Clinical nutrition ESPEN · 2017
Effects of dietary omega-3 on dystrophic cardiac and diaphragm muscles as evaluated by 1H magnetic resonance spectroscopy: Metabolic profile and calcium-related proteins.
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Maurício Adriana Fogagnolo, de Carvalho Samara Camaçari, Santo Neto Humberto, Marques Maria Julia
Аннотация
BACKGROUND & AIMS: Duchenne muscular dystrophy (DMD) is characterized by the absence of dystrophin and muscle degeneration. Calcium dysregulation and oxidative stress also contribute to the disease progression. We evaluated the potential therapeutic benefits of supplementation with omega-3 on the metabolic profile, calcium-related proteins and oxidative stress response in the heart and diaphragm (DIA) of the mdx mouse model of DMD at later stages of the disease (13 months).
METHODS: Mdx mice (8 months old) received omega-3 via a dietary supplement for 5 months. Metabolites were analyzed by 1H magnetic resonance spectroscopy. Muscle total calcium was evaluated by inductively coupled plasma-optical emission spectrometry. Calsequestrin, TRPC1 and 4-HNE were determined via Western blot.
RESULTS: Omega-3 decreased the metabolites taurine (related to calcium regulation and oxidative stress), aspartate (related to inflammation) and oxypurinol (related to oxidative stress) in the heart (aspartate) and DIA (taurine, aspartate and oxypurinol). Omega-3 also significantly decreased total calcium and TRPC1 levels in cardiac and DIA muscles and increased the levels of calsequestrin (cardiac and skeletal) and decreased the oxidative stress marker 4-HNE.
CONCLUSIONS: The current study suggests that supplementation with omega-3 may generate therapeutic benefits on dystrophy progression, at later stages of the disease, with changes in the metabolic profile that may be correlated to omega-3 therapy.
METHODS: Mdx mice (8 months old) received omega-3 via a dietary supplement for 5 months. Metabolites were analyzed by 1H magnetic resonance spectroscopy. Muscle total calcium was evaluated by inductively coupled plasma-optical emission spectrometry. Calsequestrin, TRPC1 and 4-HNE were determined via Western blot.
RESULTS: Omega-3 decreased the metabolites taurine (related to calcium regulation and oxidative stress), aspartate (related to inflammation) and oxypurinol (related to oxidative stress) in the heart (aspartate) and DIA (taurine, aspartate and oxypurinol). Omega-3 also significantly decreased total calcium and TRPC1 levels in cardiac and DIA muscles and increased the levels of calsequestrin (cardiac and skeletal) and decreased the oxidative stress marker 4-HNE.
CONCLUSIONS: The current study suggests that supplementation with omega-3 may generate therapeutic benefits on dystrophy progression, at later stages of the disease, with changes in the metabolic profile that may be correlated to omega-3 therapy.