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Completed Phase 1 Interventional Accepts healthy volunteers

Preprandial Ghrelin Effect

ClinicalTrials.gov ID: NCT02913703

Public ClinicalTrials.gov record NCT02913703. 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.

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Official title

Effect of Preprandial Ghrelin on Postprandial Glucose Tolerance

Brief summary

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

Background and Significance: The peptide hormone ghrelin drives hunger and feeding behavior, making it a focus of obesity research. Released mainly by the stomach and proximal small intestine, ghrelin peaks prior to meals, potentially priming the gut for anticipated nutrients. After eating, ghrelin abruptly declines, with levels varying 2- to 3-fold between the fasted and fed states. Interestingly, in obesity and type 2 diabetes (T2D), this pattern is disrupted. Individuals with these disorders have chronically suppressed ghrelin levels and little variation before and after meals. Although ghrelin's preprandial rise and postprandial fall is a well-established phenomenon, its role in regulating glucose metabolism is unclear. In mice, increasing preprandial ghrelin levels improves glucose tolerance through enhanced glucagon-like peptide-1 (GLP-1) secretion. Ghrelin also stimulates GLP-1 secretion from mouse and human intestinal L-cells in vitro. These findings suggest enhanced postprandial GLP-1 as a novel role for the preprandial ghrelin surge. A ghrelin-incretin enteroendocrine axis could also explain the poor postprandial GLP-1 secretion and glucose tolerance in subjects with T2D, given their preprandial hypoghrelinemia. The investigators' preliminary data demonstrate that in humans, increasing circulating ghrelin to a supraphysiologic range worsened glucose tolerance, despite increased GLP-1 secretion. The discrepancy between these findings and the ones from rodents could be due to difference in study design and/or species. For example, the investigators' study used a continuous ghrelin infusion, which resulted in elevated levels of ghrelin pre- and postprandially. Elevated postprandial ghrelin likely mitigated the positive effects of increased GLP-1 secretion by raising levels of glucagon and other counter-regulatory hormones. This study seeks to delineate the interactions between ghrelin and GLP-1 in the regulation of glucose tolerance, beta-cell function, and insulin sensitivity. The investigators hypothesize that increased preprandial ghrelin will enhance GLP-1 secretion and consequently improve glucose tolerance in healthy subjects and those with T2D. Confirmation of these hypotheses would advance the investigators understanding of the control of glucose homeostasis and have important clinical and therapeutic implications. Modulating ghrelin levels may provide a novel therapeutic strategy to improve glucose tolerance in individuals with T2D, which affects an estimated 350 million people worldwide.

Study identification

NCT ID
NCT02913703
Recruitment status
Completed
Study type
Interventional
Phase
Phase 1
Lead sponsor
Jenny Tong, MD, MPH
Other
Enrollment
80 participants

Conditions and interventions

Interventions

Drug · Other

Eligibility (public fields only)

Age range
18 Years to 70 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 10, 2017
Primary completion
Nov 30, 2018
Completion
Nov 30, 2018
Last update posted
Mar 11, 2019

2017 – 2018

United States locations

U.S. sites
1
U.S. states
1
U.S. cities
1
Facility City State ZIP Site status
Duke Center For Living Durham North Carolina 27705

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 NCT02913703, 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 Mar 11, 2019 · Synced Sep 2, 2026

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