Mitochondrial biogenesis study on different animal models of obesity : role of nitric oxide. Obesity is associated with chronic low-grade inflammation. Thus, at metabolically relevant sites, including adipose tissue and muscle, there is abnormal production of proinflammatory cytokines such as TNF-alpha. Here we demonstrate that eNOS expression was reduced, with a concomitant reduction of mitochondrial biogenesis and function, in white and brown adipose tissue and in the soleus muscle of 3 different animal models of obesity. The genetic deletion of TNF receptor 1 in obese mice restored eNOS expression and mitochondrial biogenesis in fat and muscle; this was associated with less body weight gain than in obese wild-type controls. Furthermore, TNF-alpha downregulated eNOS expression and mitochondrial biogenesis in cultured white and brown adipocytes and muscle satellite cells of mice. The NO donors DETA-NO and SNAP prevented the reduction of mitochondrial biogenesis observed with TNF-alpha. Our findings demonstrate that TNF-alpha impairs mitochondrial biogenesis and function in different tissues of obese rodents by downregulating eNOS expression and suggest a novel pathophysiological process that sustains obesity.

Studio della mitocondriogenesi in diversi modelli animali di obesità : ruolo dell'ossido nitrico / A. Cardile ; M. Carruba, A.E. Panerai. DIPARTIMENTO DI FARMACOLOGIA, CHEMIOTERAPIA E TOSSICOLOGIA MEDICA, 2006. 18. ciclo, Anno Accademico 2005/2006.

Studio della mitocondriogenesi in diversi modelli animali di obesità : ruolo dell'ossido nitrico

A. Cardile
2006

Abstract

Mitochondrial biogenesis study on different animal models of obesity : role of nitric oxide. Obesity is associated with chronic low-grade inflammation. Thus, at metabolically relevant sites, including adipose tissue and muscle, there is abnormal production of proinflammatory cytokines such as TNF-alpha. Here we demonstrate that eNOS expression was reduced, with a concomitant reduction of mitochondrial biogenesis and function, in white and brown adipose tissue and in the soleus muscle of 3 different animal models of obesity. The genetic deletion of TNF receptor 1 in obese mice restored eNOS expression and mitochondrial biogenesis in fat and muscle; this was associated with less body weight gain than in obese wild-type controls. Furthermore, TNF-alpha downregulated eNOS expression and mitochondrial biogenesis in cultured white and brown adipocytes and muscle satellite cells of mice. The NO donors DETA-NO and SNAP prevented the reduction of mitochondrial biogenesis observed with TNF-alpha. Our findings demonstrate that TNF-alpha impairs mitochondrial biogenesis and function in different tissues of obese rodents by downregulating eNOS expression and suggest a novel pathophysiological process that sustains obesity.
2006
Settore BIO/14 - Farmacologia
CARRUBA, MICHELE
PANERAI, ALBERTO EMILIO
Doctoral Thesis
Studio della mitocondriogenesi in diversi modelli animali di obesità : ruolo dell'ossido nitrico / A. Cardile ; M. Carruba, A.E. Panerai. DIPARTIMENTO DI FARMACOLOGIA, CHEMIOTERAPIA E TOSSICOLOGIA MEDICA, 2006. 18. ciclo, Anno Accademico 2005/2006.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/63130
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