Impaired beta cell glucose sensitivity and whole-body insulin sensitivity as predictors of hyperglycaemia in non-diabetic subjects

Aims/hypothesis: The aim of this prospective study was to investigate predictors of deteriorating glucose tolerance in subjects of British extraction. Methods: A total of 156 non-diabetic subjects (86 with a family history of type 2 diabetes) underwent a 75-g OGTT and anthropometric assessment at baseline and 5 years later. Pancreatic beta cell function and whole-body insulin sensitivity were studied by model assessment. Subjects were classified as progressors if glucose tolerance moved one or more steps from normal, impaired fasting glucose, impaired glucose tolerance and diabetes over the follow-up period. Results: At baseline, the progressors (n=22) had increased adiposity and a higher proportion of familial diabetes and abnormal glucose tolerance than non-progressors. Baseline pancreatic beta cell sensitivity to changes in glucose (p < 0.02) and whole-body insulin sensitivity (p < 0.0001) were decreased in the progressors. Logistic regression revealed that baseline and follow-up changes in beta cell glucose sensitivity and insulin sensitivity, rather than the classical clinical predictors (adiposity, familial diabetes and glucose levels), were the key independent predictors of progression (explaining over 50% of the progression). Conclusions/interpretation: Impaired pancreatic beta cell glucose sensing and whole-body insulin sensitivity predict progression to hyperglycaemia. Strikingly, these pathophysiological changes override the importance of the clinical risk factors and highlight potential metabolic targets for prevention strategies

Primary and tertiary health professionals' views on the health-care of patients with co-morbid diabetes and chronic kidney disease - A qualitative study

Background: Health-care for co-morbid diabetes and chronic kidney disease (CKD) is often sub-optimal. To improve health-care, we explored the perspectives of general practitioners (GPS) and tertiary health-care professionals concerning key factors influencing health-care of diabetes and CKD. Methods: A total of 65 health professionals were purposively sampled from Australia's 2 largest cities to participate in focus groups and semi-structured interviews. Four focus groups were conducted with GPS who referred to 4 tertiary health services in Australia's 2 largest cities, with 6 focus groups conducted with tertiary health-care professionals from the 4 tertiary health services. An additional 8 semi-structured interviews were performed with specialist physicians who were heads of diabetes and renal units. All discussions were facilitated by the same researcher, with discussions digitally recorded and transcribed verbatim. All qualitative data was thematically analysed independently by 2 researchers. Results: Both GPS and tertiary health-care professionals emphasised the importance of primary care and that optimal health-care was an inter-play between patient self-management and primary health-care, with specialist tertiary health-care support. Patient self-management, access to specialty care, coordination of care and a preventive approach were identified as key factors that influence healthcare and require improvement. Both groups suggested that an integrated specialist diabetes-kidney service could improve care. Unit heads emphasised the importance of quality improvement activities. Conclusions: GPS and tertiary health-care professionals emphasised the importance of patient self-management and primary care involvement in the health-care of diabetes and CKD. Supporting GPS with an accessible, multidisciplinary diabetes-renal health service underpinned by strong communication pathways, a preventive approach and quality improvement activities, may improve health-care and patient outcomes in co-morbid diabetes and CKD