http://www.cnr.it/ontology/cnr/individuo/prodotto/ID24177
The L-4F mimetic peptide prevents insulin resistance through increased levels of HO-1, pAMPK, and pAKT in obese mice (Articolo in rivista)
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- The L-4F mimetic peptide prevents insulin resistance through increased levels of HO-1, pAMPK, and pAKT in obese mice (Articolo in rivista) (literal)
- Anno
- 2009-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1194/jlr.M800610-JLR200 (literal)
- Alternative label
Peterson SJ, Drummond G, Hyun Kim D, Li M, Positano V, Vanella L, Piccolomini F, Rodella LF, Gastaldelli A, Kusmic C, L'Abbate A, Kappas A, Abraham NG. (2009)
The L-4F mimetic peptide prevents insulin resistance through increased levels of HO-1, pAMPK, and pAKT in obese mice
in Journal of lipid research (Print)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Peterson SJ, Drummond G, Hyun Kim D, Li M, Positano V, Vanella L, Piccolomini F, Rodella LF, Gastaldelli A, Kusmic C, L'Abbate A, Kappas A, Abraham NG. (literal)
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- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Departments of Pharmacology and Medicine, New York Medical College, Valhalla, NY 10595; Central
National Research Institute of Clinical Physiology and Scuola Superiore Sant'Anna and CNR Institute
of Clinical Research,Pisa, Italy; and The Rockefeller University, New York 10021 (literal)
- Titolo
- The L-4F mimetic peptide prevents insulin resistance through increased levels of HO-1, pAMPK, and pAKT in obese mice (literal)
- Abstract
- We examined mechanisms by which L-4F reducesobesity and diabetes in obese (ob) diabetic mice. We hypothesized that L-4F reduces adiposity via increased pAMPK, pAKT, HO-1, and increased insulin receptor phosphorylation in ob mice. Obese and lean mice were divided into five groups: lean, lean-L-4F-treated, ob, ob-L-4F-treated, and ob- L-4F-LY294002. Food intake, insulin, glucose adipocyte stem
cells, pAMPK, pAKT, CB1, and insulin receptor phosphorylation were determined. Subcutaneous (SAT) and visceral adipose tissue (VAT) were determined by MRI and hepatic lipid content by magnetic resonance spectroscopy. SAT and VAT volumes decreased in ob-L-4F-treated animals compared with control. L-4F treatment decreased hepatic lipid content and increased the numbers of small adipocytes (P< 0.05) and phosphorylation of insulin receptors. L-4F decreased CB1 in SAT and VAT and increased pAKT and pAMPK in endothelium. L-4F-mediated improvement in endothelium was prevented by LY294002. Inhibition of pAKT and pAMPK by LY294002 was associated with an increase in glucose levels. Upregulation of HO-1 by L-4F produced adipose remodeling and increased the number of small differentiated adipocytes. The anti-obesity effects of L-4F are manifested by a decrease in visceral fat content with reciprocal increases in adiponectin, pAMPK, pAKT, and phosphorylation of insulin receptors with improved insulin sensitivity. (literal)
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