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Aims/Introduction The purpose of the present study was to examine glycemic control in suboptimally controlled type 2 diabetes provided by a structured education group using the Diabetes Conversation Map™ ( CM™) vs usual care in a university-based hospital primary care clinic. Materials and Methods This was a randomized, pragmatic clinical trial. Patients with type 2 diabetes were randomly assigned to structured education or usual care groups. The primary outcome was the difference in the mean change of glycated hemoglobin (HbA1c) from baseline to 12 months. Secondary outcomes included the percentage achieving therapeutic HbA1c goal and self-behavioral changes. Results A total of 245 patients were randomly assigned to two groups ( CM™ group n = 121; usual care group, n = 116). The absolute reduction of HbA1c was significantly greater in the CM™ group at 3 and 6 months (Δ = −0.59% and Δ = −1.13%, P < 0.01), but the difference was no longer statistically significant at 9 and 12 months (Δ = −0.43% and Δ = −0.49%), based on an intention-to-treat analysis. A per-protocol analysis showed the significant change was maintained at 12 months (Δ = −0.67%). In the intervention group, greater percentages of patients achieved their American Association of Diabetes Educators Self-Care Behaviours™ framework ( AADE7) behavioral goals at 3 months, in particular being active, problem-solving, reducing risk and health coping. Conclusions In type 2 diabetic patients with suboptimally controlled glucose, there were greater improvements in glucose control and self-care behavioral goals in those who underwent the CM™ education program compared with outcomes achieved in patients receiving usual care. [ABSTRACT FROM AUTHOR]

Aims Diabetes mellitus increases the risk of stroke, but the mechanisms are unclear. The present study tested the hypothesis that diabetes mellitus disturbs the brain microcirculation and increases the susceptibility to cerebral damage in a middle cerebral artery occlusion ( MCAO) model of ischemia. Methods Diabetes was induced by streptozocin in mice expressing green fluorescent protein in endothelial cells (Tie2- GFP mice). Four weeks later, they were subjected to transient (20 min) MCAO. In vivo blood flow was measured by two-photon laser-scanning microscopy ( TPLSM) in cerebral arteries, veins, and capillaries. Results There was a significant decrease in red blood cell ( RBC) velocity in capillaries in diabetic mice as assessed by TPLSM, yet the regional cerebral blood flow, as assessed by laser Doppler flowmetry, was maintained. Brain capillary flow developed turbulence after MCAO only in diabetic mice. These mice sustained increased neurological deficits after MCAO which were accompanied by an exaggerated degradation of tight junction proteins and blunted Ca MKII phosphorylation in cerebral tissues indicating disruption of the blood-brain barrier and disturbed cognitive potential. Conclusion Diabetic mice are more susceptible to disturbances of cerebral capillary blood flow which may predispose them to neurovascular defects following ischemia. [ABSTRACT FROM AUTHOR]

Background Defining the impact of diabetes and related risk factors on brain cognitive function is critically important for patients with diabetes. Aims To investigate the alterations in hippocampal serine/threonine kinases signaling in the early phase of type 1 and type 2 diabetic rats. Methods Early experimental diabetes mellitus was induced in rats with streptozotocin or streptozotocin/high fat. Changes in the phosphorylation of proteins were determined by immunoblotting and immunohistochemistry. Results Our data showed a pronounced decrease in the phosphorylation of Ca2+/calmodulin-dependent protein kinase II (Ca MKII) in the hippocampi of both type 1 and type 2 diabetic rats compared with age-matched control rats. Unexpectedly, we found a significant increase in the phosphorylation of synapsin I ( Ser 603) and Glu R1 ( Ser 831) in the same experiment. In addition, aberrant changes in hippocampal protein kinase C ( PKC) and protein kinase A ( PKA) signaling in type 1 and type 2 diabetic rats were also found. Moreover, PP1α and PP2 A protein levels were decreased in the hippocampus of type 1 diabetic rats, but significantly up-regulated in type 2 diabetic rats. Conclusions The disturbance of Ca MKII/ PKA/ PKC phosphorylation in the hippocampus is an early change that may be associated with the development and progression of diabetes-related cognitive dysfunction. [ABSTRACT FROM AUTHOR]