# Mechanisms of diabetes remission induced by FGF1

> **NIH NIH R01** · UNIVERSITY OF WASHINGTON · 2020 · $441,250

## Abstract

Project Summary
Type 2 diabetes (T2D) is among the most common and costly challenges confronting modern society.
Although current treatment regimens can transiently normalize glycemia, lasting diabetes remission has yet to
be achieved through nonsurgical means. This changed with our recent finding that central administration of
fibroblast growth factor 1 (FGF1) can restore normal blood glucose levels to both rat and mouse models of
T2D in a manner that is sustained for weeks or months. Our interrogation of underlying mechanisms supports
the hypothesis tested in this proposal that FGF1 action in the brain of diabetic animals re-sets the defended
level of glycemia to the normal range, and our preliminary data point strongly to the mediobasal hypothalamus
(MBH) as a key target for this effect. The overarching goal of the proposed studies is to employ FGF1 as a tool
with which to understand how glucoregulatory neurocircuits can be remodeled so as to lower the defended
blood glucose level. In this context, FGF1 is used as a tool how this brain effect is achieved. Proposed studies
seek to identify both the discrete MBH neurocircuits involved in this FGF1 effect and the underlying cellular and
molecular mechanisms, based in part on our preliminary evidence that cross-talk between FGF receptors and
integrin receptors is required for FGF1-induced diabetes remission. To delineate the specific cell types and
molecular mediators involved, we will employ single cell transcriptomics, histochemistry, biochemistry,
pharmacology and electrophysiology, along with established energy homeostasis and glucose metabolic
phenotyping methods, in rodent models of T2D. A comprehensive understanding of how FGF1 action in the
MBH induces diabetes remission will shed new light on how glucose homeostasis is controlled by the brain and
on the potential of interventions that target the brain to improve treatment outcomes for patients with T2D.

## Key facts

- **NIH application ID:** 10000898
- **Project number:** 5R01DK083042-24
- **Recipient organization:** UNIVERSITY OF WASHINGTON
- **Principal Investigator:** Michael W Schwartz
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $441,250
- **Award type:** 5
- **Project period:** 1994-09-01 → 2022-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10000898

## Citation

> US National Institutes of Health, RePORTER application 10000898, Mechanisms of diabetes remission induced by FGF1 (5R01DK083042-24). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10000898. Licensed CC0.

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