# Mechanism of Glucose-dependent insulinotropic polypeptide (GIP) on Splanchnic Venous Capacitance in Postural Tachycardia Syndrome

> **NIH NIH R01** · VANDERBILT UNIVERSITY MEDICAL CENTER · 2022 · $806,487

## Abstract

Project summary
Postural Tachycardia Syndrome (POTS) affects ~3 million adults in the United States. These patients have a
poor quality of life due to chronic presyncopal symptoms and tachycardia that occur upon standing. Our
research has shown that meals rich in carbohydrates significantly exacerbate presyncopal symptoms in POTS,
however, the underlying mechanism that explains this clinical observation remains unknown.
Accordingly, our group conducted a preliminary study to evaluate the pathophysiology of POTS’ excessive
orthostatic tachycardia after glucose intake; we surveyed the hemodynamic and neurohormonal changes that
occurred after a 75-gr oral glucose challenge for up to 2-hrs (postprandial period) in POTS patients and healthy
controls. Compared with fasting conditions, the ingestion of glucose worsened upright tachycardia in POTS
patients, which was associated with a more robust reduction in upright stroke volume compared with healthy
controls. With regards to the disproportionate decrease in upright stroke volume in POTS patients, this could,
in part, be explained by a significant blood pooling in the splanchnic circulation. The splanchnic circulation is
the largest blood volume reservoir of the human body, storing ~25% of the total blood volume. Upon standing,
there is a significant blood pooling, which occurs mostly in the splanchnic veins. Finally, our study has also
shown that 30-min after the ingestion of 75-gr of glucose, POTS patients had a selectively increased secretion
of the glucose-dependent insulinotropic polypeptide (GIP) hormone compared with healthy controls. This
hormone has vasodilatory properties in the splanchnic circulation. Importantly, the increase in GIP secretion
was time-dependently associated with a fall in upright stroke volume after glucose intake in POTS.
Consequently, these findings point to the potential contribution of GIP in the pathophysiology of the increased
postprandial orthostatic tachycardia and presyncopal symptoms in POTS patients. As such, the overall goal of
this proposal is to investigate the mechanisms underlying the exacerbation of orthostatic tachycardia and
POTS presyncopal symptoms in response to glucose ingestion. Specifically, we will evaluate the contribution
of GIP on the changes in the splanchnic venous capacitance after oral glucose and during upright posture in
POTS patients.

## Key facts

- **NIH application ID:** 10522696
- **Project number:** 1R01HL159203-01A1
- **Recipient organization:** VANDERBILT UNIVERSITY MEDICAL CENTER
- **Principal Investigator:** Cyndya Adriana Shibao
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $806,487
- **Award type:** 1
- **Project period:** 2022-08-01 → 2027-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10522696

## Citation

> US National Institutes of Health, RePORTER application 10522696, Mechanism of Glucose-dependent insulinotropic polypeptide (GIP) on Splanchnic Venous Capacitance in Postural Tachycardia Syndrome (1R01HL159203-01A1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10522696. Licensed CC0.

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