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Defining the Molecular and Physiological Mechanisms of Pancreatic Islet Cell Dysfunction Which Lead to Type 2 Diabetes

NCT02505308 · Status: COMPLETED · Phase: NA · Type: INTERVENTIONAL · Enrollment: 328

Last updated 2019-09-25

No results posted yet for this study

Summary

Defects in insulin secretion are central to the pathogenesis of type 2 diabetes (T2D) but the molecular basis and physiological consequences of those defects are poorly understood, impeding efforts to develop novel therapeutic approaches. Key questions remain unanswered, such as the extent to which T2D-associated islet dysfunction reflects endogenous defects in beta-cell mass or function, as opposed to disruption of external factors impinging on the beta-cells, such as incretins.

Recently the investigators have identified several genetic variations (DNA changes) associated with the production and processing of insulin in non-diabetic individuals and now aim to explore in more detail the role of these genetic variations. Utilising a "recruit by genotype" approach, they will identify individuals with and without genetic variants of interest from existing databases of research volunteers. The investigators will collect detailed medical history and measurements, fasted and stimulated blood samples for the profiling of insulin-related hormones and metabolites. The resulting genetic and non-genetic data will be used to improve understanding of the role of genetic variation on insulin secretion and sensitivity defects that lead to the development of T2D.

Conditions

Interventions

OTHER

Glucose-Potentiated Arginine-Induced Insulin Secretion

Intravenous catheters are inserted into antecubital veins in both arms. One arm is used for infusion of glucose/amino acid (Arginine). The other arm is used for intermittent sampling.

Sponsors & Collaborators

  • University of Exeter

    collaborator OTHER

  • University of Oxford

    collaborator OTHER

  • Oxford University Hospitals NHS Trust

    collaborator OTHER

  • Royal Devon and Exeter NHS Foundation Trust

    lead OTHER

Principal Investigators

  • Timothy M Frayling (Prof), PhD · University of Exeter

Study Design

Allocation
NON_RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
DOUBLE
Model
PARALLEL

Eligibility

Min Age
16 Years
Max Age
75 Years
Sex
ALL
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2015-03-04
Primary Completion
2019-03-31
Completion
2019-08-31

Countries

  • United Kingdom

Study Locations

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Entities

Diseases

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT02505308 on ClinicalTrials.gov