Joon Ha
Howard University, DC·Mathematics & Statistics
Type 2 diabetes often develops slowly and then suddenly. Blood sugar creeps upward for years and then rises sharply when the disease begins.
- Fields
Mathematics & Statistics
Medicine & Clinical Research
Physiology
- Topics
type 2 diabetes
mathematical biology
mathematical modeling
- Grants
- 1 known grant, through Aug 2029
What they work on
- Identify a slow manifold, a boundary within a physiological model of beta-cell function and insulin sensitivity, that separates progression to type 2 diabetes from staying healthy.
- Explain the sharp rise in blood glucose at diabetes onset, and how the threshold shifts with genetic and environmental factors, using mathematical models of beta-cell mass and insulin secretion capacity.
- Validate the diabetes progression models against longitudinal clinical data from studies of Southwest Native Americans.
- Estimate personalized model parameters from short-timescale data and use them to predict each patient's long-term progression, building a data-derived slow manifold to guide therapy.
More about the research
This pattern suggests the body crosses a tipping point. But blood sugar itself cannot serve as that threshold. This project uses mathematics to find what the tipping point really is, and how genes and lifestyle move a person toward it or away from it.
Why it matters
A clear, mathematically defined threshold for diabetes onset could help people with prediabetes and type 2 diabetes. Diabetes educators could use it to motivate patients to keep up lifestyle changes. Personalized model estimates may support individualized treatment. The threshold could also help researchers decide which metabolic factors to target in biological and clinical studies before running experiments.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Michelle Kimple
University of Wisconsin-Madison, WI·Pharmacology
Determine how the EP3 receptor affects separate cellular pools of calcium and cAMP in mouse and human beta cells, and how these changes alter insulin secretion and beta-cell mass, using cellular imaging.
Jonathan Campbell
Duke University, NC·Physiology
Test whether pericytes, cells lining blood vessels, are the main GIP receptor (GIPR)-expressing cells in fat tissue, using mouse models that mark and lineage-trace GIPR-positive cells over time.
Laura Alonso
Weill Medical College of Cornell University, NY·Physiology
Identify the causes of beta-cell dysfunction and glucose intolerance after 14 days of continuous ATF6 activation in living mice, using molecular, morphological and tissue-homeostasis experiments.
The school
Howard University: 8 labs on PI Pages, $102M a year on research, 102 research doctorates a year.
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