Samuel Stephens
University of Iowa, IA·Physiology
Type 2 diabetes develops when the insulin-making beta cells of the pancreas can no longer keep up with the body's demand. In people with the disease, these cells store less insulin and release more of its unfinished precursor, proinsulin.
- Fields
Physiology
Biochemistry
Medicine & Clinical Research
- Topics
type 2 diabetes
beta cell
pancreatic islet
- Grants
- 1 known grant, through Jun 2027
What they work on
- Establish how glucose metabolism in beta cells supplies reducing molecules that control the redox state of the endoplasmic reticulum, using imaging of proinsulin trafficking reporters in human and rodent diabetes models.
- Define the key molecular mediators that buffer endoplasmic reticulum redox capacity and allow proinsulin, insulin's precursor, to fold and leave the ER efficiently in pancreatic beta cells.
- Determine how proinsulin folding, including formation of misfolded proinsulin clumps linked by disulfide bonds, affects redox balance in the beta-cell endoplasmic reticulum.
More about the research
Why this happens is not fully understood. Restoring beta-cell function could be an important way to treat the disease.
Why it matters
Loss of insulin release from beta cells marks the shift from insulin resistance to full Type 2 diabetes. Identifying how disrupted glucose and redox metabolism impairs insulin production could point to ways of restoring beta-cell function. This may lead to new therapeutic strategies for people with Type 2 diabetes.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Rafael Arrojo E Drigo
Vanderbilt University, TN·Physiology
Determine how calorie restriction, high-fat diet, aging and ER stress change beta cell epigenetic marks, gene activity, function and lifespan, using single-cell multiome sequencing and in vivo function measurements.
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.
The school
University of Iowa: 32 labs on PI Pages, $703M a year on research, 418 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.