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Background and Aim: In today’s digital world, people with type 1 and 2 diabetes turn to peers on social media to exchange information and support. However, little is known about what the online sharing of diabetes-related information implies for the clinical encounter. This study examines how information that stems from social media is discussed in clinical encounters between healthcare professionals (HCPs) and people with diabetes (PWD) . Methods: We conducted semi-structured interviews with 25 PWD aged 22-76 (type 1: n= 17, type 2: n=8) and HCPs (nurses n=9, medical doctors n=7, dieticians n=3) . The participants were recruited from the diabetes outpatient care setting in Denmark. Two researchers independently developed a thematic coding framework that was compared, revised, and then applied to analyze each interview. Subsequently, overarching themes were identified across the whole data set. Results: The first theme suggests that HCPs tend to have a ‘blind spot’ towards information that stems from social media: Most HCPs have not asked whether PWD retrieve information from social media and most PWD present information that is accessed on social media without naming their source. The second theme reflects that clinical dialogues about online information rest upon trustful relationships: PWD find online peer exchanges valuable and request for HCPs to acknowledge this. Still, PWD navigate large amounts of information and treatment advice online, and while PWD may seek to discuss their information in clinical encounters, initiating these dialogues is sensitive to the reactions of HCPs. Discussion: The results suggest that HCPs should encourage curious dialogues about how PWD retrieve diabetes-related information. This serves for HCPs to learn what PWD gain from peers online and for HCPs to be able to offer their expertise to support PWD who are navigating large flows of information and advice online. Disclosure E.M.Kjærulff: None. M.A.Nexo: None. U.Bjerre-christensen: None. H.Langstrup: None. Funding Innovation Fund Denmark (Ref.no. 9163-00016B)

The Practical Diabetology (PD) course for multidisciplinary health care professionals (HCPs) is directed at building a team-based approach to diabetes care delivery. Participants were asked to apply course learning to identify deficiencies in care delivery in their own settings and develop action plans to improve care and continuing self-development. The objective of the study was to evaluate the short- and mid-term impact of seven PD courses held between March 2011 and March 2012. Three methods of assessment were carried out: an end of course evaluation; pre- and post-tests to assess gain in knowledge and change in attitudes; and self-assessment of action plan implementation at six months to determine level of behaviour change. In total, 327 multidisciplinary HCPs participated in the seven PD courses. End of course evaluation indicated that the PD course was valued by course participants in terms of relevance of the topics and learning experience. A significant gain in knowledge and positive changes in attitudes were seen immediately post course in both groups. Of the 160 action plans prepared by participating teams (consisting of at least two members each – one medical and one non-medical HCP), 68 (42.5%) were implemented. At six months, continued positive change was demonstrated through self-assessment of action plan implementation. PD courses were appreciated by the participants; significant gain in knowledge and positive change in selected attitudes were seen in the short term. Implementation of action plans helped enhance participants’ competency for teamwork, problem solving and self-development skills. Copyright © 2015 John Wiley & Sons.

Type 1 diabetes (T1D) is characterized by selective autoimmune destruction of the insulin producing beta-cells in the islets of Langerhans. When the beta-cells are destroyed exogenous administration of insulin is necessary for maintenance of glucose homeostasis. Allogeneic islet transplantation has been used as a means to circumvent the need for insulin administration and has in some cases been able to restore endogenous insulin production for years. However, long life immunosuppression is needed to prevent the graft from being rejected and destroyed. Changes in protein expression pattern during spontaneous diabetes development in the diabetes prone BioBreeding rat (BB-DP) have previously been described. In the present study, we have investigated if any of the changes seen in the protein expression pattern during spontaneous diabetes development are also present during allograft rejection of BB-DP rat islets. Two hundred neonatal islets were syngeneically transplanted under the kidney capsule of 30 day old BB-DP rats and removed prior to and at onset of diabetes. Allogeneically transplanted islets from BB-DP rats were removed before onset of allograft rejection and at maximal islet graft inflammation (rejection). The protein expression profiles of the transplants were visualised by two-dimensional gel (2-DG) electrophoresis, analysed and compared. In total, 2590 protein spots were visualised and of these 310 changed expression (p < 0.01) in syngeneic islet transplants in the BB-DP rats from 7 days after transplantation until onset of diabetes. In BB-DP islets transplanted to WK rats 53 protein spots (p < 0.01) showed changes in expression when comparing islet grafts removed 7 days after transplantation with islet grafts removed 12 days after transplantation where mononuclear cell infiltration is at its maximum. Only four protein spots (1%) were significantly changed in both syngeneic (autoimmune) and allogeneic islet destruction. When comparing protein expression changes in syngeneic BB-DP islet transplants from 37 days after transplantation to onset of diabetes with protein expression changes in allografts from day 7 to 12 after transplantation only three spot were found to commonly change expression in both situations. In conclusion, a large number of protein expression changes were detected in both autoimmune islet destruction and allogeneic islet rejection, only two overlaps were detected, suggesting that autoimmune islet destruction and allogeneic islet rejection may result from different target cell responses to signals induced by the cellular infiltrate. Whether this reflects activation of distinct signalling pathways in islet cells is currently unknown and need to be further investigated.

