Diana Elizondo
University of Maryland-Baltimore County, MD·Physiology·Early-career
Obesity sharply raises the risk of type 2 diabetes (T2D), but not everyone with obesity becomes metabolically unhealthy. Part of the difference lies in how fat tissue grows.
- Fields
Physiology
Microbiology & Immunology
Biochemistry
- Topics
obesity
type 2 diabetes
adipose tissue
- Grants
- 1 known grant, through Mar 2029
What they work on
- Determine how TGases in myeloid cells, including macrophages, drive adipose tissue inflammation and unhealthy fat expansion in obesity, using conditional knockout mice.
- Define the role of TGases in Th17 cells and adipocytes in fat tissue fibrosis, extracellular matrix remodeling and immune cell dynamics during weight gain.
- Test whether deleting TGases at chosen times with a novel lentiviral Cre system changes fat cell expansion and whole-body insulin sensitivity in obese mice.
More about the research
Fat can expand in a healthy way by adding more fat cells (hyperplasia), or in an unhealthy way by swelling existing cells (hypertrophy). Unhealthy growth brings inflammation, scarring (fibrosis) and poor blood sugar control. Understanding what tips fat tissue toward the unhealthy path could point to ways to prevent diabetes.
Why it matters
Obesity-related type 2 diabetes affects millions of people. By showing how TGase enzymes in specific immune and fat cells push fat tissue toward inflammation and insulin resistance, this work may reveal new drug targets. Such targets could help prevent or reverse the metabolic disease that follows unhealthy weight gain.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sona Kang
University of California-Berkeley, CA·Physiology
Define how FAM3D, a protein genetically linked to type 2 diabetes, suppresses heat production and mitochondrial function in mouse and human brown fat cells.
Margo Emont
University of Chicago, IL·Physiology·Early-career
Track how human adipocyte subpopulations change during weight loss, using single-nucleus RNA sequencing of fat tissue collected during and after bariatric surgery.
Philipp Scherer
University of Texas Southwestern Medical Center, TX·Physiology
Adjust insulin signaling only in mouse fat cells, by lowering insulin receptor levels on demand, switching on an artificial insulin receptor, or manipulating the signaling brake PTEN. Measure the effects on whole-body metabolism.
The school
University of Maryland-Baltimore County: 7 labs on PI Pages, $151M a year on research, 90 research doctorates a year.
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