Jennifer completed her BSc in Anatomy with first class honours from Glasgow University in 2002. Following a year travelling she undertook an MSc in Oncology at Nottingham University achieving a distinction in 2004. The MSc dissertation focused on The Mechanisms of EMAP-II- induced lymphocyte apoptosis, supervised by Dr C Murray. Her first position in 2004 was a Research assistant at The Human Reproductive Science Unit in Edinburgh. This position was in collaboration with Ardana Bioscience and involved screening of compounds for the induction of apoptosis in prostate cancer cell lines. In 2007 Jennifer moved to Dundee University to undertake a Research assistant position within the Cardiovascular and Diabetes Medicine department. Since her appointment within CVDM Jennifer has worked on a number of projects which have focused on complications associated with disease such as obesity, Type I and Type II diabetes and Alzheimer’s. Jennifer has spent the last 5 years working for Professor Rory McCrimmon focusing on Defective counter regulation associated with recurrent hypoglycaemia. She has been heavily involved in establishing and managing the Dundee metabolic phenotyping centre under direct supervision of Professor McCrimmon.
Metabolic dysfunction and in particular Diabetes (both Type 1 and Type 2) can have a profound impact upon multiple systems within the body. At present Jennifer is involved in a number of projects looking at the various aspects of metabolic dysfunction.
Her current research for Professor McCrimmon investigates the role of the cytokine, IL-6 in the modulation of whole body response to hypoglycaemia as well as the adaptation to repeated hypoglycaemia.
Another research project due to start focuses on the characterisation of the role of NPAT in metformin regulation of body weight and glycemic control. This project will be working with Dr Calum Sutherland and in an example of GWAS data moving to biological function.
Diabetes also increases the risk of cardiovascular disease, primarily mediated through micro- and macrovascular dysfunction. In a study performed in collaboration with Dr Faisel Khan (University of Dundee) and Prof Maria Gomez (Lund University, Sweden) the team have demonstrated a potential therapeutic role of NFAT inhibition in hyperglycemia induced endothelial dysfunction.
Over the past 5 years Jennifer has worked at establishing the Dundee Metabolic Phenotyping Service. During this time she has collaborated with a number of groups within the University including Prof Mike Ashford, Dr Graham Rena, Dr Will Fuller, Dr Calum Sutherland and Dr Li Kang. She is currently involved in a number of phenotyping studies accessing the response of various genotypes to metabolic stress factors such as high fat feeding.
I deliver teaching in all aspects of in vivo techniques, to any staff and students within and out with the University of Dundee.
McNeilly AD,Gallagher JR, Dinkova-Kostova A, Hayes, JD, Ashford MLJ, Sharkey J & McCrimmon RJ (2014) Intermittent hypoglycaemia affects memory in a mouse model of type 1diabetes Diabetes under review
Beall, C., Hamilton, D.L., Gallagher, J., Logie, L., Wright, K.Y., Soutar, P.M., Dadak, S., Ashford, F., Haythorne E., Jovanovic, A., McCrimmon, R.J., Ashford, M.L. Mouse hypothalamic GT1-7 cells demonstrate AMPK-dependent intrinsic glucose-sensing behaviour (In Press Diabetologia).
Watterson KR, Bestow D, Gallagher J, Hamilton DL, Ashford FB, Meakin PJ, Ashford ML. Anorexigenic and Orexigenic Hormone Modulation of Mammalian Target of Rapamycin Complex 1 Activity and the Regulation of Hypothalamic Agouti-Related Protein mRNA Expression.Neurosignals. 2012 Mar 28
Meakin PJ, Harper AJ, Hamilton DL, Gallagher J, McNeilly AD, Burgess LA, Vaanholt LM, Bannon KA, Latcham J, Hussain I, Speakman JR, Howlett DR, Ashford ML. Reduction in BACE1 decreases body weight, protects against diet-induced obesity and enhances insulin sensitivity in mice. Biochem J. 2012 Jan 1;441(1):285-96.
Ning K, Miller LC, Laidlaw HA, Watterson KR, Gallagher J, Sutherland C, Ashford ML.J. Leptin-dependent phosphorylation of PTEN mediates actin restructuring and activation of ATP-sensitive K+ channels. Biol Chem. 2009 Apr 3;284(14):9331-40.