To evaluate if improvements in the quality of diabetes care in Indian clinics can be obtained by simple self-surveillance PC-based software. Method Nineteen Indian diabetes clinics were introduced to the principles of quality assurance (QA), and to a software program, the Steno Quality Assurance Tool (SQAT). Data was entered for an initial 3 months period. Subsequently data were analyzed by the users, who designed plans to improve indicator status and set goals for the upcoming period. A second data entry period followed after 7–9 months. Results QA data was analyzed from 4487 T2DM patients (baseline) and 4440 (follow-up). The average examination frequency per clinic of the following indicators increased significantly: lipid examination (72–87%) ( p =0.007), foot examination (80–94%) ( p =0.02), HbA1c investigation (59–77%) ( p =0.006), and urine albumin excretion investigation (72–87%) ( p =0.006). Outcome parameters also improved significantly: mean (SD) fasting and post prandial BG reduced from 144(16) to 132(16)mg/dl ( p =0.02) and 212(24)–195(29)mg/dl ( p =0.03), respectively. Systolic BP reduced from 139(6) to 133(4) ( p =0.0008)mmHg and diastolic BP from 83(3) to 81(3)mmHg ( p =0.002). Conclusion Quality of diabetes care can be improved by applying SQAT, a QA self-surveillance software that enables documentation of changes in process and outcome indicators.

Recently, the synthetic immunomodulator Linomide (quinoline-3-carboxamide, LS 2616) was reported to prevent IDDM and insulitis in NOD mice. The mechanism for this protective effect is not known. The cytokine interleukin 1 (IL-1) may be a pathogenetic factor in the initial destruction of the beta-cells leading to IDDM. This study was undertaken to investigate the influence of Linomide on IL-1beta induced diabetogenic and hormonal changes in the rat in vivo, and on IL-1beta mediated synthesis of NO and inhibition of insulin secretion in isolated islets of Langerhans ex vivo. Normal male Wistar Kyoto rats received 4.0 microg/kg of recombinant human IL-1beta (rhIL-1beta) i.p. daily for 5 days with or without Linomide (8-9 mg/kg/day) in the drinking water. Litters of neonatal Wistar rats were pretreated for 3 days with injections of 10 mg/kg of Linomide i.p., and pancreatic islets of Langerhans were isolated for ex vivo studies. Linomide alone caused significant hypercorticosteronemia, hypoglucagonemia, lymphopenia and neutrophilia. Linomide had no effect on IL-1beta induced hyperglycemia, hyperglucagonemia, lymphopenia, neutrocytosis, or hypercorticosteronemia on day three and hypocorticosteronemia on day five. Further, Linomide did not prevent rhIL-1beta mediated reduction in insulin secretion or increase in NO synthesis ex vivo. In conclusion, Linomide does not seem to exert its protective effect on IDDM development via inhibition of interleukin 1 action on islet insulin release or NO production, but the increase in plasma corticosterone may contribute to the understanding of the immunomodulatory effects of Linomide.

Type 1 Diabetes Mellitus is characterized by selective destruction of the pancreatic beta-cells in the islets of Langerhans and insulitis. Subcutaneous insulin injections given to diabetes prone BioBreeding (BB-DP) rats reduce diabetes incidence. The underlying mechanism(s) are not known in detail. Previously, we showed that transplantation of 200 syngeneic neonatal islets under the kidney capsule is useful for studying molecular events during diabetes development in BB-DP rats. In the present study we tested if prophylactic insulin treatment of syngeneically transplanted BB-DP rats would protect both islets in situ and transplanted islets from destruction.BB-DP rats received transplants of 200 syngeneic neonatal islets under the kidney capsule at 30 days of age. They were given a subcutaneous insulin or placebo implant and were compared to control rats. Blood glucose was measured three times weekly. In total, 193 rats were transplanted and rats were sacrificed 7, 23, 50, 90 days post-transplantation or at onset of diabetes. Pancreatic and transplant sections were stained for insulin and mononuclear cell infiltration and insulitis was graded.Eight (19%) rats developed diabetes in the insulin-treated group and 19 (63%) and 19 (65%) rats in the control and placebo, respectively (p = 0.0002 and p = 0.0001). Onset of diabetes in the insulin treated group was delayed compared to control and placebo, (102, 77 and 81 days of age, respectively (p = 0.0001 and p = 0.0001)). Insulin treatment diminished mononuclear cell infiltration in the islets at day 50 after transplantation compared to placebo. Infiltration pattern in islets in situ correlates with infiltration in transplants (r is 0.9076 and p0.001).These results suggest that insulin-treatment of syngeneically transplanted BB-DP rats considerably decreases the incidence of diabetes and that this model is well suited for studying molecular changes in the islet transplants.

