Patients' education, and its impact on care outcomes, resource consumption and working conditions: data from the International Diabetes Management Practices Study (IDMPS).

AIM: To evaluate the impact of diabetes education provided to patients with type 2 diabetes mellitus (T2DM) in non-controlled studies ("real-world conditions") on quality of care, resource consumption and conditions of employment. METHODS: This cross-sectional study and longitudinal follow-up describe the data (demographic and socioeconomic profiles, clinical characteristics, treatment of hyperglycaemia and associated cardiovascular risk factors, resource consumption) collected during the second phase (2006) of the International Diabetes Management Practices Study (IDMPS). Patients received diabetes education directly from the practice nurse, dietitian or educator, or were referred to ad hoc group-education programmes; all programmes emphasized healthy lifestyle changes, self-care and active participation in disease control and treatment. Educated vs non-educated T2DM patients (n=5692 in each group), paired by age, gender and diabetes duration, were randomly recruited for the IDMPS by participating primary-care physicians from 27 countries in Eastern Europe, Asia, Latin America and Africa. Outcome measures included clinical (body weight, height, waist circumference, blood pressure, foot evaluation), metabolic (HbA(1c) levels, blood lipid profile) and biochemical control measures. Treatment goals were defined according to American Diabetes Association guidelines. RESULTS: T2DM patients' education significantly improved the percentage of patients achieving target values set by international guidelines. Educated patients increased their insulin use and self-care performance, had a lower rate of chronic complications and a modest increase in cost of care, and probably higher salaries and slightly better productivity. CONCLUSION: Diabetes education is an efficient tool for improving care outcomes without having a major impact on healthcare costs.

Symptoms of depression and diabetes-specific emotional distress are associated with a negative appraisal of insulin therapy in insulin-naïve patients with Type 2 diabetes mellitus. A study from the European Depression in Diabetes [EDID] Research Consortium.

AIMS: A meta-analysis concluded that depression is associated with poor glycaemic control in Type 2 diabetes (DM2). In DM2 patients with deteriorating glycaemic control, the initiation of insulin therapy is often postponed. The aim of the present study was to determine whether symptoms of depression and diabetes-specific emotional distress are associated with a more negative appraisal of insulin therapy. METHODS: We collected cross-sectional data in two outpatient university clinics in Istanbul, Turkey. The study sample consisted of 154 insulin-naïve patients with DM2. A self-report questionnaire was used to obtain demographic and clinical data. Main instruments were the Centre for Epidemiologic Studies Depression Scale, (CES-D), the Problem Areas In Diabetes scale (PAID) and the Insulin Treatment Appraisal Scale (ITAS). RESULTS: Analysis of variance revealed that patients with a higher depression score rated insulin therapy significantly more negative then patients with lower depression scores. Moreover, 47% of patients with a high depression score had a negative appraisal of insulin therapy on 7 or more of the 20 ITAS-items, compared to 25 to 29% of those with low-moderate depression scores. Multiple regression analyses showed that a negative appraisal of insulin therapy was significantly associated with higher depression and diabetes-distress scores and low education, but not with sex, age or duration of diabetes. CONCLUSIONS: Our results suggest that in insulin-naïve Type 2 diabetes patients, higher levels of depression and diabetes-distress tend to be associated with more negative beliefs about insulin. Whether these negative attitudes translate into postponing initiation of insulin therapy needs to be tested in longitudinal research.

Increased intestinal permeability as a cause of fluctuating postprandial blood glucose levels in Type 1 diabetic patients.

BACKGROUND: In diabetic patients, postprandial glucose levels, which have a major impact on metabolic control, are determined by the rate of nutrient delivery into the intestine, absorption of nutrients from the small intestine, and the metabolism of the absorbed nutrients by the liver. The present study addresses whether Type 1 diabetic patients have increased intestinal permeability and intestinal permeability predicts postprandial glucose variability. MATERIAL AND METHODS: Thirty Type 1 diabetic patients together with 15 sex- and age-matched healthy controls were enrolled in the study. After an overnight fasting all patients and controls received 100 micro Ci 51Cr of EDTA as a radioactive tracer and the percentage of the isotope excreted in a 24-h urinary specimen was the permeability measure. Instant blood glucose was measured just before the test, and the patients performed and recorded self-monitoring of fasting and 2nd-hour postprandial blood glucose levels during the following week. RESULTS: We found that intestinal permeability is increased in Type 1 diabetic patients compared with age- and sex-matched healthy controls. Increased intestinal permeability is related at least in part to the instant blood glucose level and the presence of diabetic autonomic neuropathy. CONCLUSION: Increased intestinal permeability leads to higher variation in postprandial blood glucose levels, thereby worsening metabolic control.

Higher blood pressure in normoalbuminuric type 1 diabetic patients with a familial history of type 2 diabetes.

