John Fowlkes
University of Kentucky, KY·Physiology
People with type 1 diabetes, whose bodies make little or no insulin, have thinner bones and break them more easily than people without diabetes. This condition, called diabetic bone disease, starts early in the illness, yet it is still unclear why it happens.
- Fields
Physiology
Medicine & Clinical Research
Biology
- Topics
type 1 diabetes
diabetic bone disease
osteoporosis
- Grants
- 1 known grant, through Apr 2027
What they work on
- Determine how deficiencies of insulin and insulin-like growth factor 1 (IGF-1) each contribute to diabetic bone disease at the tissue, cellular and molecular levels in models of type 1 diabetes.
- Define the overlapping and independent effects of insulin and IGF-1 on osteoblastogenesis, the formation of bone-building cells, by tracing the downstream signaling pathways each hormone uses.
- Explore the therapeutic potential of insulin and IGF-1 for preventing and treating diabetic bone disease by identifying signaling pathways that could become treatment targets.
More about the research
A common idea blames high blood sugar, but this project focuses on a different suspect: the loss of insulin and of insulin-like growth factor 1 (IGF-1), a related hormone that drives growth.
Why it matters
People with type 1 diabetes face a higher risk of osteoporosis and fragility fractures. By showing how missing insulin and IGF-1 weaken bone, this work could point to signaling pathways that serve as treatment targets, and could inform the use of insulin or IGF-1 to prevent or reverse diabetic bone disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Erica Scheller
Washington University in St Louis, MO·Physiology
Define how fat breakdown in constitutive bone marrow adipocytes supports osteoblast bone formation during high sympathetic nerve activity, and test whether this protection persists in aged and post-menopausal states.
Cornelia Peterson
Tufts University, MA·Medicine & Clinical Research·Early-career
Test how turning the insulin/insulin-like growth factor signaling (IIS) pathway up or down with drugs and genetic tools changes MYC levels, behavior and gene activity in cultured normal and tumor meibocytes, the oil-producing eyelid gland cells.
Ronald Kwon
University of Washington, WA·Genetics
Identify genes near 56 bone mineral density-linked genomic regions that cause adult skeletal defects when disrupted, using a reverse genetic screen and a new phenotyping strategy in zebrafish.
The school
University of Kentucky: 34 labs on PI Pages, $528M a year on research, 319 research doctorates a year.
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