Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:B6ZGS2 (Peroxisome proliferator activated receptor gamma)
 44 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adiponectin is a protein hormone involved in maintaining energy homeostasis in metabolically active tissues. It enhances glucose and lipid metabolism via activation of AMP-dependent kinase (AMPK) in skeletal muscle and liver. Energy homeostasis is vital for the heart to work as a pump. In this study, we investigated whether adiponectin and its receptors are expressed in adult ventricular cardiomyocytes. We observed adiponectin transcript and protein in cultured ventricular cardiomyocytes isolated from adult rat, by quantitative real-time PCR, ELISA assays, Western blots, and immunofluorescent staining. In addition, we detected adiponectin receptor (AdipoR1 and AdipoR2) expression in the heart. AdipoR1 was expressed in rat myocardium at a level of approximately 50% of that in skeletal muscle; whereas adipoR2 was expressed at a similar level to that in liver. Rosiglitazone, a Peroxisome proliferator activated receptor gamma (PPARgamma) activator, substantially elevated expression of adiponectin in cultured cardiomyocytes and its secretion into cultured media. Rosiglitazone also increased adipoR1 and adipoR2 expression in cardiomyocytes. Treatment of recombinant globular adiponectin in cultured cardiomyocytes increased fatty acid oxidation and glucose uptake via activation of AMPK, suggesting a role for adiponectin in cardiac energy metabolism. Together, these data establish the existence of a local cardiac-specific adiponectin system that is regulated by PPARgamma. Moreover, these findings indicate a role for adiponectin on normal myocardial energy homeostasis, in part, through the activation of AMPK.
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PMID:Adiponectin and its receptors are expressed in adult ventricular cardiomyocytes and upregulated by activation of peroxisome proliferator-activated receptor gamma. 1753 4

Peroxisome proliferator activated receptor gamma (PPAR-gamma) agonists are involved in the regulation of inflammatory responses and recent studies suggest that PPAR-gamma ligands may have potential for the treatment of allergic airway disease. This study investigated the effect of the PPAR-gamma agonist, rosiglitazone, on nasal mucous allergic inflammation and galectin-3 gene expression in a murine model of allergic rhinitis (AR mice). Rosiglitazone resulted in a statistically significant attenuation of the increased numbers of inflammatory cells and Th2 cytokine levels in nasal cavity lavage fluid of AR mice. Furthermore, the expression of galectin-3 in the nasal mucosa of AR mice was statistically significantly increased. Overexpression of galectin-3 was markedly suppressed by rosiglitazone treatment. These data suggest that the PPAR-gamma agonist, rosiglitazone, may have potential in the development of therapies for allergic rhinitis.
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PMID:Rosiglitazone attenuates allergic inflammation and inhibits expression of galectin-3 in a mouse model of allergic rhinitis. 1865 80