Ignite Creation Date:
2024-05-06 @ 7:07 PM
Last Modification Date:
2024-10-26 @ 3:00 PM
Study NCT ID:
NCT05900193
Status:
COMPLETED
Last Update Posted:
2023-06-12
First Post:
2023-06-02
Brief Title:
Sucralose and Lactisole Additions to OGTT in Humans
Sponsor:
Rutgers The State University of New Jersey
Organization:
Rutgers The State University of New Jersey
Study Overview
Official Title:
Activation and Inhibition of the Sweet Taste Receptor T1R2-T1R3 Differentially Affect Glucose Tolerance in Humans
Status:
COMPLETED
Status Verified Date:
2023-06
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
SLOGTT
Brief Summary:
In the present study our objective was to determine whether T1R2-T1R3 influences glucose metabolism bidirectionally via hyperactivation with sucralose and inhibition with sodium lactisole in mixture with glucose loads during tolerance tests in humans In 12 healthy participants we conducted oral glucose tolerance tests OGTTs of 75 g glucose with and without the addition of the T1R2-T1R3 agonist sucralose 5 mM We also conducted OGTTs in 10 healthy participants with and without the addition of a T1R2-T1R3 antagonist sodium lactisole 2 mM Plasma glucose insulin and glucagon were measured before during and after OGTTs up to 120 minutes post-prandially We also assessed individual participants sweet taste responses to sucralose their sensitivities to sweetness inhibition by lactisole and their BMIs
Detailed Description:
The sweet taste receptor T1R2-T1R3 is expressed in taste bud cells where it conveys sweetness and also in intestinal enteroendocrine cells where it may facilitate glucose absorption and assimilation There is evidence in mice through genetic knockout studies that T1r2-T1r3 is involved in endocrine and enteroendocrine responses to glucose loads Yet our understanding of the impact of T1R2-T1R3 on human glucose metabolism is less clear In the present study our objective was to determine whether T1R2-T1R3 influences glucose metabolism bidirectionally via hyperactivation with sucralose and inhibition with sodium lactisole in mixture with glucose loads during tolerance tests in humans In 12 healthy participants we conducted oral glucose tolerance tests OGTTs of 75 g glucose with and without the addition of the T1R2-T1R3 agonist sucralose 5 mM We also conducted OGTTs in 10 healthy participants with and without the addition of a T1R2-T1R3 antagonist sodium lactisole 2 mM Plasma glucose insulin and glucagon were measured before during and after OGTTs up to 120 minutes post-prandially We also assessed individual participants sweet taste responses to sucralose their sensitivities to sweetness inhibition by lactisole and their BMIs The addition of sucralose to glucose elevated plasma insulin responses to the OGTT Sucralose-sensitive participants those who rated sucralose as sweetest had a more pronounced elevation in peak plasma insulin to sucralose glucose with early increases in plasma glucose and insulin area-under-the-curve AUC within the first 15 minutes In lactisole-sensitive participants whose sweetness was suppressed by low levels of lactisole the addition of lactisole to glucose in the OGTT decreased plasma glucose AUC Participants with higher BMI 24 kgm2 tended to be hyper-responsive to added sucralose nearly doubling their peak levels of insulin to the sucralose glucose OGTT Manipulation of the T1R2-T1R3 receptor with a non-caloric agonist and an antagonist demonstrates that T1R2-T1R3 helps regulate glucose handling and metabolism in humans Importantly participants with BMI 24 kgm2 tended to rate sucralose as sweeter and showed exaggerated insulin increases when it was added to their OGTT
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None