Muscle triglyceride synthesis and insulin sensitivity (M-FAT)
Research type
Research Study
Full title
Role of alternative pathways of triglyceride synthesis in determining insulin sensitivity in muscle (M-FAT)
IRAS ID
191701
Contact name
Jason Gill
Contact email
Sponsor organisation
NHS Greater Glasgow & Clyde
Duration of Study in the UK
3 years, 6 months, 1 days
Research summary
One of the major factors determining a person’s risk of developing adult-onset diabetes is a reduced ability of muscle to respond to the hormone insulin to take up sugar from the blood. This is called ‘insulin resistance’. One key factor in this process is a build-up of fat (called triglyceride) within muscle. However, similarly high levels of triglyceride are found in the muscles of highly trained athletes who are highly insulin-sensitive (the opposite of insulin resistant). We have evidence that this is because the triglyceride in these two cases is not the same and is made from two different sources by two different processes within the muscle. We hypothesise that an enzyme called DGAT2 makes triglyceride from glucose and acts as a source of molecules that contribute to insulin resistance, whereas an enzyme called DGAT1 acts to store triglyceride safely for use by the muscle during physical activity. These alternative routes may, therefore, give rise to 'good' triglyceride in highly insulin-sensitive people and 'bad' triglyceride in insulin-resistant people at risk of developing diabetes. We will examine whether the ratio of these enzymes in muscle contributes to the likelihood of developing type 2 diabetes, as altering this ratio may offer a strategy for reducing the risk of developing the disease. We will also investigate whether differences in fat storage and release in adipose (fat) tissue influences these processes in muscle.
REC name
West of Scotland REC 4
REC reference
16/WS/0002
Date of REC Opinion
14 Jan 2016
REC opinion
Favourable Opinion