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Completed Phase 1 Interventional Accepts healthy volunteers

Mechanisms of Cerebrovascular Control

ClinicalTrials.gov ID: NCT02936687

Public ClinicalTrials.gov record NCT02936687. Field values are reproduced from the official study page; the official ClinicalTrials.gov record remains the source of truth for eligibility, enrollment, and contact information.

ClinicalTrials.gov public records Last synced Sep 4, 2026, 5:47 PM EDT

Data is sourced from official ClinicalTrials.gov public API records. Always review the official ClinicalTrials.gov record for the latest information.

Official title

Mechanisms of Cerebrovascular Control: Acute Insulin Surges Lead to Brain Hypoperfusion in Human Metabolic Syndrome

Brief summary

Reproduced verbatim from the official ClinicalTrials.gov record. Not medical advice.

The objective of this study is to identify insulin-specific cerebral blood flow (CBF) control mechanisms, and establish cerebrovascular responsive baseline in younger (18-45 yrs) metabolic syndrome adults (MetSyn) who are at substantial risk of stroke and other types of cardiovascular mortality even if they never develop diabetes. The central hypothesis is that vasodilator actions of insulin are impaired in MetSyn due to loss of dilator and gain of constrictor signals. This study will focus on 2 mechanisms that likely limit CBF in MetSyn: 1) Disruption of nitric oxide (NO) vasodilation, and 2) Exaggerated endothelin (ET-1) constriction. Three specific aims will be addressed: Aim 1: To test the hypothesis that physiologic surges of insulin acutely increase CBF in young adults, but adults with MetSyn exhibit paradoxical insulin-mediated vasoconstriction. Aim 2: To test the hypotheses that key mechanisms responsible for poor CBF in MetSyn are shifts in NO and ET-1 signaling. Specifically, in healthy controls, NO mediates robust dilation, with little to no ET-1 constriction. In contrast, adults with MetSyn exhibit uncoupled NO synthase (NOS) and exaggerated ET-1 constriction. Aim 3: To test the hypothesis that insulin regulation of CBF is regionally distinct (e.g. Middle Cerebral Artery (MCA) reactive than Anterior Cerebral Artery (ACA) or basilar), and the negative effects of insulin resistance (IR) are similarly regionally specific.

Study identification

NCT ID
NCT02936687
Recruitment status
Completed
Study type
Interventional
Phase
Phase 1
Enrollment
59 participants

Conditions and interventions

Eligibility (public fields only)

Age range
18 Years to 45 Years
Sex
All
Healthy volunteers
Accepts healthy volunteers

This page does not interpret eligibility. Detailed inclusion and exclusion criteria are on the official ClinicalTrials.gov record.

Study timeline

Start date
Jan 30, 2017
Primary completion
Jun 30, 2021
Completion
Sep 29, 2021
Last update posted
Oct 17, 2021

2017 – 2021

United States locations

U.S. sites
1
U.S. states
1
U.S. cities
1
Facility City State ZIP Site status
University of Wisconsin, Madison Madison Wisconsin 53706

Site contact phone numbers, emails, and investigator names are intentionally not displayed here. Open the official ClinicalTrials.gov record for site contact information.

About this trial record page

What this page shows
Public field values for ClinicalTrials.gov record NCT02936687, including study identification, conditions, interventions, eligibility (age, sex, healthy volunteer), timeline, and U.S. site list.
What this page does not do
No medical advice, eligibility judgments, treatment recommendations, study quality scoring, or AI-generated medical summaries. No site contact phone numbers, emails, or investigator names.
Where the data comes from
Sourced from the official ClinicalTrials.gov public API. The official record is the source of truth.
Last refresh
Last update posted Oct 17, 2021 · Synced Sep 4, 2026

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Open the official record

The complete protocol, eligibility criteria, and contact information for NCT02936687 live on ClinicalTrials.gov.

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