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Metabolic Regulation

Staff List

Professor AOYAMA Toshifumi
Assistant Professor NAKAJIMA Takero

Contact

E-mail : aoyamato(at)shinshu-u.ac.jp
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Summary of Activity

This laboratory has examined the physiological, pharmacological, and toxicological roles of PPAR (peroxisomal proliferator-activated receptor) in many kinds of organs and tissues.

This laboratory has also developed the analytical method for sulfatides and examined its relation with specific diseases.

Research Projects

Roles of PPARa activation in the development of HCC with HCV infection

 

Development of preventive methods against HCC appearance with HCV infection

 

Roles of PPARa activation in the development of inflammation in kidney abnormalities

 

Roles of PPARa activation in cholesterol / bile acids metabolism

 

Roles of PPARa activation in the development of NASH and ASH

 

Roles of PPARa activation in hepatic triglyceride homeostasis

 

Roles of PPARa activation in renal triglyceride homeostasis

 

Roles of PPARa activation in cardiac triglyceride homeostasis

 

Roles of PPARa activation in testicular cholesterol homeostasis

 

Roles of sulfatides in coagulation

 

Roles of sulfatides as oxidative stress scavenger

 

Roles of sulfatides in sulfur metabolism

Major Publications

1. Nagaya, T., ---, Aoyama, T. (2010) Down-regulation of SREBP-1c is associated with the development of burned-out NASH.  J Hepatol. (in press).

2. Okiyama, W., ---, Aoyama, T. (2009) Polyenephosphatidylcholine prevents alcoholic liver disease in PPARa-null mice through attenuation of increases in oxidative stress.  J Hepatol. 50: 1236-1246.

3. Tanaka, N., --- , Aoyama T. (2008) PPARa activation is essential for HCV core protein-induced hepatic steatosis and hepatocellular carcinoma in mice. J Clin. Invest. 118: 683-694.

4. Kamijo, Y., --- , Aoyama, T. (2007)  PPAR alpha protects proximal tubular cells from acute fatty acid toxicity. J Am Soc Nephrol. 18: 3089-3100.

5. Kamijo, Y., --- , Aoyama, T. (2007)  PPARa protects against glomerulonephritis induced by long-term exposure to the plasticizer di-(2-ethylhexyl) phthalate. J Am Soc Nephrol. 18: 176-188.