BSc (Hons), PhD
Professor of Metabolic Physiology
- BHF Senior Basic Science Research Fellow
Integrative Physiology (Systems Biology)
I am heading the Metabolic Research Group together with Professor Fredrik Karpe. My research focuses on the alterations in metabolism with nutritional state and substrates (e.g. sugars, fatty acids) along with the associated metabolic consequences of obesity. We perform whole body human physiological studies to understand the metabolic integration between tissues.
The current focus of my research is on understanding liver fat metabolism, as perturbations in this have the potential to impact widely on metabolic health. Accumulation of fat within the liver underlies the spectrum of conditions known as non-alcoholic fatty liver disease (NAFLD) and this is a risk factor for cardiovascular disease and diabetes. The liver is a major player in fat metabolism; it integrates endogenous and exogenous fatty acids and the accumulation or loss of liver fat represents the balance between input and removal pathways. However, the regulation of the metabolic partitioning of fatty acids within the human liver is poorly understood. We use a combination of approaches, including human in vivo, ex vivo, and in vitro cellular models along metabolically-labelled substrates (stable-isotope tracers) to probe relevant pathways involved liver fat metabolism. By understanding the regulation of these pathways, this may lead to interesting new therapeutic approaches to prevent and/or treat NAFLD.
I was awarded a British Heart Foundation Senior Fellowship in Basic Science in 2015. Prior to this, I was awarded the Gridlers’ Health Research Council (NZ) Career Development Fellowship, which enabled me to come and undertake post-doctoral work at the University of Oxford in 2004 and I held a British Heart Foundation Intermediate Fellowship in Basic Science from 2011-2015.
Dysregulation of hepatic metabolism with obesity: factors influencing glucose and lipid metabolism
Nagarajan SR. et al, (2021), Proceedings of the Nutrition Society, 1 - 23
Distinct contributions of metabolic dysfunction and genetic risk factors in the pathogenesis of non-alcoholic fatty liver disease.
Luukkonen PK. et al, (2021), J Hepatol
Overfeeding Saturated Fat Increases LDL (Low-Density Lipoprotein) Aggregation Susceptibility While Overfeeding Unsaturated Fat Decreases Proteoglycan-Binding of Lipoproteins.
Ruuth M. et al, (2021), Arterioscler Thromb Vasc Biol
Adipocyte NR1D1 dictates adipose tissue expansion during obesity.
Hunter AL. et al, (2021), Elife, 10
Prolyl-4-hydroxylase 3 maintains β-cell glucose metabolism during fatty acid excess in mice.
Nasteska D. et al, (2021), JCI Insight