117,860 research outputs found
Experimental colitis: decreased Octn2 and Atb0+ expression in rat colonocytes induces carnitine depletion that is reversible by catnitine-loaded liposomes.
No full textCarnitine transporters have recently been implicated in susceptibility to inflammatory bowel disease (IBD). Because carnitine is required for beta-oxidation, it was suggested that decreased carnitine transporters, and hence reduced carnitine uptake, could lead to impaired fatty acid oxidation in intestinal epithelial cells, and to cell injury. We investigated this issue by examining the expression of the carnitine transporters OCTN2 and ATB0+, and butyrate metabolism in colonocytes in a rat model of IBD induced by trinitrobenzene sulfonic acid (TNBS). We found that Octn2 and Atb0+ expression was decreased in inflammatory samples at translational and functional level. Butyrate oxidation, evaluated based on CO2 production and acetyl-coenzyme A synthesis, was deranged in colonocytes from TNBS-treated rats. Treatment with carnitine-loaded liposomes corrected the butyrate metabolic alterations in vitro and reduced the severity of colitis in vivo. These results suggest that carnitine depletion in colonocytes is associated with the inability of mitochondria to maintain normal butyrate beta-oxidation. Our data indicate that carnitine is a rate-limiting factor for the maintenance of physiological butyrate oxidation in colonic cells. This hypothesis could also explain the contradictory therapeutic efficacy of butyrate supplementation observed in clinical trials of IBD.-D'Argenio, G., Calvani, M., Casamassimi, A., Petillo, O., Margarucci, S., Rienzo, M., Peluso, I., Calvani, R., Ciccodicola, A., Caporaso, N., and Peluso, G. Experimental colitis: decreased Octn2 and Atb0+ expression in rat colonocytes induces carnitine depletion that is reversible by carnitine-loaded liposomes
Use of propionyl L-carnitine for the preparation of a medicament for the treatment of glaucoma.
No full textUso della propionil L-carnitina per la preparazione di un medicamento
per il trattamento del glaucom
Acetyl-L-carnitine feeding to unloaded rats triggers in soleus muscle the coordinated expression of genes involved in mitochondrial biogenesis
No full textThe expressional profile of mitochondrial transcripts and of genes involved in the mitochondrial biogenesis pathway induced by ALCAR daily supplementation in soleus muscle of control and unloaded 3-month-old rats has been analyzed. It has been found that ALCAR treatment is able to upregulate the expression level of mitochondrial transcripts (COX I, ATP6, ND6, 16 S rRNA) in both control and unloaded animals. Interestingly, ALCAR feeding to unloaded rats resulted in the increase of transcript level for master factors involved in mitochondrial biogenesis (PGC-1alpha, NRF-1, TFAM). It also prevented the unloading-induced downregulation of mRNA levels for kinases able to transduce metabolic (AMPK) and neuronal stimuli (CaMKIIbeta) into mitochondrial biogenesis. No significant effect on the expressional level of such genes was found in control ALCAR-treated rats. In addition, ALCAR feeding was able to prevent the loss of mitochondrial protein content due to unloading condition. Correlation analysis revealed a strong coordination in the expression of genes involved in mitochondrial biogenesis only in ALCAR-treated suspended animals, supporting a differentiated effect of ALCAR treatment in relation to the loading state of the soleus muscle. In conclusions, we demonstrated the ability of ALCAR supplementation to promote only in soleus muscle of hindlimb suspended rats an orchestrated expression of genes involved in mitochondrial biogenesis, which might counteract the unloading-induced metabolic changes, preventing the loss of mitochondrial proteins
La formazione per il sostegno. Valutare la didattica in un'ottica di qualità (speech ammesso a convegno)
No full textEsito di una ricerca pluriennale condotta nell'organizzazione di corsi di formazione per insegnanti di sostegno
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