Laura Alonso
Weill Medical College of Cornell University, NY·Physiology
Diabetes develops when the pancreas's beta cells can no longer make enough insulin. One cause of beta-cell failure is stress in the endoplasmic reticulum (ER), the cell compartment where insulin and other proteins are built and folded.
- Fields
Physiology
Medicine & Clinical Research
Biology
- Topics
diabetes
pancreatic beta cells
insulin
- Grants
- 1 known grant, through Dec 2026
What they work on
- 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.
- Determine the cellular and molecular basis by which beta-cell function recovers in mice once chronic activation of ATF6, an ER stress-response transcription factor, is allowed to switch off.
- Define the molecular mechanisms through which ATF6 drives both beneficial effects, such as beta-cell proliferation and survival, and harmful effects, such as loss of beta-cell function.
- Identify conditions under which ATF6's benefits can be separated from its harms, using tools that activate ATF6 in beta cells with precise timing, either outside the body or in live mice.
More about the research
ER stress contributes to type 2 diabetes, type 1 diabetes and some inherited forms of the disease. Cells respond to ER stress through three main pathways. One is run by ATF6, a transcription factor (a protein that switches genes on). ATF6 expands the ER's capacity and helps cells survive stress. The lab and others have also found that ATF6 helps beta cells multiply when the body needs more insulin, in both mouse and human beta cells. Activating ATF6 has therefore been proposed as a way to increase beta-cell numbers, but it may also cause harm.
Why it matters
Beta-cell failure underlies type 2, type 1 and some inherited forms of diabetes. Boosting the ATF6 pathway has been proposed as a way to grow more insulin-producing cells. Learning why prolonged ATF6 activation harms beta cells, how they recover, and whether benefits can be separated from harms could guide whether ATF6 can be safely used. This could form the basis for new approaches that keep beta cells healthy to prevent or treat diabetes.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Samuel Stephens
University of Iowa, IA·Physiology
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.
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
Weill Medical College of Cornell University: 35 labs on PI Pages, $1.6B a year on research, 59 research doctorates a year.
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