The Role of Phosphodiesterase 3B in the Regulation of Human Adipose Tissue Biology and Systemic Glucose and Lipid Homeostasis

Study code
NBR247

Lead researcher
Dr Maria Chondronikola

Study type
Participant re-contact

Institution or company
University of Cambridge

Researcher type
Academic

Speciality area
Metabolic and Endocrine Disorders

Recruitment Site
National

Summary

We are inviting individuals to join this experimental medicine study aiming to understand the role an enzyme called Phosphodiesterase 3B (PDE3B) has on fat tissue and metabolism.

Some changes in our DNA called “mutations” affect our proteins making them less effective. Having less of this protein PDE3B might protect people from developing type 2 diabetes, heart attacks or stroke.

To clarify the role of this protein in humans, we propose to study people who have this mutation on their genetic make-up and compare them with people who don’t. This will help us answer these questions: 1) How does having a less functioning PDE3B protein affect the fat tissue? 2) How does it affect the ability of the body to control the sugar and lipid levels in the blood?

Participants will complete a telephone questionnaire and attend for a screening visit, which includes a medical examination and blood tests before and after drinking a sugary drink, and an XRay scan called DEXA. Food patterns and exercise will be assessed the following week with some questions and by wearing a smartwatch sensor. After that, participants will return for an in-depth metabolic visit with collection of blood and fat tissue samples.

The NIHR BioResource can identify people who either do or do not have this mutation based on their genetic make-up. It provides us with a great opportunity to study how people with or without the mutation handle fat, sugars and lipids in their bodies.

These investigations will help us understand more about the role of PDE3B in humans and possibly develop new ways to prevent or fight conditions like type 2 diabetes, fatty liver, heart attacks or stroke.