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Lewis, M. P.

Publications and source records attributed to Lewis, M. P..

2 recordsLinked to original sources

γ-Linolenic acid increases expression of key regulators of lipid metabolism in human skeletal muscle cells.

Control of skeletal muscle fat metabolism is regulated acutely through Peroxisome Proliferator Activated Receptor (PPAR) {delta} activation and its downstream intracellular targets. The purpose of this study was to determine whether fatty acids with high binding affinity for PPAR{delta} can elevate the expression of genes related to fatty acid oxidation and indicators of mitochondrial biogenesis in cultured human skeletal myotubes. Myotubes were treated for 72 hours with one of four conditions: (i) Control (CON); (ii) Eicosapentaenoic acid (EPA 250M); (iii) {gamma}-linolenic acid ({gamma}-LA 250M); (iv) PPAR{delta} Agonist (GW501516 10nM). Incubation with {gamma}-LA induced increases in the gene expression of CD36 (p= 0.005), HADHA (p= 0.022) and PDK4 (p=0.025) in comparison with CON, with no further differences observed between conditions. Furthermore, intensity of MitoTracker(R) Red immunostaining in myotubes increased following incubation with {gamma}-LA (p[≤] 0.001) and EPA (p= 0.005) however these trends were not mirrored in the expression of PGC-1 as might be expected. Overall, {gamma}-LA elevates levels the transcription of key intracellular regulators of lipid metabolism and transport in human myotubes, which may be clinically beneficial in the control of metabolic diseases.

cell biology

Monosodium Iodoacetate delays regeneration and inhibits hypertrophy in skeletal muscle cells in vitro

ObjectiveOsteoarthritis (OA) is a musculoskeletal disease which contributes to severe morbidity. The monosodium iodoacetate (MIA) rodent model of OA is now well established, however the effect of MIA on surrounding tissues post injection has not been investigated and as such the impact on phenotypic development is unknown. The aim of this investigation was to examine the impact of MIA incubation on skeletal muscle cells in vitro, to provide an indication as to the potential influence of MIA administration of skeletal muscle in vivo.\n\nMethodsC2C12 skeletal muscle myotubes were treated with either 4.8M MIA or 10M Dexamethasone (DEX, positive atrophic control) up to 72hrs post differentiation and sampled for morphological and mRNA analyses.\n\nResultsSignificant morphological effects (fusion index, number of myotubes and myotube width, p<0.05) were evident, demonstrating a hypertrophic phenotype in control (CON) compared to a hyperplasic phenotype in MIA and DEX. Increases in MAFbx mRNA were also evident between conditions, with post-hoc analysis demonstrating significance between CON and DEX (p<0.001), but not between CON and MIA (p>0.05).\n\nConclusionsThese data indicate a significant impact of both DEX and MIA on regeneration and hypertrophy in vitro and suggest differential activating mechanisms. Future investigations should determine whether skeletal muscle regeneration and hypertrophy is affected in the in vivo rodent model and the potential impact this has on the OA phenotypic outcome.

cell biology