Western diets have changed dramatically over the last 30 years with a significant increase in consumption of processed foods that are high in calories, but nutrient deplete. There is general consensus that the rising prevalence of obesity and type II diabetes is related to consumption of these processed and calorie-dense foods. Recently it has also been suggested that excessive consumption of these foods may also increase the risk of developing cardiovascular disease (CVD) due to the high levels of phosphate preservatives used to enhance flavor and shelf life of these products.

Hyperphosphatemia is a serious consequence of chronic kidney disease, leading to increased vascular calcification and cardiovascular morbidity and mortality. New evidence is emerging that post-prandial fluctuations in serum phosphate concentration also correlate with increased CVD risk in a normal population. The kidney is generally considered to be the main organ involved in the regulation of phosphate homeostasis; however, data is now emerging to suggest this may not be the case and that different regions of the small intestine play distinct functional roles in this process. My research aims to further investigate the role of this organ in phosphate balance and to investigate the use of specific transporter inhibitors to directly target intestinal phosphate transport. This approach has the potential to be used to control hyperphosphatemia in chronic kidney disease and to reduce phosphate toxicity and subsequent CVD risk in the general population.

The cellular processes of glucose transport are similar in the kidney and small intestine, although different transport proteins are involved. Novel mechanisms for controlling intestinal glucose transport have recently been identified and it is likely, although not yet confirmed, that these processes will be similar in the kidney.  My research investigates the mechanisms involved in renal glucose reabsorption and how these processes are altered by diet, obesity and diabetes. The aim is to identify novel therapeutic targets to blunt renal, as well as intestinal, glucose reabsorption for the treatment of obesity and diabetes.