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Liu Lab

 
 
 
Personnel: 
Jun Liu, M.D., Ph.D.
Associate Consultant, HEALth Program, Mayo Clinic in Arizona
Assistant Professor, Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine
Adjunct Faculty Member, Molecular and Cellular Biology Interdisciplinary Graduate Program, Arizona State University School of Life Sciences
 
Description: 

Dr. Liu's research focuses on the molecular mechanisms underlying obesity. Obesity has become a major global health threat due to its strong association with prevalent metabolic problems such as insulin resistance, diabetes and non-alcoholic fatty liver disease. Two things occur in obesity: (1) enhanced fatty acid storage as triglycerides in adipose tissue; and (2) overflow of free fatty acids and fatty acid-derived toxic lipids to other peripheral tissues. Protection against lipotoxicity in nonadipose tissues requires a carefully regulated balance in adipose tissue between triglyceride synthesis from fatty acids and triglyceride breakdown to release free fatty acids. Adipose triglyceride lipase (ATGL) is the rate-limiting enzyme mediating triglyceride breakdown or lipolysis, and thus is a critical determinant of storage/release of fatty acids. The primary interest of Dr. Liu's laboratory is to better understand the fundamental mechanisms that control the enzyme action of ATGL and how their alterations lead to the development of the aforementioned metabolic problems.

Recently, Dr. Liu's laboratory made an exciting discovery that a small protein named G0S2 can act as a molecular brake on ATGL-catalyzed lipolysis. G0S2 can interact directly with ATGL to suppress its enzyme activity. Additionally, G0S2 expression in adipose tissue and liver is reciprocally regulated during feeding-fasting-refeeding cycle, implicating a novel mechanism for the nutritional control of triglyceride mobilization and inter-organ flux of fatty acids. As usual, new insights raise many new questions. For example:

What is the biochemical mechanism by which G0S2 inhibits ATGL?
How does G0S2 work coordinately with other regulatory components in the lipolytic machinery?
Are there other proteins that interact with and modulate ATGL and/or G0S2?
What is the physiologic relevance of G0S2 in modulating adipose lipolysis and hepatic lipid homeostasis?
In diet-induced obesity, is G0S2 expression in adipose tissue altered and thereby contributing to elevated plasma fatty acid levels, peripheral lipotoxicity and insulin resistance?
What are the roles of G0S2 and other lipolytic modulators in the development of nonalcoholic fatty liver disease?

Dr. Liu and his colleagues are currently pursuing answers to all these important questions using a wide variety of experimental approaches, including cutting-edge proteomic, biochemical and cell biologic techniques. The Liu laboratory has also engineered animals to produce more or less G0S2, and is now vigorously testing whether these animals are more or less prone to metabolic diseases when obesity is induced by high fat feeding.

Laboratory Members

Postdoctoral Fellows
Xiaodong Zhang, PhD
Xitao Xie, PhD

Technical Staff
Alicia Saarinen, BS

Ph.D. Students
Bradlee Heckmann