I grew up in Taiyuan, the Capital of Shanxi province, China. I planned to be a physician who would help people with their health problems, as I chose clinical medicine as my major during my undergraduate studies. But experiences during my internship changed my mind. I decided to pursue a higher degree in Pharmacology since I realized that only when more efficient medicine/therapeutic methods are developed can the physicians truly help the patients out of their suffering. Thus I entered the graduate school in Peking University and obtained a MS. Later I came to the U.S to pursue my PhD Degree at KUMC.
Research Interests
As a PhD student in Dr. Klaassen’s lab, my thesis project is to determine dose-response hepatotoxic effects of bile acids and their regulation of hepatic genes in mice.
Bile acids (BAs) are well known to form micelles for facilitating the elimination of cholesterol in bile as well as emulsifiers for the absorption of lipids and lipid-soluble vitamins from the intestine. Within the last decade, BAs have been found to be ligands that regulate the homeostasis of cholesterol, bile acids, glucose, lipids, and energy by activation of a number of cellular receptors, such as nuclear receptors: farnesoid X receptor (FXR/Fxr), pregnane X receptor (PXR/Pxr), and vitamin D receptor (VDR) , as well as the membrane receptor TGR5.
Even though all BAs are derived from the precursor cholesterol, they have different physiological and pathological effects For example, CDCA is the most potent endogenous agonist of the farnesoid X receptor (FXR), whereas CA has little effects on FXR, rather it activates the cell surface receptor TGR5 triggering the transformation of inactive thyroid hormone T4 into active T3, causing increased energy expenditure. LCA is considered to be the most toxic bile acid, whereas UDCA and CDCA are thought to have hepato-protective effects, and are used in the treatment of cholestatic liver diseases.
To determine the physiological effects of individual BAs, they have usually been added to the diet. For example, feeding mice with 0.5 and 1% CA caused decreased expression of bile-acid-uptake transporter Ntcp. At such doses, CA caused liver damage indicated by increased serum ALT . Thus, it is not clear whether the changes caused by the bile acids are due to bile acid signaling or a consequence of their toxicity. In addtion, it is not clear from the literature, which doses of bile acids are non-toxic and which are toxic. Therefore, my study will provide useful information inregard to the toxic effects of individual BAs in the diets, namely, CA, CDCA, DCA, and LCA, as well as UDCA.
Contact Information
Peizhen (Sunny) Song
Department of Pharmacology, Toxicology, and Therapeutics
The University of Kansas Medical Center
MS1018
3901 Rainbow Blvd.
Kansas City, KS 66160
Phone: (913) 588-9248
Fax: (913) 588-7501
E-Mail: psong@kumc.edu
Updated 9/5/08
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The University of Kansas Medical Center