Role of Alpha-to-beta Cell Communication to Adapt Insulin Secretion to Insulin Resistance.

NCT ID: NCT07224334

Last Updated: 2025-11-13

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

NOT_YET_RECRUITING

Clinical Phase

PHASE1

Total Enrollment

30 participants

Study Classification

INTERVENTIONAL

Study Start Date

2025-11-30

Study Completion Date

2026-12-31

Brief Summary

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Glucagon secretion from α-cells has long been viewed as primarily a counterregulatory mechanism - e.g. an agent with a role to prevent blood sugar from decreasing to levels that compromise function. Our group, along with other researchers, have begun to identify a much more complex role for α-cells, raising questions about when and how glucagon may influence blood glucose levels. This proposal looks to detail proglucagon peptide secretion from α-cells and the impact this has on β-cell function and glucose tolerance, in preclinical studies of human islets and translational studies in human subjects.

This protocol registration describes Aim 2 from this NIH grant which involves 2 study populations and separate protocols but addresses a common question. Aim 3 in the grant is focused on a separate hypothesis and will be conducted and published separately from Aim 2.

Detailed Description

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Subjects will undergo screening for medical history, medication usage, and blood work; those who qualify will be offered participation. Study participation will last approximately 4-5 weeks depending on appointment availability.

Aim 2A: Each participant will have two 5-hour hyperglycemic clamp procedures to test the effect of fasting glucagon-like peptide 1 (GLP-1) action before and after experimental insulin resistance. The effect of endogenous proglucagon peptides (glucagon and GLP-1) to stimulate insulin secretion will be determined by blockade of the GLP-1 receptor with the antagonist exendin-9 (Ex-9) during glucose infusions. Insulin secretion experiments will be repeated before and after induction of insulin resistance. To induce insulin resistance, subjects will take dexamethasone, a synthetic glucocorticoid that has been shown in published studies and in a pilot study by our group to reduce insulin sensitivity by \~30%.

Aim 2B: This study will recruit non-diabetic subjects with obesity. They will be studied on two occasions using a 3 hr procedure with a hyperglycemic clamp to measure insulin secretion, followed by a hyperinsulinemic, euglycemic clamp to measure insulin sensitivity. This procedure will be done 2 times, once with saline infused during hyperglycemia as a control, and once with exendin-9 given during hyperglycemia to determine the role of GLP-1 receptor action.

Conditions

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Diabetes (DM)

Keywords

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insulin secretion insulin sensitivity GLP-1 alpha- to beta-cell communication

Study Design

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Allocation Method

RANDOMIZED

Intervention Model

CROSSOVER

Each subject will have paired, single day experiments performed within 4-5 weeks.
Primary Study Purpose

BASIC_SCIENCE

Blinding Strategy

SINGLE

Participants

Study Groups

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Aim 2A: Glucose-stimulated insulin secretion with and without GLP-1 receptor blockade

Aim 2A: Each subject will have a 5 hr experiment with sequential hyperglycemic clamps separated by a 90-minute washout. Blood glucose will be increased with an intravenous (IV) infusion of 20% dextrose and maintained stable at a level of 2.5-3.0 mM above fasting glucose for 90 minutes. Following the washout, a second, identical hyperglycemic clamp will be performed. Subjects will receive either saline or exendin-9 (600 pmol/kg/min) during the clamps; in 10 subjects the saline/clamp will be first and in 10 subjects the exendin-9/clamp will be first; the orders will be assigned randomly.

Intervention: The interventions here are the experimental hyperglycemia with and without exendin-9

Group Type PLACEBO_COMPARATOR

Exendin-9 is a 30 amino acid peptide that is an established competitive antagonist of the GLP-1 receptor. Subjects will receive exendin-9 by intravenous infusion at a rate of 600 pmol/kg/min

Intervention Type DRUG

Subjects in Aim 2A will receive exendin-9 on both experimental days and dexamethasone for one week before their second experimental day.

Subjects in Aim 2B will receive exendin-9 on one of their two experimental days.

