# Characterizing the role of novel long non coding RNA in diabetes onset and progression

> **NIH NIH F32** · UNIVERSITY OF COLORADO DENVER · 2020 · $51,322

## Abstract

During pancreas development cells receive and respond to signals that direct their decisions towards specific
lineages. In the past few decades collaborative efforts have allowed us to gain extensive knowledge about
pancreas development, islet composition and cell fate specification and function. Furthermore the increasing
availability of human pancreas samples have allowed us to explore the similarities and differences between
human and mouse pancreas biology. Although this significant progress has improved our understanding of
islet cell biology and diabetes we have still not been able to identify mutations that contribute to Type 1 and
Type 2 diabetes, suggesting that we are missing some key regulators. One of the most significant findings in
genome biology is that most of the genome is transcribed and produces a large variety of non-coding RNAs.
One of the non-coding RNA subtypes shown to be important in most aspects of biology are the long noncoding
RNAs (lncRNAs) that are characterized by their lack of protein coding potential and length of more than 200
nucleotides. We hypothesize that tissue specific lncRNAs play important roles in specialized cell-
specific functions, and that dysregulation of lncRNAs might result in cellular dysfunctions to cause
disorders, such as diabetes. We have identified several potential candidate conserved lncRNAs whose
expression changes during diabetes. In this proposal we will focus on lncRNA 6330403K07Rik (633), a
previously uncharacterized lncRNA that is conserved in mouse and humans, and whose expression increases
significantly in multiple mouse models of beta cell dysfunction. Human GWAS studies on diabetic subjects
have also identified SNPs in the vicinity of the 633 human ortholog. I will assess expression profile and timeline
of 633 upregulation during Type 2 diabetes onset and progression in db/db mice and test the effects of 633
overexpression in beta cells, in vitro and in vivo. Additionally, I will delete 633 in a diabetic mouse model to
determine the extent of its contribution to the beta cell dysfunction. This project provides us with a unique
opportunity to understand how the upregulation of a lncRNA might impact diabetes onset and progression. The
proposed approaches will allow me to identify important molecular mechanisms involved in diabetes
progression and has the potential to develop crucial therapeutic targets.

## Key facts

- **NIH application ID:** 9883627
- **Project number:** 5F32DK118803-02
- **Recipient organization:** UNIVERSITY OF COLORADO DENVER
- **Principal Investigator:** Laura Ioana Hudish
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $51,322
- **Award type:** 5
- **Project period:** 2019-07-01 → 2021-02-27

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9883627

## Citation

> US National Institutes of Health, RePORTER application 9883627, Characterizing the role of novel long non coding RNA in diabetes onset and progression (5F32DK118803-02). Retrieved via AI Analytics 2026-06-01 from https://api.ai-analytics.org/grant/nih/9883627. Licensed CC0.

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