Do people with diabetes who need to talk want to talk?

Aim. To examine whether the people with diabetes who ask for psychological support are those who are experiencing clinically significant levels of psychological distress.
Method. In total 300 people with diabetes were asked to complete psychometrically validated questionnaires that assessed subjective need and objective psychological distress.
Results. High levels of psychological distress were reported: 25% of the sample reported depressive symptomatology, 41% reported clinically significant levels if anxiety and 51% reported a degree of binge eating behaviour. Participants also indicated a desire to talk to diabetes professionals about various problem areas in diabetes. Chi-square analysis demonstrated that those reporting psychological distress, especially depression, were most likely to indicate a desire to talk to somebody about living with diabetes.
Conclusions. Those who want to talk are those who need to talk. Future service development issues should acknowledge the needs and expressed wishes of service users.

Providing psychological services for people with diabetes

Previous research and service development guidelines have highlighted the importance of psychological issues in diabetes care, and both people with diabetes and diabetes professionals recognise the need for specialist psychological input. This article outlines the development of a service delivery model for psychological services in diabetes care, based on a patient needs assessment and the advice of diabetes professionals. This involved an assessment of the psychological needs of people with diabetes within an urban Health Trust in Northern Ireland, and the collation of the views of local diabetes professionals. Questionnaires to assess for depression, anxiety, binge eating behaviour and diabetes-specific worries were completed by 300 people with diabetes. The participants were accessed through both primary and secondary care diabetes teams. As expected, a high level of psychological distress relative to population norms was illustrated by the patient needs assessment. Particularly high levels of binge eating behaviour were reported, and levels of distress were higher for community-managed patients than for hospital-managed patients. The diabetes professionals unanimously agreed that there is a need for specialist psychological input and contributed to the service delivery model which is outlined in this article.

A novel, long-acting agonist of glucose-dependent insulinotropic polypeptide suitable for once-daily administration in type 2 diabetes

Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone with a potentially therapeutic role in type 2 diabetes. Rapid degradation by dipeptidylpeptidase IV has prompted the development of enzyme-resistant N-terminally modified analogs, but renal clearance still limits in vivo bioactivity. In this study, we report long-term antidiabetic effects of a novel, N-terminally protected, fatty acid-derivatized analog of GIP, N-AcGIP(LysPAL(37)), in obese diabetic (ob/ob) mice. Once-daily injections of N-AcGIP(LysPAL(37)) over a 14-day period significantly decreased plasma glucose, glycated hemoglobin, and improved glucose tolerance compared with ob/ob mice treated with saline or native GIP. Plasma insulin and pancreatic insulin content were significantly increased by N-AcGIP(LysPAL(37)). This was accompanied by a significant enhancement in the insulin response to glucose together with a notable improvement of insulin sensitivity. No evidence was found for GIP receptor desensitization and the metabolic effects of NAcGIP(LysPAL(37)) were independent of any change in feeding or body weight. Similar daily injections of native GIP did not affect any of the parameters measured. These data demonstrate the ability of once-daily injections of N-terminally modified, fatty acid-derivatized analogs of GIP, such as N-AcGIP(LysPAL(37)), to improve diabetes control and to offer a new class of agents for the treatment of type 2 diabetes.

Diabetes-induced activation of protein kinase C inhibits store-operated Ca2+ uptake in rat retinal microvascular smooth muscle.

AIMS/HYPOTHESIS: To assess the effects of diabetes-induced activation of protein kinase C (PKC) on voltage-dependent and voltage-independent Ca2+ influx pathways in retinal microvascular smooth muscle cells. METHODS: Cytosolic Ca2+ was estimated in freshly isolated rat retinal arterioles from streptozotocin-induced diabetic and non-diabetic rats using fura-2 microfluorimetry. Voltage-dependent Ca2+ influx was tested by measuring rises in [Ca2+]i with KCl (100 mmol/l) and store-operated Ca2+ influx was assessed by depleting [Ca2+]i stores with Ca2+ free medium containing 5 micromol/l cyclopiazonic acid over 10 min and subsequently measuring the rate of rise in Ca2+ on adding 2 mmol/l or 10 mmol/l Ca2+ solution. RESULTS: Ca2+ entry through voltage-dependent L-type Ca2+ channels was unaffected by diabetes. In contrast, store-operated Ca2+ influx was attenuated. In microvessels from non-diabetic rats 20 mmol/l D-mannitol had no effect on store-operated Ca2+ influx. Diabetic rats injected daily with insulin had store-operated Ca2+ influx rates similar to non-diabetic control rats. The reduced Ca2+ entry in diabetic microvessels was reversed by 2-h exposure to 100 nmol/l staurosporine, a non-specific PKC antagonist and was mimicked in microvessels from non-diabetic rats by 10-min exposure to the PKC activator phorbol myristate acetate (100 nmol/l). The specific PKCbeta antagonist LY379196 (100 nmol/l) also reversed the poor Ca2+ influx although its action was less efficacious than staurosporine. CONCLUSION/INTERPRETATION: These results show that store-operated Ca2+ influx is inhibited in retinal arterioles from rats having sustained increased blood glucose and that PKCbeta seems to play a role in mediating this effect.