Bo Wang
University of Illinois Urbana-Champaign, IL·Physiology
The liver acts as the body's fat and sugar control center. When it goes wrong, the results include two of the most common chronic diseases: atherosclerosis, the build-up of fatty plaques in arteries, and type 2 diabetes.
- Fields
Physiology
Biochemistry
Medicine & Clinical Research
- Topics
lipid metabolism
atherosclerosis
type 2 diabetes
- Grants
- 2 known grants, through May 2029
What they work on
- Examine how SEC16B, a scaffold protein on the endoplasmic reticulum, regulates the formation of lipid droplets (fat-storage bodies) in liver cells, using cell-culture and in vivo experiments.
- Determine the function and mechanism of SEC16B in VLDL metabolism, the packaging and secretion of fat-carrying particles from the liver, and assess whether SEC16B could be a therapeutic target for atherosclerosis.
- Elucidate how the phospholipid makeup of liver cell membranes, shaped by the remodeling enzyme Lpcat3, controls insulin signaling and insulin sensitivity.
- Test whether abnormal Lpcat3 expression drives selective insulin resistance in type 2 diabetes, where insulin fails to curb glucose production but still promotes fat production.
- Evaluate whether targeting Lpcat3 can reduce hyperglycemia and hypertriglyceridemia (high blood sugar and blood fats) in type 2 diabetes.
More about the research
This research asks how the liver's internal membranes and compartments decide where fats go: whether they are stored, packaged and secreted into the blood, or used to process insulin signals. One project focuses on a scaffold protein that sits at a key cellular checkpoint for fat export. The other focuses on an enzyme that reshapes the fat molecules making up cell membranes.
Why it matters
Atherosclerosis and type 2 diabetes are growing public health burdens. Many people still have heart disease risk even after LDL-lowering drugs such as statins. By defining how SEC16B controls fat export from the liver, and how the membrane-remodeling enzyme Lpcat3 shapes insulin action, this work may reveal new drug targets. Such targets could lower blood triglycerides and blood sugar in patients with cardiovascular disease or type 2 diabetes.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Kamran Atabai
University of California-San Francisco, CA·Physiology
Determine the cellular mechanism by which insulin moves MFGE8, a secreted protein, through the endoplasmic reticulum and Golgi to the muscle cell surface, where it binds the αvβ5 integrin.
Karin Bornfeldt
University of Washington, WA·Medicine & Clinical Research
Test whether higher plasma APOC3, a protein that controls triglyceride-rich particles, tracks with build-up of a mid-sized lipoprotein particle and worsening insulin resistance and arterial stiffness in youth with type 1 or type 2 diabetes followed over time.
Rita Basu
University of Alabama at Birmingham, AL·Medicine & Clinical Research
Map the daytime pattern of liver glucose production after meals in adults with type 2 diabetes using a stable-isotope triple-tracer approach, while estimating insulin action and beta-cell responsiveness.
The school
University of Illinois Urbana-Champaign: 41 labs on PI Pages, $907M a year on research, 870 research doctorates a year.
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