BACKGROUND: To address whether type 1 diabetic patients with type 2 diabetic first degree relatives are different from others in terms of cardiovascular risk factors, insulin resistance and daily insulin dosage. METHODS: We studied 18 type 1 diabetic patients with type 2 diabetic first degree relatives and 36 type 1 diabetic patients without such relatives. Patients with diabetic complications (including microalbuminuria) were excluded. The groups were similar in terms of baseline characteristics. We measured systolic and diastolic blood pressures, body mass index, waist circumference, total cholesterol, triglycerides, LDL, VLDL, HDL, daily insulin dosage and insulin sensitivity. Insulin sensitivity was tested using insulin tolerance test. RESULTS: Type 1 diabetic patients having first degree relatives with type 2 diabetes had significantly higher systolic and diastolic blood pressures (although within the normal range) than others (p < 0.001). They were more insulin resistant according to insulin tolerance test and were using higher daily insulin dosages. In this group, waist circumference, triglyceride and VLDL levels also tended to be higher, but differences were not significant statistically. Total cholesterol, LDL and HDL levels were similar in both groups. CONCLUSION: Family history of type 2 diabetes increases blood pressure and decreases insulin sensitivity in type 1 diabetic patients. Thus such patients should be treated more aggressively in terms of both cardiovascular risk factors and glucose control.

The role of coping with disease in adherence to treatment regimen and disease control in type 1 and insulin treated type 2 diabetes mellitus.

BACKGROUND: Coping is defined as the behavioral and cognitive efforts used in an attempt to deal with stressful events. The objective of this study was to explore the relationship between coping with diabetes and the following outcome variables in type 1 and insulin treated type 2 diabetes mellitus: glycemic control, microangiopathic complications, adherence to self monitoring of blood glucose, adherence to insulin injections, and adherence to diet. METHODS: Subjects were 196 insulin treated adult diabetes patients visiting an outpatient clinic at a government university hospital in Istanbul, Turkey. Coping with disease was measured with the Turkish version of the Diabetes Coping Measure and adherence to treatment regimen was measured with a questionnaire adapted from the subscales of the Summary of Diabetes Self-Care Activities Questionnaire. Data on patients' HbA(1c) levels and severity of microangiopathic complications were obtained from their medical records. RESULTS: Partial correlations controlling for background variables suggested that coping was a good predictor of outcome for both type 1 and insulin treated type 2 diabetes mellitus. These associations were more pronounced for type 1 patients when compared to type 2 patients. Regressing the outcome variables on the two second-order coping factors (obtained by a factor analysis) also supported the hypothesis that coping is an important construct in explaining the outcome variables. Finally, the effect of coping on HbA(1c) was only partially mediated by adherence. CONCLUSION: Coping with diabetes-related issues is an important factor in both types of diabetes, with type 1 patients showing slightly stronger associations. Therefore, training and education programs for diabetic adults might benefit from including a component that is aimed at improving coping with issues specific to diabetes.

Does instantaneous blood glucose affect vibration perception threshold measurement using biothesiometer?

Diabetic neuropathy is a common and troublesome complication of diabetes mellitus. Vibration sensation is a measure of large fiber nerve conduction, which is very commonly affected in diabetes. The present study addresses the question of whether vibration perception threshold (VPT) measurement using a biothesiometer is reproducible under different levels of blood glucose at different hours of the day. Seventy-five diabetic patients, 31 insulin-dependent diabetes mellitus and 44 non-insulin-dependent diabetes mellitus, with mean age 50.33+/-14.22 years (21-70 years) and diabetes duration of 14.3+/-10.6 years (1-60 years) were included in the study. Forty-one patients were male and 34 were female. In conclusion, VPT was found to be reproducible under different blood glucose levels at different hours of the day, which is affected only by the height of the patient.

Chronic hyperglycemia triggers loss of pancreatic beta cell differentiation in an animal model of diabetes.

Differentiated pancreatic beta cells are unique in their ability to secrete insulin in response to a rise in plasma glucose. We have proposed that the unique constellation of genes they express may be lost in diabetes due to the deleterious effect of chronic hyperglycemia. To test this hypothesis, Sprague-Dawley rats were submitted to a 85-95% pancreatectomy or sham pancreatectomy. One week later, the animals developed mild to severe chronic hyperglycemia that was stable for the next 3 weeks, without significant alteration of plasma nonesterified fatty acid levels. Expression of many genes important for glucose-induced insulin release decreased progressively with increasing hyperglycemia, in parallel with a reduction of several islet transcription factors involved in beta cell development and differentiation. In contrast, genes barely expressed in sham islets (lactate dehydrogenase A and hexokinase I) were markedly increased, in parallel with an increase in the transcription factor c-Myc, a potent stimulator of cell growth. These abnormalities were accompanied by beta cell hypertrophy. Changes in gene expression were fully developed 2 weeks after pancreatectomy. Correction of blood glucose by phlorizin for the next 2 weeks normalized islet gene expression and beta cell volume without affecting plasma nonesterified fatty acid levels, strongly suggesting that hyperglycemia triggers these abnormalities. In conclusion, chronic hyperglycemia leads to beta cell hypertrophy and loss of beta cell differentiation that is correlated with changes in c-Myc and other key transcription factors. A similar change in beta cell differentiation could contribute to the profound derangement of insulin secretion in human diabetes.

