# A pathway linking gut osmolarity to thirst

> **NIH NIH F32** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2021 · $66,390

## Abstract

PROJECT SUMMARY/ABSTRACT
Fluid intake is precisely regulated to match physiological need. This is imperative to maintain fluid homeostasis
and ultimately for survival, although the underlying mechanisms remain poorly understood. Critically, the body
needs to be able to sense the osmolarity of ingested fluids, as different osmolarities can have opposing
impacts on physiological need and behavioral responses. It has been recently demonstrated that the
gastrointestinal tract is the locale that detects and communicates fluid osmolarity in real-time to central thirst
circuits, but the specific mechanisms underlying this osmosensation are completely unknown.
The aim of this proposal is to identify the key cell types and afferent neural pathways that detect osmolarity in
the gut and relay this information to the brain to control thirst. The hypothesis proposed here is that this
happens in two steps. First, specialized chemosensory cells in the gut, called enteroendocrine cells, detect the
osmolarity of the gut lumen. These cells then communicate with the brain by activating adjacent vagal sensory
neurons. Aim 1 will determine the role of enteroendocrine cells in thirst and osmosensation, whereas Aim 2 will
focus on the vagus nerve. These experiments will be done using genetic and virally mediated tools to target
and manipulate, for the first time, specific enteroendocrine and vagal cell types in awake, behaving mice. The
effect manipulating these cell types has on fluid intake will be measured, and the corresponding activity of thirst
neurons in the subfornical organ that track gut osmolarity will be monitored using calcium imaging in vivo.
These data will reveal fundamental mechanisms that allow the body to appropriately respond to ingested
substances and maintain fluid homeostasis. Ultimately, these experiments will advance our understanding of
basic physiologic processes in the gut and how fluid and salt are handled by the body; dysregulation of these
processes contributes to conditions like hypertension and gastrointestinal disorders.

## Key facts

- **NIH application ID:** 10116167
- **Project number:** 5F32DK124984-02
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** Brooke Jarvie
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $66,390
- **Award type:** 5
- **Project period:** 2020-03-01 → 2023-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10116167

## Citation

> US National Institutes of Health, RePORTER application 10116167, A pathway linking gut osmolarity to thirst (5F32DK124984-02). Retrieved via AI Analytics 2026-05-21 from https://api.ai-analytics.org/grant/nih/10116167. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*
