Phoenix, Arizona




In cases of caloric surplus, adipocytes serve as a fuel depot by synthesizing triglycerides from fatty acids and glucose for storage. During starvation and extended exercise, beta-adrenergic hormones stimulate the lipolytic process in which triglycerides are broken down into fatty acids and glycerol. Subsequently, free fatty acids and glycerol are released into circulation to supply energy to other tissues and organs.

The research of Jun Liu, M.D., Ph.D., is focused on identifying the molecular mechanisms governing triglyceride breakdown in adipose tissue. In 2004, three groups independently discovered adipose triglyceride lipase (ATGL) as the rate-limiting enzyme in lipolysis.

Recent work in Dr. Liu's laboratory has identified a protein named G0S2 as a potent inhibitor of ATGL, providing a new piece to the complex lipolysis puzzle. G0S2 protein is highly abundant in adipose tissue and liver. G0S2 interacts directly with ATGL to suppress its enzyme activity.

Depletion of endogenous G0S2 in adipocytes using siRNA accelerates basal and hormone-stimulated lipolysis, whereas overexpression of G0S2 using recombinant adenovirus diminishes the rate of lipolysis in both adipocytes and adipose tissue explants.

Additionally, G0S2 expression in adipocytes and hepatocytes is reciprocally regulated by insulin and lipolytic stimulators such as beta-adrenergic agonists and TNF-alpha, implicating a potential mechanism for the efficient hormonal regulation of triglyceride mobilization.

Focus areas

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?
  • What is the in vivo 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 level and insulin resistance?
  • What are the roles of G0S2 and other lipolytic regulators 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 biochemical analyses, cell biology and in vivo physiologic measurements.

Their model systems include cultured and freshly isolated primary cells, tissue explants, and genetically engineered animals.

Significance to patient care

Obesity has been implicated to predispose a set of disorders, such as insulin resistance, hyperglycemia and dyslipidemia. Insulin resistance is a strong, independent contributor to the onset of type 2 diabetes.

Increased lipolysis in obesity contributes to elevated circulating fatty acids, resulting in the lipid accumulation in muscle and liver, which in turn inhibits insulin sensitivity.

Accordingly, a better understanding of the precise mechanisms for lipolytic regulation is needed to overcome insulin resistance and type 2 diabetes.


See my publications


Joint Appointment

  1. Senior Associate Consultant, Division of Endocrinology, Department of Internal Medicine

Administrative Appointment

  1. Senior Associate Consultant II-Research, Research Laboratories

Academic Rank

  1. Associate Professor of Biochemistry and Molecular Biology


  1. Post Doctoral Fellowship Life Sciences Institute, University of Michigan
  2. Ph.D. - Microbiology University of Virginia
  3. Graduate Fellowship - Molecular Medicine University of Virginia
  4. MD - Clinical Medicine Shanghai Medical University

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