Induction of long-term glycemic control in newly diagnosed type 2 diabetic patients by transient intensive insulin treatment.

OBJECTIVE: Type 2 diabetes is a slowly progressive disease, in which the gradual deterioration of glucose tolerance is associated with the progressive decrease in beta-cell function. Hyperglycemia per se has deleterious effects on both beta-cell function and insulin action, which are partially reversible by the short-term control of blood glucose levels. We hypothesized that the induction of euglycemia, using intensive insulin therapy at the time of clinical diagnosis, could lead to a significant improvement in insulin secretion and action and thus alter the clinical course of the disease. RESEARCH DESIGN AND METHODS: Thirteen newly diagnosed diet-unresponsive type 2 diabetic patients were treated with continuous subcutaneous insulin infusion (CSII) for 2 weeks and followed longitudinally while being treated with diet alone. RESULTS: Four patients were considered therapeutic failures since CSII failed to induce euglycemia (n = 1) or glucose control deteriorated within 6 months after CSII (n = 3). The remaining nine patients were maintained on diet alone with adequate control from 9 to > 50 months (median +/- SE, 26 +/- 4.8 months). In five patients, glycemic control deteriorated after 9-36 months, but a repeat 2-week CSII treatment reestablished control in four patients. One of these patients underwent a third CSII treatment 13 months later. At the time this article was written, six patients of the initial group were still controlled without medication 16-59 months (median +/- SE, 45.5 +/- 6.6 months) after the initiation of treatment. Body weight remained unchanged in all patients. CONCLUSIONS: These findings suggest that in a significant proportion of type 2 diabetic patients who fail to respond to dietary measures, short-term intensive insulin treatment can effectively establish responsiveness, allowing long-term glycemic control without medication. Further studies are required to establish whether simpler treatment regimens could be equally effective. If the hypothesis offered here finds support, present approaches to the management of newly diagnosed type 2 diabetes may need to be revised.

Lipid metabolism alterations in patients with gestational diabetes mellitus associated fetal macrosomia.

Fetal macrosomia is commonly associated with gestational diabetes mellitus (GDM) which may lead to various complications. It has been suggested that some other metabolites apart from maternal hyperglycemia are responsible for the genesis of macrosomia. Lipid metabolism changes in GDM patients having macrosomic fetuses were studied. A lipid tolerance test (10% Lipovenous solution) was performed in 14 GDM. Pre- and post-infusion plasma lipid levels and their elimination rates were measured and compared to the ones of 8 non diabetic control pregnant women. HbA1c, basal glucose and triglyceride levels were found to be higher in GDM group and significantly higher levels of triglycerides persisted throughout the infusion. FFA, glycerol and phospholipid levels increased following infusion in both groups without significant differences. Glucose, C-peptide and insulin levels remained unchanged after the infusion. Increased basal triglycerides with slowed triglyceride metabolism may be responsible for the fetal macrosomia in mild GDM patients whose fasting blood glucose are below 105 mg/dl. A better metabolic control that provides plasma lipid regulation as well as glucose control may forestall the occurrence of fetal macrosomia.

Safety and efficacy of [Lys(B28), Pro(B29)]-human insulin in patients with diabetes mellitus.

The primary objectives of this study were to assess the efficacy and safety of Lys(B28), Pro(B29) in the treatment of patients with diabetes mellitus and to compare Lys(B28), Pro(B29) to currently available regular insulin with respect to quality of life. This study was designed as an open-label, non-comparative one. The number of patients enrolled in the trial was 39. At Visit 1 (week 0), blood samples for fasting, 1- and 2-hour postprandial blood glucose, and HbA1c were taken. At Visit 2 (week 6) and Visit 3 (week 12), fasting, 1- and 2-hour postprandial blood glucose, and HbA1c levels were measured again. There was no significant change in HbA1c, fasting blood glucose and 1- and 2-hour postprandial blood glucose levels. The 1- and 2-hour postprandial blood glucose excursions decreased significantly from Visit 1 to Visit 3. There were no serious adverse events during the study. Half of the patients had less hypoglycemia with LysPro insulin, while 25% had an increase in episodes. Thirty percent of patients were more satisfied with LysPro insulin than with the short-acting insulin that they had previously used. In conclusion, LysPro therapy can be regarded as safe, since there were no unexpected adverse events and no changes in the usual physical parameters.

Phosphoinositide metabolism and insulin secretion.

Secretion of insulin from beta cells of the pancreatic islets is regulated by glucose, its anaerobic metabolism and its metabolites. The phospholipids of the cell membrane the phosphoinositides are broken down by the activation of the enzyme phospholipase C either through the occupation of the receptor by an agonist or through the metabolism of glucose in the anaerobic glycolytic pathway. The hydrolysis of the phosphotidyl inositide-bisphosphate yields to the generation of Inositol 1, 4, 5-trisphosphate and diacylglycerol. Ins-1, 4, 5-P3 increases the intracellular Ca2+ by releasing the sequestered Ca2+ in the endoplasmic reticulum and diacylglycerol activates the enzyme protein kinase C.