Interleukin 1beta (IL-1) is cytotoxic to rat pancreatic beta-cells in vitro, and increased expression of IL-1 mRNA is found in the islets of Langerhans during development of diabetes in BB/Wor/Mol-BB2 (BB-DP) rats and NOD mice. It has been proposed that IL-1 induces a race between protective and deleterious proteins in the beta-cells during development of diabetes, and that heat shock proteins 70 and 90, and manganese superoxide dismutase, all inducible by IL-1 are potentially protective proteins. We have established a database of approximately 2000 neonatal rat-islet proteins by two-dimensional gel (2-D gel) electrophoresis of [35S]-methionine labelled neonatal Wistar Furth rat islets. In these IL-1 was shown to up- or down-regulate the islet-expression level of 99, and to induce de novo synthesis of 6 proteins. The identity of most of the IL-1 induced proteins is unknown and under study. In this study we wished to investigate if changes in protein expression induced in vitro by IL-1 stimulation of islets are also seen in vivo during spontaneous development of diabetes in BB-DP rats, and during islet allograft rejection. Two-hundred neonatal BB-DP rat islets were grafted under the kidney capsule of either 30-day-old BB-DP rats killed at onset of diabetes or of 30-day-old Wistar Kyoto (WK) rats, killed 12 days after grafting. Proteins in excised islet-grafts and in vitro IL-1 exposed isolated neonatal BB-DP rat islets were labelled with [35S]-methionine, and processed for 2-D gel electrophoresis. Fluorographs of the gels were analysed by computer. A total of 1815 proteins were found in 3 of 3 12.5% polyacrylamide gels. Interleukin-1 was found to change expression level of 82 of these proteins (22 up- and 60 down-regulated) in neonatal BB-DP rat islets in vitro. Of these 82 proteins 33 (4 up- and 29 down-regulated) also changed level of expression during disease occurrence in syngeneic islet grafts from diabetic BB-DP rats, and 29 (4 up- and 25 down-regulated) during rejection of BB-DP islets grafted to WK rats. Changes in the expression level of 14 (3 up- and 11 down-regulated) of the 82 proteins altered by IL-1 in vitro were only found in syngeneic islet grafts in diabetic BB-DP rats, and changes in the expression level of 8 (2 up- and 6 down-regulated) of these 82 proteins expression were only found in BB-DP islet allografts in WK recipients. Identification of these proteins may be important in understanding the mechanisms of islet destruction during development of insulin-dependent diabetes mellitus and during islet allograft rejection.

During development of IDDM mononuclear cell infiltration is seen in the islets of Langerhans in both man and rodent models. This process is not synchronized in time and space. To create a synchronized model for investigation of the cellular and molecular events during IDDM development, we isolated and transplanted 200 neonatal BB-DP rat islets under the kidney capsule of 30 day old BB-DP rats. Islet transplantations were also carried out from Wistar Furth (WF) to WF rats, from WF to Wistar Kyoto (WK) rats and from WK to BB-DP rats to compare disease occurrence in an islet syngraft with changes in islet syngrafts or allografts in non-diabetes prone recipients and with changes in islet allografts in diabetes prone recipients, respectively. Pancreata and grafts were harvested at pre-scheduled time points before onset of diabetes and at onset of diabetes, and stained for insulin, MHC class I, MHC class II, alphabeta-TCR, CD4, CD8 or ED1. Diabetes incidence in the syngrafted BB-DP rats was 75% at 78 +/- 5 days of age. The incidence and time of onset of IDDM was unaffected by islet syngrafting. Positive correlations were found between the percentage of infiltrated islets in situ and the number of infiltrating cells in the islet syngraft from the same BB-DP rats (p = 0.003-p < 0.0001, r = 0.5-0.7). The number of infiltrating cells regardless of cell type in the graft was inversely correlated to the graft insulin content (p = 0.0003-p < 0.0000, r = -0.6 to -0.8). The graft insulin content was 70% and 90% in BB-DP rats before onset of diabetes and BB-DP rats not developing diabetes respectively, and 30% in the diabetic rats (p < 0.01). Interestingly only 5% of the allografted BB-DP rats developed diabetes. No correlation was found between the number of infiltrating cells in the graft and islets in situ in the BB-DP rats not developing diabetes. Only baseline infiltration was seen in grafts from syngrafted WF rats. In allografted WF islet to WK rats graft rejection was seen 12 days after transplantation. No correlation was found between the number of infiltrating cells in the graft and islets in situ. In conclusion the cellular infiltration in syngeneic but not allogeneic islets grafted to 30 day old BB-rats mirrors that seen in islets in situ. Syngeneic islet grafting in BB-DP rats may be useful for studying the cellular and molecular events during the development of IDDM.