Defining the Physiological Mechanisms of Risk Genes for Hyperglycaemia, Insulin Resistance and Type 2 Diabetes
NCT02723110 · Status: UNKNOWN · Type: OBSERVATIONAL · Enrollment: 40
Last updated 2016-06-22
Summary
Recent genetic association studies have identified variants in the Peptidyl-Glycine alpha-amidating mono-oxygenase (PAM) gene that increase the risk of diabetes likely through a defect in beta-cell function. This has been followed up and supported by novel kinetic assays and cellular studies. This investigation will recall heterozygous carriers of the risk allele at rs78408340 and age, BMI and gender matched controls from the Oxford Biobank. The study will compare the incretin effect, glucagon-like peptide-1(GLP-1), insulin, glucose levels and PAM protein activity in individuals both with and without the risk variant. The aim of the study is to gain mechanistic insight into the effect of the variant on human physiology and diabetes pathogenesis.
Conditions
Interventions
- OTHER
-
4 Hour Frequently Sampled Oral Glucose Tolerance Test
Blood glucose level(BGL) every 5 min, blood for hormone, biochemical analysis at -15,0,15,30,45,60,90,120,180, 240
- OTHER
-
Isoglycaemic Clamp
Glucose infusion over 4 hours to reproduce OGTT glucose curve to allow measurement of incretin effect. BGL every 5 min, blood for hormone, biochemical analysis at -15,0,15,30,45,60,90,120,180, 240
Sponsors & Collaborators
-
University of Exeter
collaborator OTHER - collaborator OTHER_GOV
-
University of Oxford
lead OTHER
Eligibility
- Min Age
- 30 Years
- Max Age
- 65 Years
- Sex
- ALL
- Healthy Volunteers
- Yes
Timeline & Regulatory
- Start
- 2015-06-30
- Primary Completion
- 2016-07-31
- Completion
- 2016-07-31
Countries
- United Kingdom
Study Locations
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