# Regulation of energy and glucose homeostasis by endogenous hypothalamic FGF1

> **NIH NIH R03** · UNIVERSITY OF WASHINGTON · 2022 · $132,375

## Abstract

Project Summary
Over the past 3 decades, obesity and type 2 diabetes (T2D) have emerged as among the most common and
costly chronic diseases confronting modern society. Treatment outcomes for patients affected with obesity or
T2D have shown minimal improvement due to the absence of non-surgical medical treatments that have
sustained efficacy. Therefore, an urgent need for new, more effective treatment options therefore exists, and
strategies targeting the brain have important potential to meet this need. As one example of relevant preclinical
work, our group has recently shown that signaling in the brain by exogenous administration of members of the
fibroblast growth factor (FGF) family produces potent weight-loss and anti-diabetic effects. Our K08 proposal
focused on the integrated central and peripheral mechanisms underlying the sustained anti-diabetic action of
exogenous FGF1 in rodent models of obesity and T2D. In this application, we propose a parallel line of studies
that will investigate the role of endogenous hypothalamic FGF1 signaling in the regulation of energy and glucose
homeostasis. We have recently found that FGF1 is endogenously expressed by tanycytes and cells distributed
in a number of key hypothalamic areas implicated in the control of body weight and glucose. Further, we have
observed that endogenous hypothalamic FGF1 expression is regulated fasting and refeeding and in preliminary
studies that deleting FGF1 from either hypothalamic neurons or tanycytes induces weight gain and glucose
intolerance on chow diet. These data support the premise that endogenous hypothalamic FGF1 signaling plays
a physiologic role in the regulation of energy and glucose homeostasis. We will investigate this hypothesis by
determining the specific hypothalamic nuclei and cell types that express FGF1, identify which of these
populations respond to acute and chronic changes in metabolic status and diet, and the extent to which disrupting
endogenous hypothalamic FGF1 signaling is sufficient to promote the development of obesity and glucose
intolerance. The data obtained from these investigations will form the basis of a new line of research centered
on endogenous hypothalamic FGF1 signaling as a novel target to treat obesity and T2D.

## Key facts

- **NIH application ID:** 10368119
- **Project number:** 5R03DK128383-02
- **Recipient organization:** UNIVERSITY OF WASHINGTON
- **Principal Investigator:** Jarrad M Scarlett
- **Activity code:** R03 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $132,375
- **Award type:** 5
- **Project period:** 2021-04-01 → 2023-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10368119

## Citation

> US National Institutes of Health, RePORTER application 10368119, Regulation of energy and glucose homeostasis by endogenous hypothalamic FGF1 (5R03DK128383-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10368119. Licensed CC0.

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