Glucose stimulated insulin secretion with or without GLP-1 receptor blockade and insulin resistance

Aim 2A: Subjects will be treated with 6 mg dexamethasone once daily for 7 days to induce insulin resistance before repeating the 5 hr glucose clamp study. The infusion of glucose with saline and exendin-9 will be performed identically to the first study.

Intervention: The intervention in this arm is the induction of insulin resistance with dexamethasone treatment.

Group Type ACTIVE_COMPARATOR

Exendin-9 is a 30 amino acid peptide that is an established competitive antagonist of the GLP-1 receptor. Subjects will receive exendin-9 by intravenous infusion at a rate of 600 pmol/kg/min

Intervention Type DRUG

Subjects in Aim 2A will receive exendin-9 on both experimental days and dexamethasone for one week before their second experimental day.

Subjects in Aim 2B will receive exendin-9 on one of their two experimental days.

Aim 2B: Glucose stimulated insulin secretion and insulin sensitivity

Aim 2B: Each subject will have a 3-hour experiment with a 90-minute hyperglycemic clamp at a level of 2.5-3.0 mM above fasting glucose followed by a 60 minute hyperinsulinemic (80 units/meter2 Body Surface Area/minute), euglycemic clamp.

Group Type PLACEBO_COMPARATOR

Dexamethasone

Intervention Type DRUG

Dexamethasone 6 mg daily

Aim 2B: Glucose stimulated insulin secretion with GLP-1 receptor blockade and insulin sensitivity

Aim 2B: Subjects will have an identical hyperglycemic clamp but with infusion of exendin-9 (600 pmol/kg/min). Exendin-9 infusion will be stopped before the following hyperinsulinemic clamp that will be conducted identically to the control arm. Allocation of subjects in Aim 2B to the study with and without exendin-9 will be randomized.

Intervention: The intervention in this study is the administration of exendin-9 during experimental hyperglycemia.

Group Type ACTIVE_COMPARATOR

Exendin-9 is a 30 amino acid peptide that is an established competitive antagonist of the GLP-1 receptor. Subjects will receive exendin-9 by intravenous infusion at a rate of 600 pmol/kg/min

Intervention Type DRUG

Subjects in Aim 2A will receive exendin-9 on both experimental days and dexamethasone for one week before their second experimental day.

Subjects in Aim 2B will receive exendin-9 on one of their two experimental days.

Interventions

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Exendin-9 is a 30 amino acid peptide that is an established competitive antagonist of the GLP-1 receptor. Subjects will receive exendin-9 by intravenous infusion at a rate of 600 pmol/kg/min

Subjects in Aim 2A will receive exendin-9 on both experimental days and dexamethasone for one week before their second experimental day.

Subjects in Aim 2B will receive exendin-9 on one of their two experimental days.

Intervention Type DRUG

Dexamethasone

Dexamethasone 6 mg daily

Intervention Type DRUG

Eligibility Criteria

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Inclusion Criteria

* age 18-45
* Body Mass Index (BMI) \< 27.0
* Fasting plasma glucose of ≤ 95 mg/dL or HbA1c value ≤ 5.8% as measured at screening visit


* Age 35-60
* Body Mass Index (BMI) 27.0-35
* Fasting plasma glucose of \< 125 mg/dL or HbA1c value \< 6.5% as measured at screening visit

Exclusion Criteria

* Active medical disease: e.g. active infectious, inflammatory, neurodegenerative or mental health disorders
* Personal history of diabetes or pancreatitis
* Personal history of cardiac, gastrointestinal, renal or liver disease
* Immediate family history of diabetes
* Renal insufficiency (eGFR \< 60 mL/kg/min)
* Anemia (hematocrit \< 34%) as measured at screening visit
* Pregnant females
* Consumption of daily medications that alter glucose metabolism of GI function (glucocorticoids, psychotropics, narcotics, metoclopramide)
* Apparent sensitivity to the study peptide as determined by the skin test


* Active medical disease: e.g. active infectious, inflammatory, neurodegenerative or mental health disorders
* Personal history of diabetes or pancreatitis
* Personal history of cardiac, gastrointestinal, renal or liver disease
* Immediate family history of diabetes
* Renal insufficiency (eGFR \< 60 mL/kg/min)
* Anemia (hematocrit \< 34%) as measured at screening visit
* Pregnant females
* Consumption of daily medications that alter glucose metabolism of GI function (glucocorticoids, psychotropics, narcotics, metoclopramide)
* Apparent sensitivity to the study peptide as determined by the skin test
Minimum Eligible Age

18 Years

Maximum Eligible Age

60 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

NIH

Sponsor Role collaborator

David D'Alessio, M.D.

