Identifying gestational-induced changes in islet macrophages as a potential target for beta-cell expansion
Ended Project Grant Awarded Last action
- Award ID
- F31GM150237
- Recipient
-
University Of Alabama At Birmingham UEI YND4PLMC9AN7
- Awarding agency
-
National Institute of General Medical Sciences
National Institutes of Health, Department of Health and Human Services
- Obligated
- $165,712
Award facts
- Assistance listing
- 93.859 Biomedical Research and Research Training
- Completion date
- Place of performance
- Birmingham, AL 35294, USA
Award details come from USAspending.gov.
Description
- Abstract
- (30 line max) diabetes mellitus is the leading cause of kidney failure, heart disease, and stroke, affecting 537 million people worldwide. Diabetes is diagnosed as an increase in blood glucose due to insufficient or ineffective insulin production by the pancreatic SS-cell. The inability of the SS-cell to adapt to changes in physiologic demand results in hyperglycemia. Under select conditions, such as injury and high-FAT diet, the SS-cell is capable of expansion, increasing in size and/or number to increase insulin production. Therefore, one potential strategy for mitigating hyperglycemic events is to stimulate SS-cell replication. A crucial component for SS-cell maturation and SS-cell expansion in the adult pancreas is macrophages which support tissue growth through the production of cytokines and stimulatory factors. In models of injury, macrophages shift from their basal classically activated proinflammatory state to a more alternatively-activated anti-inflammatory state, supportive of tissue remodeling through the production of anti-inflammatory cytokines, such as TGF-SS. Robust SS-cell proliferation has also been measured during pregnancy as a result of reductions in insulin sensitivity and increased fetal demand, making pregnancy an ideal model for investigating expansion in mature SS-cells under non-pathologic conditions. SS-cell expansion during gestation and macrophage contribution to maternal SS-cell growth has not been fully elucidated. I will assess changes in macrophage quantity and phenotype throughout pregnancy. I will determine the source of macrophage accumulation within the islet and whether IT is a critical component for SS-cell expansion in late gestation. I will also determine whether depletion of islet resident macrophages impairs SS-cell expansion in late gestation. I hypothesize that pregnancy drives islet macrophages to an alternatively-activated phenotype, necessary for maternal SS-cell expansion. To test this hypothesis, i will explore the following two aims: (1) characterize the macrophage population within the islet throughout gestation. (2) establish the requirement of macrophages for maternal SS-cell expansion in late gestation. The completion of these aims will identify macrophage-specific responses during pregnancy and their effects on SS-cell expansion. 1
Transactions
| Action | Obligated | Date |
|---|---|---|
| Amendment | $42,491 | |
| Amendment | $1,280 | |
| Amendment | $40,647 | |
| Amendment | $40,647 | |
| Amendment | $0 | |
| Amendment | $40,647 | |
| Original award | $0 |
Quick answers
Who received award F31GM150237?
F31GM150237 was awarded to University Of Alabama At Birmingham by National Institute of General Medical Sciences (National Institutes of Health) on July 22, 2024.
How much is award F31GM150237 worth?
$165,712 has been obligated on F31GM150237.
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