Dr Andrew Thomas

Job Title:            Principal Lecturer
Room No:          D2.04d
Telephone No: + 44 (0) 29 2041 6844
Email Address:  AThomas@cardiffmet.ac.uk



Molecular biology, genetics, cell biology, biotechnology, Bioinformatics, pharmacology.


In general, my research interests concentrate on the molecular mechanisms involved in chronic systemic inflammation and subsequent accelerated atherosclerosis associated with type 2 diabetes and obesity. Specifically, I am interested in the role of hyperglycaemia and advanced glycated end-products (AGEs), and their respective receptor (AGER), in the development of atherosclerotic lesions. I am also interested in the way in which PPAR gamma ligands (both synthetic and natural) and exercise and diet can modulate intracellular signalling cascades, alter gene expression and ultimately interfere with the atherosclerotic and inflammatory pathways that are central to the pathological complications associated type 2 diabetes. The overall outcome of this research is to elucidate the beneficial molecular effects that drug intervention, alteration of diet and increased physical activity can have on insulin resistance and diabetes-associated atherosclerosis. Iis envisaged that the knowledge gained during this research will ultimately be translated to create more effective preventative, treatment and management schemes for obesity and diabetes. 


2008 onwards:

1.  Cullen, T. Thomas, A.W. Webb, R. Hughes, M.G. "The relationship between interleukin-6 in saliva, venous and capillary plasma, at rest and in response to exercise" Cytokine (in press).
2.  Davies, N.A., Watkeys, L., Butcher, L., Potter, S., Hughes, M.G.1, Moir, H.2, Morris, K., Thomas, A.W. and Webb, R. "The Roles of Oxidative Stress, Oxidised Lipoproteins and AMPK in Exercise-Associated PPARg Signalling within Human Monocytic Cells" Free Radical Research (in press).
3.  Thomas AW, Davies NA, Moir H, Watkeys L, Ruffino JS, Isa SA, Butcher LR, Hughes MG, Morris K, Webb R.(2012) Exercise-associated generation of PPARγ ligands activates PPARγ signalling events and upregulates genes related to lipid metabolism.J Appl Physiol; 112(5):806-15.
4.  Moir H, Hughes MG, Potter S, Sims C, Butcher LR, Davies NA, Verheggen K, Jones KP, Thomas AW, Webb R. (2010) Exercise-induced immunosuppression: roles of reactive oxygen species and 5'-AMP-activated protein kinase dephosphorylation within immune cells. Appl Physiol.108(5):1284-92
5.  Caddy, J., Isa, S., Adam, E., Roberts, A., Lang, D., Morris, R.H.K., Thomas, A.W. Webb, R. (2010) Rosiglitazone induces the unfolded protein response, but has no effect on cell viability, in monocytic and vascular smooth muscle cells. Biochem Biophys Res Commun 400(4):689-95
6.  Yakeu, G. Butcher, L. Webb, R. Roberts, A. Thomas, AW, Backx, K., James, P,E Morris, K. (2010) "Low-intensity exercise triggers monocyte polarisation into the M2 anti-inflammatory phenotype" Atherosclerosis. 212(2):668-73.
7.  Isa, S.A., Mainwaring, L.S., Webb. R. and Thomas, A.W. (2009): "The Non-Genomic Effects of High Doses of Rosiglitazone on Cell Growth and Apoptosis in Cultured Monocytic Cells" Bayero Journal of Pure and Applied Sciences 2(2): pp.1-8.
8.  Butcher, L., Backx, K., Roberts, A., Thomas, A., Webb, R., and Morris, K. (2008): "Low-intensity exercise exerts beneficial effects on plasma lipids via PPARg" Medicine & Science in Sports & Exercise 40 (7), pp. 1–7.
9.  Caddy, J., Singh, N., Atkin, L., Ahluwalia, M., Roberts, A.W., Lang, D., Thomas, A.W. and Webb, R. (2008): "Rosiglitazone Transiently Disturbs Calcium Homeostasis in Monocytic Cells" Biochemical Biophysical Research Communications 366, p.149-155.