Diabetes is characterized by hyperglycaemia due to impaired insulin secretion and aberrant glucagon secretion resulting from changes in pancreatic islet cell function and/or mass. The extent to which hyperglycaemia per se underlies these alterations remains poorly understood. Here we show that β-cell-specific expression of a human activating KATP channel mutation in adult mice leads to rapid diabetes and marked alterations in islet morphology, ultrastructure and gene expression. Chronic hyperglycaemia is associated with a dramatic reduction in insulin-positive cells and an increase in glucagon-positive cells in islets, without alterations in cell turnover. Furthermore, some β-cells begin expressing glucagon, whilst retaining many β-cell characteristics. Hyperglycaemia, rather than KATP channel activation, underlies these changes, as they are prevented by insulin therapy and fully reversed by sulphonylureas. Our data suggest that many changes in islet structure and function associated with diabetes are attributable to hyperglycaemia alone and are reversed when blood glucose is normalized.

Many clinicians working in healthcare simulation struggle with competing dual identities of clinician and educator, whilst those who harmonise these identities are observed to be highly effective teachers and clinicians. Professional identity formation (PIF) theories offer a conceptual framework for considering this dilemma. However, many clinician simulation educators lack practical guidance for translating these theories and are unable to develop or align their dual identities.An unusual experience involving the first author’s suspension of disbelief as a simulation facilitator sparked a novel reflection on his dual identity as a clinician and as a simulation educator. He re-framed his clinician and simulation ‘hats’ as cooperative and fluid rather than competing and compartmentalised. He recognised that these dual identities could flow between clinical and simulation environments through leaky ‘blended boundaries’ rather than being restricted by environmental demarcations.This personal story is shared and reflected upon to offer a practical ‘hats and boundaries’ model. Experimenting with the model in both clinical and simulation workplaces presents opportunities for PIF and alignment of dual identities. The model may help other clinician simulation educators navigate the complexities of merging their dual identities.

Gastric-bypass associated hyperammonaemia (GaBHA) is an under-recognised cause of non-hepatic encephalopathy that is associated with significant mortality and has limited reporting in published literature. GaBHA has been reported predominately in middle-aged females with a past surgical history of Roux-En-Y surgical procedure. Individuals may present at any stage post-surgery and an important minority may have an undiagnosed inherited metabolic disorder. We report a case of a 49 year old woman who presented acutely with encephalopathy, a significantly elevated plasma ammonia level, and substantial multifactorial nutritional deficiency which required correction with intensive enteral and parenteral nutritional support. This case represented a diagnostic and management challenge for acute medical physicians and the multidisciplinary team involved.