# Contribution of Renal Tubule Insulin Receptor on Proximal Tubule Sodium Transport and Hypertension int he Metabolic Syndrome

> **NIH NIH K08** · UNIVERSITY OF IOWA · 2020 · $151,140

## Abstract

Project Summary / Abstract
Hypertension in patients with Metabolic Syndrome incurs a large financial, societal, and health cost in the
United States. Despite several lines of evidence that hypertension in the Metabolic Syndrome has a distinct
cause from idiopathic (essential) hypertension, this cause is not known and patients are treated empirically.
Contributions from many labs over the last 30 years have supported the hypothesis that enhanced insulin
signaling in the kidney plays a critical role in the pathogenesis of this disease. The Applicant's preliminary data
confirms the hypothesis that insulin action in the kidney contributes to hypertension in a mouse model of
Metabolic Syndrome and suggests that proximal tubular sodium transport may be increased, expanding blood
volume, and increasing blood pressure. The Applicant has (1) characterized: a mouse model to study the
intersection of the kidney, blood pressure, and Metabolic Syndrome and (2) generated a novel inducible tubule
insulin receptor knockout mouse to study the contribution of insulin receptor signaling to sodium transport and
blood pressure. In addition to the Applicant's contributions, the mentoring and scientific environment make him
an ideal candidate to develop independence in renal physiology research addressing this important question.
Here, the Applicant proposes three aims to study the contribution of insulin receptor signaling in the Metabolic
Syndrome to acute pressure natriuresis (Aim 1), to regulators of proximal tubule sodium transporter activity in
response to acute and chronic hypertension (Aim 2), and to patterns within the proximal tubule epithelial cell
transcriptome generated by insulin receptor signaling, the Metabolic Syndrome, or both (Aim 3). Successful
completion of these aims will begin to bridge the gap in knowledge between the role of insulin in whole animal
physiology and transporter activity and regulation in individual cells. In addition, through this training
mechanism the Applicant will learn the skills to successfully conduct independent research in basic science
nephrology.

## Key facts

- **NIH application ID:** 10001474
- **Project number:** 5K08DK114567-05
- **Recipient organization:** UNIVERSITY OF IOWA
- **Principal Investigator:** Jonathan Nizar
- **Activity code:** K08 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $151,140
- **Award type:** 5
- **Project period:** 2019-05-01 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10001474

## Citation

> US National Institutes of Health, RePORTER application 10001474, Contribution of Renal Tubule Insulin Receptor on Proximal Tubule Sodium Transport and Hypertension int he Metabolic Syndrome (5K08DK114567-05). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10001474. Licensed CC0.

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