Ignite Creation Date:
2024-06-16 @ 11:48 AM
Last Modification Date:
2024-10-26 @ 3:30 PM
Study NCT ID:
NCT06424106
Status:
RECRUITING
Last Update Posted:
2024-05-21
First Post:
2024-05-13
Brief Title:
Effect of Glucagon on Fasting Insulin Secretion and Glucose Metabolism in Subjects Without Type 2 Diabetes
Sponsor:
Mayo Clinic
Organization:
Mayo Clinic
Study Overview
Official Title:
Effect of Glucagon on Fasting Insulin Secretion and Glucose Metabolism in Subjects Without Type 2 Diabetes
Status:
RECRUITING
Status Verified Date:
2024-10
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:
None
Brief Summary:
Fasting hyperglycemia contributes disproportionately to nonenzymatic glycosylation and the microvascular complications of type 2 diabetes However little is known about the regulation of glucose concentrations in the fasting state relative to what is known about the postprandial state The proposed experiment is part of a series of experiments designed to establish how glucagon and insulin interact with their receptors to control fasting glucose in health and in prediabetes
Detailed Description:
The interaction between α-cell and β-cell function to regulate fasting glucose is incompletely understood This is an important gap in our knowledge as fasting glucose contributes disproportionately to HbA1c and the microvascular complications of type 2 diabetes T2DM The regulation of fasting glucose in health and disease is relatively understudied
Insulin and glucagon should regulate glucose reciprocally through direct interaction insulin restrains α-cell secretion while glucagon directly stimulates β-cell secretion In addition there are indirect interactions via changes in glucose Glucagon increases endogenous glucose production EGP increasing glucose and insulin secretion Conversely insulin stimulates glucose disappearance Rd and suppresses EGP lowering glucose and stimulating glucagon
However this does not appear to occur uniformly in prediabetes For example in impaired fasting glucose IFG glucagon secretion rate GSR is inappropriate for the prevailing glucose This is not accompanied by reciprocal changes in insulin secretion rate ISR Variability in the hepatic response to glucagon and to insulin further compound the dysregulation of fasting glucose The net effect of these variables is unknown This experiment is intended to test the hypothesis that impaired glucagon-induced insulin secretion contributes to fasting hyperglycemia in IFG
Insulin and glucagon should regulate glucose reciprocally through direct interaction insulin restrains α-cell secretion while glucagon directly stimulates β-cell secretion In addition there are indirect interactions via changes in glucose Glucagon increases endogenous glucose production EGP increasing glucose and insulin secretion Conversely insulin stimulates glucose disappearance Rd and suppresses EGP lowering glucose and stimulating glucagon
However this does not appear to occur uniformly in prediabetes For example in impaired fasting glucose IFG glucagon secretion rate GSR is inappropriate for the prevailing glucose This is not accompanied by reciprocal changes in insulin secretion rate ISR Variability in the hepatic response to glucagon and to insulin further compound the dysregulation of fasting glucose The net effect of these variables is unknown This experiment is intended to test the hypothesis that impaired glucagon-induced insulin secretion contributes to fasting hyperglycemia in IFG
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