# Interrogating beta cell function and heterogeneity of C-peptide preservation in patients with type 1 diabetes or chronic pancreatitis

> **NIH NIH K23** · UNIVERSITY OF COLORADO DENVER · 2024 · $189,896

## Abstract

PROJECT SUMMARY/ABSTRACT:
Type 1 diabetes (T1D) is an increasing public health burden for which current therapies are focused on insulin
replacement. Future T1D treatments will try to preserve endogenous pancreatic beta cell function in new onset
T1D and replace beta cells via transplantation in long standing diabetes. Classically, T1D is viewed as an
autoimmune disease but beta cell loss is also driven by genetic risk factors and metabolic stress. Much has
been done to try to delay T1D progression from preclinical multiple autoantibody positivity to clinical disease, but
progression is highly heterogenous. C-peptide preservation can improve diabetes control and decrease the risk
for diabetes complications. There are a wide array of C-peptide measurements to examine endogenous beta
cell function and stress and many genes have been associated with C-peptide preservation in T1D. Less is
known about the influence of genetics on the preservation of endogenous beta cell function during the partial
remission period (PRM) or “honeymoon” after diagnosis. These factors are also likely important for patients with
chronic pancreatitis (CP) who have risk for islet loss but for whom genetic risk and metabolic stressors remain
largely unexplored. Patients with CP have severe pain and progressive endocrine insufficiency due to persistent
inflammation and hepatic insulin resistance. For patients with severe CP, total pancreatectomy with islet auto-
transplantation (TPIAT) is an attempt to preserve a patient’s endogenous beta cell function while removing the
source of their pain. Younger age and higher beta cell mass during transplantation are predictors for functional
graft survival. Less is known about the role of beta cell genetics in these patients, which I will evaluate in this
proposal.
I am an emerging researcher with experience in basic science beta cells studies and clinical research defining
heterogeneity in T1D. My goal in this career development award is to hone clinical research skills by studying
the impact of genetics and markers of beta cell function in patients with newly diagnosed T1D and in a model of
cell therapy (CP patients who have undergone TPIAT) with these aims:
1: Analyze if baseline markers of beta cell function and stress can predict PRM C-peptide preservation.
2: Evaluate if known pre-specified T1D SNPs are associated with PRM C-peptide preservation
3: Evaluate if pre-specified SNPs associated with C-peptide preservation predict insulin use and C-peptide in
CP patients who have undergone TPIAT
As part of this K23 award proposal, I outline educational, training, and scientific goals that will support my
pathway to independence. I have assembled a diverse and broad mentorship/collaborator team to support this
endeavor. This career development award will support my career goal to elucidate heterogeneity in beta cell
(dys-)function in diabetes and to develop novel cell therapy interventions.

## Key facts

- **NIH application ID:** 10910119
- **Project number:** 5K23DK136931-02
- **Recipient organization:** UNIVERSITY OF COLORADO DENVER
- **Principal Investigator:** Taylor Triolo
- **Activity code:** K23 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $189,896
- **Award type:** 5
- **Project period:** 2023-09-01 → 2026-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10910119

## Citation

> US National Institutes of Health, RePORTER application 10910119, Interrogating beta cell function and heterogeneity of C-peptide preservation in patients with type 1 diabetes or chronic pancreatitis (5K23DK136931-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10910119. Licensed CC0.

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