Heidi de Wet
Associate Professor of Physiology
Heidi de Wet received her Bachelor of Science degree from North Western University, South Africa, and was awarded a DPhil from the University of Cape Town (UCT) Medical School in 2000. She moved to the University of Oxford to pursue post-doctoral studies in 2003, where she joined the group of Professor Frances Ashcroft. Following two maternity breaks, she joined the Department of Physiology, Anatomy and Genetics as a University Lecturer in Physiology and Associate Professor. She is a Fellow and Director of Studies for Pre-clinical Medicine for St Catherine's College.
Her doctoral work in the Department of Chemical Pathology, UCT, first introduced her to the ATP-binding cassette (ABC) family of membrane transporters; these transporters have been the focus of her research ever since. Her post-doctoral research in Oxford focussed on neonatal diabetes, a rare form of type 2 diabetes, and the dysfunctional ABC transporters involved in this disease. More recently, her focus has shifted to studying the role of ABC transporters in gut endocrine K-and L-cells. These cells are involved in nutrient sensing in the small intestine and the subsequent secretion of appropriate peptide hormones that regulate several essential physiological responses to food intake.
A Ketone Ester Drink Lowers Human Ghrelin and Appetite.
Stubbs BJ. et al, (2018), Obesity (Silver Spring), 26, 269 - 273
Correction: Molecular action of sulphonylureas on KATP channels: a real partnership between drugs and nucleotides.
de Wet H. and Proks P., (2015), Biochem Soc Trans, 43
Molecular action of sulphonylureas on KATP channels: a real partnership between drugs and nucleotides.
de Wet H. and Proks P., (2015), Biochem Soc Trans, 43, 901 - 907
Sulfonylureas suppress the stimulatory action of Mg-nucleotides on Kir6.2/SUR1 but not Kir6.2/SUR2A KATP channels: a mechanistic study.
Proks P. et al, (2014), J Gen Physiol, 144, 469 - 486
Molecular mechanism of sulphonylurea block of K(ATP) channels carrying mutations that impair ATP inhibition and cause neonatal diabetes.
Proks P. et al, (2013), Diabetes, 62, 3909 - 3919