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Do individuals with a genetic predisposition for diabetes have dysfunctional fat tissue?

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  • Full or part time
    Dr K Kos
  • Application Deadline
    No more applications being accepted
  • Self-Funded PhD Students Only
    Self-Funded PhD Students Only

Project Description

The University of Exeter Medical School is seeking to attract self-funded PhD candidates of outstanding ability to join their exciting and rapidly expanding programme of internationally rated research.

Genetic profiles can help us unravel why certain people with obesity may become insulin resistant and others not. Obesity is associated with considerable metabolic complications, including diabetes and about 90% of subjects with Type 2 diabetes are being overweight or obese. About 3.8 million adults in the UK have diabetes at a cost of £10 billion per year to the NHS. Research into diabetes prevention and treatment is much needed. Fat (adipose) tissue stores surplus nutrients delivered to fat cells as triglycerides. With increasing obesity adipose tissue function becomes compromised by limitation of its capacity to take up fatty acids in form of triglycerides. A hallmark of this dysfunction is inflammation and production of surplus inflammatory hormones/cytokines secreted from fat tissue which drive insulin resistance which linits the uptake of glucose into the cells and is preceeding the development of diabetes . This also increases the risk of heart disease. At Exeter we deliver world leading research into the genetics of diabetes. Recently, we have found common genetic variations associated with a higher risk of Type 2 diabetes alongside an abnormal body fat distribution which suggests dysfunctional adipose tissue in these individuals (1). In this studentship we aim to study whether subjects with high risk genes for diabetes have compromised adipose tissue function by studying differences in adipose tissue genes commonly attributed to ‘adipose dysfunction’ and test the ability of adipose tissue of these individuals to store triglycerides. Increased understanding of the relationship of these genetic traits with adipose tissue dysfunction will aid in the development of novel therapies for people with diabetes.
This project will provide the student with a robust skill set resulting in highly employable skills in molecular biology and genetics and allow contribution to cutting edge science of wider significance.

Supervision of this project will be with the adipose tissue biologist Dr Katarina Kos and geneticist Professor Tim Frayling.

Contact name for scientific enquiries: Dr Katarina Kos [Email Address Removed]
For any other enquiries please contact: [Email Address Removed]

Applicants should be highly motivated and have, or expect to obtain, either a first or upper-second class BSc (or equivalent) in a relevant discipline. International applicants must also have IELTS [International English Language Testing System] score of 7 and above (or equivalent qualification).

Please send a CV, Covering letter (outlining your academic interests, prior research experience and reasons for wishing to undertake the project) and copies of degree transcript (giving full details of subjects studied and grades/marks obtained. This should be an interim transcript if you are still studying) to UEMS Graduate Research: [Email Address Removed]

Funding Notes

For some PhD projects, a ‘bench fee’ may apply. Bench fees are project specific and cover additional costs related to consumables, equipment and materials which are not included in the tuition fee. If bench fees do apply this will be notified as part of the application process and will be clearly stated in any offer letter.


Yaghootkar H, et al. Genetic evidence for a normal-weight "metabolically obese" phenotype linking insulin resistance, hypertension, coronary artery disease and type 2 diabetes. Diabetes 2014 (ahead of print and available on request)

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