Publications by authors named "Chabowski A"

An increased rate of fatty acid transport into skeletal muscle has been has been linked to the accumulation of intramuscular lipids and insulin resistance, and red muscles are more susceptible than white muscles in developing fatty acid-mediated insulin resistance. Therefore, we examined in Zucker diabetic fatty (ZDF) rats, relative to lean rats, 1) whether rates of fatty acid transport and transporters (FAT/CD36 and FABPpm) were upregulated in skeletal muscle during the transition from insulin resistance (week 6) to type 2 diabetes (weeks 12 and 24), 2) whether such changes occurred primarily in red skeletal muscle, and 3) whether changes in FAT/CD36 and GLUT4 were correlated. In red muscles of ZDF compared with lean rats, the rates of fatty acid transport were upregulated (+66%) early in life (week 6).

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Muscle fatty acid (FA) metabolism is impaired in obesity and insulin resistance, reflected by reduced rates of FA oxidation and accumulation of lipids. It has been suggested that interventions that increase FA oxidation may enhance insulin action by reducing these lipid pools. Here, we examined the effect of endurance training on rates of mitochondrial FA oxidation, the activity of carnitine palmitoyltransferase I (CPT I), and the lipid content in muscle of obese individuals and related these to measures of glucose tolerance.

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The fraction of free fatty acids (FFA) is present in skeletal muscles. However, there is almost no data regarding regulation in the content of this intramuscular lipid pool. We took advantage of the isolated muscle preparation to examine whether: a) increasing exogenous concentration of FFA (500microM or 700microM, 30min) b) insulin (10.

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Cellular fatty acid uptake is facilitated by a number of fatty acid transporters, FAT/CD36, FABPpm and FATP1. It had been presumed that FABPpm, was confined to the plasma membrane and was not regulated. Here, we demonstrate for the first time that FABPpm and FATP1 are also present in intracellular depots in cardiac myocytes.

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Fatty acid (FA) translocase (FAT)/CD36 is a key protein involved in regulating the uptake of FA across the plasma membrane in heart and skeletal muscle. A null mutation of FAT/CD36 reduces FA uptake rates and metabolism, while its overexpression increases FA uptake rates and metabolism. FA uptake into the myocyte may be regulated (a) by altering the expression of FAT/CD36, thereby increasing the plasmalemmal content of this protein (i.

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In obesity, the development of cardiomyopathy is associated with the accumulation of myocardial triacylglycerols (TAGs), possibly stemming from elevation of myocardial long-chain fatty acid (LCFA) uptake. Because LCFA uptake is regulated by insulin and contractions, we examined in cardiac myocytes from lean and obese Zucker rats the effects of insulin and the contraction-mimetic agent oligomycin on the initial rate of LCFA uptake, subcellular distribution of FAT/CD36, and LCFA metabolism. In cardiac myocytes from obese Zucker rats, under basal conditions, FAT/CD36 was relocated to the sarcolemma at the expense of intracellular stores.

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Because insulin has been shown to stimulate long-chain fatty acid (LCFA) esterification in skeletal muscle and cardiac myocytes, we investigated whether insulin increased the rate of LCFA transport by altering the expression and the subcellular distribution of the fatty acid transporters FAT/CD36 and FABPpm. In cardiac myocytes, insulin very rapidly increased the expression of FAT/CD36 protein in a time- and dose-dependent manner. During a 2-h period, insulin (10 nM) increased cardiac myocyte FAT/CD36 protein by 25% after 60 min and attained a maximum after 90-120 min (+40-50%).

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It has been assumed that the uptake of long chain fatty acids (LCFAs) into skeletal muscle and the heart muscle, as well as other tissues, occurred via passive diffusion. In recent years our work has shown that the LCFA uptake into skeletal muscle is a highly regulated process. The use of giant sarcolemmal vesicles obtained from skeletal muscle and heart has been used to demonstrate that LCFA uptake into these tissues occurs via a protein-mediated mechanism involving the 40 kDa plasma membrane associated fatty acid binding protein (FABPpm) and the 88 kDa fatty acid translocase, the homologue of human CD36 (FAT/CD36).

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The paper contains current data on the different ways of the liver regeneration. There is still not enough data about control of the regeneration processes in the liver. However nuclear phosphatidylinositols and sphingomyelins have been shown to play a potent role of messengers signaling.

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Although it has been suggested that tumour budding at the invasive edge of colorectal cancer is an important prognostic factor its biological significance for tumour progression is still to be evaluated. The aim of the study was to correlate tumour budding intensity with cathepsin D expression and some other clinicopathological variables of presumed or established prognostic value. 48 patients with colorectal cancer at pT3 stage, G2 grade of histological differentiation and tumour budding at the invasive edge were evaluated.

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Cathepsin D is one of the main proteolytic enzymes involved in the neoplastic process. The aim of the study was to evaluate the activity of cathepsin D in 36 colorectal adenocarcinomas (of the colon and rectum) at stage pT3 of clinical advancement and histological grade G2. The correlation of cathepsin D activity with the stage of anatomo-clinical advancement and the presence of chosen anatomo-clinical properties of the tumour was also analysed.

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The aim of the present study was to evaluate the activity of cathepsin B in 36 colorectal adenocarcinomas at stage pT3 of clinical advancement and histological grade G2. A correlation was also analysed of cathepsin B activity with the stage of anatomo-clinical advancement and the presence of chosen anatomo-clinical features of the tumour. Statistically significantly higher activity of cathepsin B was observed both in the cytosol and homogenate of the neoplastic tissue compared to its activity in the cytosol and homogenate of the adjacent unchanged tissue.

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Cathepsin D is one of the main proteolytic enzymes contributing to the development of cancer. The aim of the present study was to evaluate the expression of cathepsin D in 48 colorectal adenocarcinomas at pT3 stage of clinical advancement and G2 histologic grade. The correlation between cathepsin D expression, anatomo-clinical advancement and the presence of chosen anatomo-clinical properties of the tumours was also analysed.

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The aim of the study was to determine the usefulness of the expression of argyrophilic nucleolar organizer region proteins (AgNORs) as a marker of malignancy degree in thyroid follicular tumours. The study used the postoperative material of thyroid glands and cytologic material obtained with fine needle aspiration biopsy. Follicular adenoma, carcinoma and struma nodosa hyperplastica-type changes were analysed.

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