Julia Buckingham Award 2026 winner announced!
The British Society for Neuroendocrinology (BSN) is delighted to announce Paula-Peace James-Okoro as the 2026 winner of the Julia Buckingham Award. The Award, in honour of Professor Dame Julia Buckingham, recognises the achievement and potential of an up-and-coming scientist within the BSN.
Paula-Peace James-Okoro is currently resesarching body weight and blood glucose levels at the Institute of Metabolic Science-Metabolic Research Laboratories & MRC-Metabolic Diseases Unit, University of Cambridge, Cambridge, UK.
Upon receiving the award, Paula-Peace said:
“Receiving the 2026 BSN Julia Buckingham Award is a significant milestone in my research career, and I am incredibly honoured to be recognised for my contributions to neuroendocrinology. This award is a great encouragement to keep pushing the boundaries of my research and contributing to the field at the highest level. I am deeply grateful to the BSN for its continued commitment to supporting and recognising early-career researchers.”
As part of the award prize, Paula-Peace will be giving a 15 minute lecture on "Endogenous GIP Attenuates Nausea-Related Avoidance Behaviours in Mice" at the Early Career Meeting, Neuroendo Celebrate 2026, in September 2026.
The BSN congratulates Paula-Peace James-Okoro for her excellent contribution to the field so far and we look forward to following her career in the future.
Abstract: Endogenous GIP Attenuates Nausea-Related Avoidance Behaviours in Mice
Paula-Peace James-Okoro1, Jo Edward Lewis1, Mireia Montaner1, Fiona Mary Gribble1, Frank Reimann1
1Institute of Metabolic Science-Metabolic Research Laboratories & MRC-Metabolic Diseases Unit, University of Cambridge, Cambridge, UK.
Background: Glucagon-like peptide-1 receptor (GLP1R) agonists and dual GLP1R/glucose-dependent insulinotropic polypeptide receptor (GIPR) agonists are effective treatments for type 2 diabetes and obesity, improving glycaemic control and reducing body weight. Beyond enhancing weight loss, GIPR agonism reduces nausea and aversion associated with GLP1R agonists, likely via activation of GABAergic neurons in the area postrema (AP). However, whether endogenous GIP physiologically suppresses nausea remains unclear. We investigated whether intestinal GIP reduces avoidance behaviour in response to aversive stimuli and whether AP GIPR signalling mediates this effect.
Methods: An intersectional transgenic mouse model (Gip-Cre Å~ Vil1-p2a-FlpO-F/L-Dq) expressing hM3Dq DREADDs in intestinal K cells was used to selectively stimulate GIP release with clozapine N-oxide. In parallel, wild-type mice consumed 15%-flavoured-sucrose following water deprivation to induce endogenous GIP secretion. Flavour avoidance assays were conducted in these two models by pairing a novel flavour with aversive agents (PYY or liraglutide) in the presence or absence of GIP release. AP-specific GIPR knockdown was generated via stereotactic rAAV-Cre delivery in Giprflx/flx mice.
Results: Chemogenetic activation and sucrose ingestion elevated plasma GIP to postprandial levels. K-cell activation abolished PYY-induced flavour avoidance without affecting anorectic responses. Sucrose intake similarly reduced liraglutide-induced avoidance, an effect blocked by GIPR antagonism. Pharmacological GIPR activation suppressed avoidance in control mice but not in AP-specific GIPR knockdown mice.
Conclusion: These findings demonstrate that endogenous gut-derived GIP suppresses avoidance behaviour induced by nausea-associated stimuli, supporting a physiological anti-aversive role for GIP beyond pharmacological GIPR agonism. Furthermore, GIPR-expressing neurons in the AP mediate this anti-avoidance effect.
