Ahmad Al-Mrabeh
MRC Career Development Fellow
- Centre for Cardiovascular Science
Contact details
- Tel: +44 (0)1315371000
- Email: Ahmad.Al-Mrabeh@ed.ac.uk
Address
- Street
-
The Queen's Medical Research Institute,
Edinburgh BioQuarter,
47 Little France Crescent - City
- Edinburgh
- Post code
- EH16 4TJ
Background
I obtained a PhD in biology in 2011 from the James Hutton Institute, Dundee. Afterwards, I had undertaken several research positions between 2011-2021 becoming in 2019 a senior scientist at Newcastle University working primarily on remission of type 2 diabetes (T2D). In Aug 2021, I moved to the University of Edinburgh as a BHF Transition Research Fellow to establish my own research group around the mechanisms of T2D remission. In 2022, I was successful in securing an MRC Career Development Award to investigate the mechanisms of reversible pancreas lipotoxicity in T2D. I am interested in identification of the toxic lipids that cause pancreas dysfunction and understanding their function with aim to develop novel therapies for diabetes. My research programme involves a combination of clinical, preclinical (mouse), and ex-vivo studies.
Open to PhD supervision enquiries?
Yes
Research summary
Obesity is a major risk factor for type 2 diabetes (T2D). Weight loss by low calorie diet can induce remission of T2D. However, this is challenging to achieve and maintain in the long-term due to weight regain. Our research is centred on elucidating the mechanisms by which weight loss bring about remission of diabetes in order to develop novel therapies. Obesity also alters hepatic lipid export, leading to dyslipidaemia, a key pathophysiological feature associated with the metabolic syndrome. One reason for this is increased de novo lipogenesis (DNL), a pathway whose flux is increased in fatty liver disease and T2D. We have previously demonstrated that hepatic DNL-derived fatty acids decrease after weight loss and remission of diabetes in humans and have more recently confirmed that we can replicate this in a polygenic mouse model of T2D. The lab’s primary focus is on the DNL pathway as a potential mechanism leading to elevated lipoprotein export, intrapancreatic fat deposition, loss of acinar cell mass, and beta cell dysfunction (collectively termed “pancreas lipotoxicity”).