National Audit Data highlight persistent sub-optimum control among increasing numbers of people living with diabetes, with severe consequences for the individual and the NHS. The aim of the present review was to introduce a new cohesive, holistic model of care, tailored to individual needs to support optimum diabetes outcomes. This model of diabetes is necessary in order to understand the driving forces behind behaviour and their impact on diabetes management. Feelings (an emotional state or reaction) and beliefs (an acceptance that something is true or real) are fundamental behavioural drivers and influence diabetes self-management choices. Individually, these explain some of the complexities of behaviour and, collectively, they impact on personal motivation (rationale/desire to act) to achieve a specific outcome. Inevitably, they independently affect diabetes self-management and the environment in which individuals live. A model of care that proposes the encompassing of environment, intrinsic thought and therapy regimens to provide tailored, personalized healthcare should support enhanced diabetes self-management and outcomes from diagnosis. The Kaleidoscope model of care could be deliverable in routine care, incorporating each of the influences on diabetes self-management, and should benefit both individuals with diabetes and healthcare professionals.
The first goal of the work reported here was to prepare single-stranded DNA sequences for use in studies on the regulation of albumin gene expression. A double-stranded rat albumin cDNA clone was subcloned into the bacteriophage vector M13mp7. Single-stranded recombinant clones were screened for albumin sequences containing either the mRNA strand or the complementary strand. Two clones were selected that contained the 1,200 nucleotide long 3' end of the albumin sequence. DNA from the clone containing the mRNA strand was used as a template for DNA polymerase I to prepare a radiolabeled, single-stranded cDNA to albumin mRNA. This radiolabeled cDNA probe was used to quantitate the relative abundance of albumin mRNA in samples of total cellular RNA. DNA from the clone containing the complementary strand was used to measure relative rates of albumin gene transcription in isolated nuclei. The second goal was to use the single-stranded DNA probes to investigate the mechanism of the insulin-mediated stimulation of albumin synthesis in primary cultures of rat hepatocytes. Addition of insulin to hepatocytes maintained in hepatocytes. Addition of insulin to hepatocytes maintained in a chemically defined, serum-free medium for 40 h in the absence of any hormones resulted in a specific 1.5- to 2.5-fold stimulation of albumin gene transcription that was maximal at 3 h and was maintained above control values for at least 24 h. The relative abundance of albumin mRNA and albumin secretion increased correspondingly within 24 to 30 h. These parameters remained above control levels for at least 60 h after addition of insulin. Maximal responses were attained at an insulin concentration of 100 nM and there was a close correspondence between albumin gene transcription and albumin secretion at each concentration tested. The rate of albumin gene transcription in nuclei isolated from livers of diabetic rats was reduced to 50% of the value recorded in control nuclei. Taken together, these findings demonstrate that insulin regulates synthesis of albumin at the level of gene transcription.
Insulin-dependent diabetes mellitus (IDDM) increases the risk of developing coronary artery disease (CAD) compared with that seen in the general population, while the sex differential in rates of CAD is considerably reduced in IDDM populations. To further our understanding of these observations, the effects of gender on baseline risk factors for CAD incidence were examined. Participants in the Pittsburgh Epidemiology of Diabetes Complications (EDC) Study were recruited from the Children's Hospital of Pittsburgh IDDM registry and had been diagnosed between 1950 and 1980. Subjects completed a series of questionnaires and were given a full clinical examination at baseline (1986 through 1988) and every subsequent 2 years. This report is based on the first 4 years of follow-up. Similar incidence rates of new CAD events were observed in men and women. In neither sex was glycemic control a predictor of later CAD. Sex-specific Cox proportional hazards models showed that for men, duration of IDDM, HDL cholesterol, fibrinogen, hypertension, and smoking were all significantly associated with the onset of CAD. Hypertension, fibrinogen, and smoking were all replaced by nephropathy when this latter variable was added to the model. For women, duration, hypertension, waist-hip ratio, physical activity, and depressive symptomatology were all significant independent predictors of CAD. Nephropathy status did not enter the model for women. While 4-year incidence of CAD in IDDM varies little by sex in this population, the predictive risk factors vary considerably. In particular, the effect of renal disease was stronger in men, while the cluster of physical activity, waist-to-hip ratio, and depressive symptomatology were more important in women. These results may help explain the relatively greater impact IDDM has on CAD risk for women and suggest new potential preventive approaches.
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Stress has been proposed as a possible precipitating factor for the development of Type 1 diabetes in genetically susceptible individuals. A validated in-depth psychometric instrument (The Life Events and Difficulties Schedule) was used to investigate the role of psychosocial factors in the onset of Type 1 diabetes in islet cell antibody (ICA)-positive family members. Families with ICA-positive members had higher scores for subject focused severe life events in the 5-year period prior to the diagnosis of diabetes in a second family member compared with matched control families (1.50 +/- 0.68 (+/- SD) vs 0.32 +/- 0.37; p less than 0.03). In the same time period, these families also experienced a higher mean number of severe long-term difficulties compared with control families (1.34 +/- 0.52 vs 0.14 +/- 0.17; p less than 0.01). Scores for current total visual social contacts were greater for control families compared with case family members (12.10 +/- 1.90 vs 9.64 +/- 2.70; p less than 0.05). These results suggest that global family stress possibly in conjunction with a reduced number of social contacts may act as a trigger for the development of diabetes in a second family member and that social support may act as a buffer to stress and disease onset.
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