muscular dystrophies/carbohydrate

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Muscle wasting and carbohydrate homeostasis in Duchenne muscular dystrophy.

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Carbohydrate homeostasis was evaluated in nine patients with Duchenne muscular dystrophy (DMD), and in six age-matched normal boys. Mild carbohydrate intolerance was observed in the DMD patients during an oral glucose tolerance test. Only minor differences were observed between the DMD patients and

Protein-carbohydrate supplements improve muscle protein balance in muscular dystrophy patients after endurance exercise: a placebo-controlled crossover study.

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In healthy individuals, postexercise protein supplementation increases muscle protein anabolism. In patients with muscular dystrophies, aerobic exercise improves muscle function, but the effect of exercise on muscle protein balance is unknown. Therefore, we investigated 1) muscle protein balance

Duchenne muscular dystrophy: lack of differences in the expression of endogenous carbohydrate- and heparin-binding proteins (lectins) in cultured fibroblasts.

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Duchenne muscular dystrophy (DMD), the most severe form of inherited muscular dystrophies, is known to be caused by a deficiency of the protein "dystrophin", but the pathophysiologic consequences of this lack have not as yet been elucidated. Investigations with cultured fibroblasts point to altered

Abnormal carbohydrate metabolism in a canine model for muscular dystrophy.

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The canine golden retriever muscular dystrophy (GRMD) model is the best animal model for studying Duchenne muscular dystrophy in humans. Considering the importance of glucose metabolism in the muscles, the existence of metabolic and endocrine alterations in a wide range of muscular dystrophies, and

Overexpression of the cytotoxic T cell (CT) carbohydrate inhibits muscular dystrophy in the dyW mouse model of congenital muscular dystrophy 1A.

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A number of recent studies have demonstrated therapeutic effects of transgenes on the development of muscle pathology in the mdx mouse model for Duchenne muscular dystrophy, but none have been shown also to be effective in mouse models for laminin alpha2-deficient congenital muscular dystrophy

[Characteristics of carbohydrate-phosphorus and electrolyte metabolism in the erythrocytes of patients with progressive muscular dystrophy and in their closest relations].

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[The activity of carbohydrate-metabolizing enzymes in muscle biopsies from humans with various myodystrophies].

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INVESTIGATIONS ON CARBOHYDRATE METABOLISM IN PROGRESSIVE MUSCULAR DYSTROPHIES.

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[The behavior of some indices of carbohydrate metabolism on subjects with progressive muscular dystrophy subjected to muscular work].

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[Features of disorders of carbohydrate metabolism in progressive muscular dystrophies (review)].

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Glycosylation defects in muscular dystrophies.

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OBJECTIVE Congenital disorders of glycosylation are caused by defects in the synthesis of the glycan moiety of glycoproteins or other glycoconjugates. There has been a great explosion in the number of neuromuscular diseases caused by mutations in genes that affect carbohydrate metabolism or protein

Overexpression of the cytotoxic T cell GalNAc transferase in skeletal muscle inhibits muscular dystrophy in mdx mice.

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Duchenne muscular dystrophy (DMD) is a congenital X-linked myopathy caused by lack of dystrophin protein expression. In DMD, the expression of many dystrophin-associated proteins (DAPs) is reduced along the sarcolemmal membrane, but the same proteins remain concentrated at the neuromuscular junction

Cell-penetrating peptide-morpholino conjugates alter pre-mRNA splicing of DMD (Duchenne muscular dystrophy) and inhibit murine coronavirus replication in vivo.

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The cellular uptake of PMOs (phosphorodiamidate morpholino oligomers) can be enhanced by their conjugation to arginine-rich CPPs (cell-penetrating peptides). Here, we discuss our recent findings regarding (R-Ahx-R)(4)AhxB (Ahx is 6-aminohexanoic acid and B is beta-alanine) CPP-PMO conjugates in DMD

Mouse fukutin deletion impairs dystroglycan processing and recapitulates muscular dystrophy.

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Dystroglycan is a transmembrane glycoprotein that links the extracellular basement membrane to cytoplasmic dystrophin. Disruption of the extensive carbohydrate structure normally present on α-dystroglycan causes an array of congenital and limb girdle muscular dystrophies known as

[Excess caloric intake induced severe hypercapnia in a patient with Duchenne muscular dystrophy on noninvansive positive pressure ventilation].

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In many patients with neuromuscular diseases, respiratory failure is mainly caused by alveolar hypoventilation in their terminal stages. Malnutrition is one of the common and serious problems in patients with chronic respiratory failure. Energy consumption for breathing is remarkably high in

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