OTHER

Sponsor Role lead

Responsible Party

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David D'Alessio, M.D.

Professor of Medicine Duke University, Director Division of Endocrinology

Responsibility Role SPONSOR_INVESTIGATOR

Principal Investigators

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David D'Alessio, MD

Role: PRINCIPAL_INVESTIGATOR

Duke University

Locations

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Duke Center for Living

Durham, North Carolina, United States

Site Status

Countries

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United States

Central Contacts

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Johanna Johnson, MS

Role: CONTACT

Phone: 919-660-6766

Email: [email protected]

Alyssa Sudnick, MS

Role: CONTACT

Phone: 919-660-6769

Email: [email protected]

Facility Contacts

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Johanna Johnson, MS

Role: primary

Alyssa Sudnick, MS

Role: backup

References

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Ryan AS, Muller DC, Elahi D. Sequential hyperglycemic-euglycemic clamp to assess beta-cell and peripheral tissue: studies in female athletes. J Appl Physiol (1985). 2001 Aug;91(2):872-81. doi: 10.1152/jappl.2001.91.2.872.

Reference Type BACKGROUND
PMID: 11457805 (View on PubMed)

Jensen DH, Aaboe K, Henriksen JE, Volund A, Holst JJ, Madsbad S, Krarup T. Steroid-induced insulin resistance and impaired glucose tolerance are both associated with a progressive decline of incretin effect in first-degree relatives of patients with type 2 diabetes. Diabetologia. 2012 May;55(5):1406-16. doi: 10.1007/s00125-012-2459-7.

Reference Type BACKGROUND
PMID: 22286551 (View on PubMed)

Salehi M, Vahl TP, D'Alessio DA. Regulation of islet hormone release and gastric emptying by endogenous glucagon-like peptide 1 after glucose ingestion. J Clin Endocrinol Metab. 2008 Dec;93(12):4909-16. doi: 10.1210/jc.2008-0605. Epub 2008 Sep 30.

Reference Type BACKGROUND
PMID: 18827000 (View on PubMed)

Gray SM, Goonatilleke E, Emrick MA, Becker JO, Hoofnagle AN, Stefanovski D, He W, Zhang G, Tong J, Campbell J, D'Alessio DA. High Doses of Exogenous Glucagon Stimulate Insulin Secretion and Reduce Insulin Clearance in Healthy Humans. Diabetes. 2024 Mar 1;73(3):412-425. doi: 10.2337/db23-0201.

Reference Type BACKGROUND
PMID: 38015721 (View on PubMed)

Schirra J, Sturm K, Leicht P, Arnold R, Goke B, Katschinski M. Exendin(9-39)amide is an antagonist of glucagon-like peptide-1(7-36)amide in humans. J Clin Invest. 1998 Apr 1;101(7):1421-30. doi: 10.1172/JCI1349.

Reference Type BACKGROUND
PMID: 9525985 (View on PubMed)

Salehi M, Aulinger B, Prigeon RL, D'Alessio DA. Effect of endogenous GLP-1 on insulin secretion in type 2 diabetes. Diabetes. 2010 Jun;59(6):1330-7. doi: 10.2337/db09-1253. Epub 2010 Mar 9.

Reference Type BACKGROUND
PMID: 20215429 (View on PubMed)

Other Identifiers

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R01DK142423

Identifier Type: NIH

Identifier Source: secondary_id

View Link

Pro00116631

Identifier Type: -

Identifier Source: org_study_id