Benefits of Individualized Training in Fatigued Patients with Multiple Sclerosis.

Introduction: Chronic fatigue is the most common and debilitating symptom in people with multiple sclerosis (PwMS). Recently, exercise has been proven to alleviate chronic fatigue and improve physical functions. Tailoring the training intervention to the potential fatigue causes could optimize the beneficial effects of training on fatigue.

Insulin-sensitive glucose transporter transcript levels in calf muscles assessed with a bovine GLUT4 cDNA fragment.

Previous studies have shown that the expression of the insulin-sensitive glucose transporter (GLUT4) is lower in oxidative muscles than in glycolytic muscles in bovines and goats in contrast to observations in rats. Additional experiments in this work provide very strong arguments that the immunoreactive band detected does represent GLUT4 protein, which further validates our previous results. Therefore, to determine the level of regulation, the main objective of the present study was to measure GLUT4 mRNA amounts in various bovine muscles.

Discrete brain areas express the insulin-responsive glucose transporter GLUT4.

Whether or not glucose utilization in the brain is insulin-dependent is still a controversial issue. We looked for the presence of the insulin-sensitive glucose transporter (GLUT4) in rat brain and obtained the following results: (1) poly(A) RNAs from the hypothalamus and anterior medulla oblongata hybridize with a cDNA probe for GLUT4; (2) reverse transcription-polymerase chain reaction (RT-PCR) on RNA from various brain nuclei detects GLUT4 transcripts; (3) immunocytochemistry, using a polyclonal antibody to GLUT4; reveals a specific immunostaining pattern, whereas both electronic microscopy and double immunofluorescence staining, using a neurofilament protein marker, indicate a neuronal localization. These results are discussed in terms of a putative neuromodulator role of insulin, via glucose utilization, in brain areas involved in the regulation of fuel metabolism.

DNase I hypersensitivity sites and nuclear protein binding on the fatty acid synthase gene: identification of an element with properties similar to known glucose-responsive elements.

We have shown previously that fatty acid synthase (FAS) gene expression is positively regulated by glucose in rat adipose tissue and liver. In the present study, we have identified in the first intron of the gene a sequence closely related to known glucose-responsive elements such as in the L-pyruvate kinase and S14 genes, including a putative upstream stimulatory factor/major late transcription factor (USF/MLTF) binding site (E-box) (+ 292 nt to + 297 nt). Location of this sequence corresponds to a site of hypersensitivity to DNase I which is present in the liver but not in the spleen.

[Medium-chain acyl-CoA dehydrogenase deficiency: contribution of molecular biology].

Background: Medium-chain acyl-CoA dehydrogenase deficiency is the most frequent cause of defective congenital fatty acid oxidation. Its molecular characterization is now possible. Case n.