia [ 115 , 116 ]. The resulting CD36 translocation and an associated increase in fatty acid uptake might restore the substrate balance under these conditions.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Endosomal v-ATPase as a Sensor Determining Myocardial Substrate Preference

et al. 2022

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The heart is a metabolically flexible omnivore that can utilize a variety of substrates for energy provision. To fulfill cardiac energy requirements, the healthy adult heart mainly uses long-chain fatty acids and glucose in a balanced manner, but when exposed to physiological or pathological stimuli, it can switch its substrate preference to alternative substrates such as amino acids (AAs) and ketone bodies. Using the failing heart as an example, upon stress, the fatty acid/glucose substrate balance is upset, resulting in an over-reliance on either fatty acids or glucose. A chronic fuel shift towards a single type of substrate is linked with cardiac dysfunction. Re-balancing myocardial substrate preference is suggested as an effective strategy to rescue the failing heart. In the last decade, we revealed that vacuolar-type H+-ATPase (v-ATPase) functions as a key regulator of myocardial substrate preference and, therefore, as a novel potential treatment approach for the failing heart. Fatty acids, glucose, and AAs selectively influence the assembly state of v-ATPase resulting in modulation of its proton-pumping activity. In this review, we summarize these novel insights on v-ATPase as an integrator of nutritional information. We also describe its exploitation as a therapeutic target with focus on supplementation of AA as a nutraceutical approach to fight lipid-induced insulin resistance and contractile dysfunction of the heart.

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Supplementation with a phenolic-rich fraction from Ilex kudingcha improves inflammatory stress, gastrocnemius weights, and foreleg muscle grip strength in murine squamous cell carcinoma (SCC7)-bearing mice

Chao,

Yang,

et al. 2024

Food Bioscience

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Enhanced Muscle Strength in Dyslipidemic Mice and Its Relation to Increased Capacity for Fatty Acid Oxidation

Cited by 3 publications

References 47 publications

Rosiglitazone Ameliorates Cardiac and Skeletal Muscle Dysfunction by Correction of Energetics in Huntington’s Disease

Rosiglitazone Ameliorates Cardiac and Skeletal Muscle Dysfunction by Correction of Energetics in Huntington’s Disease

Endosomal v-ATPase as a Sensor Determining Myocardial Substrate Preference

Supplementation with a phenolic-rich fraction from Ilex kudingcha improves inflammatory stress, gastrocnemius weights, and foreleg muscle grip strength in murine squamous cell carcinoma (SCC7)-bearing mice

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