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AimsPeriodontal disease (PD) is a chronic inflammation of periodontal tissue associated with infection from specific anaerobic pathogens contained in dental plaque. Both type 1 and type 2 diabetes are associated with an increased prevalence of PDs. A two-way relationship between diabetes and periodontitis has been proposed, with diabetes increasing the risk for periodontitis, and periodontal inflammation negatively affecting glycaemic control. To date, the relationship between PD and glucose variability in type 1 diabetes has not been evaluated. To investigate the prevalence of PD in patients with type 1 diabetes and its association with glycemic control and glucose variability.MethodsIn this cross-sectional study, all enrolled patients were scheduled to attend both a diabetologic and a periodontal visit. HbA1c, glucose coefficient of variation (CV), loss of clinical attachment (CAL), and periodontal probing depth (PPD) were collected.Results136 patients were included in the analysis. The prevalence of PD was 63%. A significant correlation was found between mean CAL and glucose CV (r = 0.31,p = 0.002), but not with HbA1c. Mean PPD was also associated with glucose CV (r = 0.27 and 0.044), but not with HbA1c. In a multiple linear regression model, with mean CAL as dependent variable, age, glucose CV, and smoking habit resulted significantly associated (r = 0.23,p = 0.013;r = 0.33,p = 0.001;r = 0.34,p ConclusionsPD is associated with glucose variability in patients with type 1 diabetes also after adjusting for the main confounders.

Self-monitoring of blood glucose (SMBG) represented a major breakthrough in the treatment of type 1 diabetes. The aim of the present meta-analysis is to assess the effect of continues glucose monitoring (CGM) and flash glucose monitoring (FGM), on glycemic control in type 1 diabetes. The present analysis includes randomized clinical trials comparing CGM or FGM with SMBG, with a duration of at least 12 weeks, identified in Medline or clinicaltrials.gov. The principal endpoint was HbA1c at the end of the trial. A secondary endpoint was severe hypoglycemia. Mean and 95% confidence intervals for HbA1c and Mantel–Haenzel odds ratio [MH-OR] for severe hypoglycemia were calculated, using random effect models. A sensitivity analysis was performed using fixed effect models. In addition, the following secondary endpoints were explored, using the same methods: time in range, health-related quality of life, and treatment satisfaction. Separate analyses were performed for trials comparing CGM with SMBG, and those comparing CGM + CSII and SMBG + MDI and CGM-regulated insulin infusion system (CRIS) and CSII + SMBG. CGM was associated with a significantly lower HbA1c at endpoint in comparison with SMBG (− 0.24 [− 0.34, − 0.13]%); CGM was associated with a significantly lower risk of severe hypoglycemia than SMBG. Treatment satisfaction and quality of life were not measured, or not reported, in the majority of studies. FGM showed a significant reduction in the incidence of mild hypoglycemia and an increased treatment satisfaction, but no significant results are shown in HbA1c. CGM + CSII in comparison with SMBG + MDI was associated with a significant reduction in HbA1c. Only two trials with a duration of at least 12 weeks compared a CRIS with SMBG + CSII; HbA1c between the two treatment arms was not statistically significant (difference in means: − 0.23 [− 0.91; 0.46]%; p = 0.52). GCM compared to SMBG has showed a reduction in HbA1c and severe hypoglycemia in patient with type 1 diabetes. The comparison between CGM + CSII and SMBG + MDI showed a large reduction in HbA1c; it is conceivable that the effects of CSII + CGM on glycemic control additives. The only comparison available between FGM and SMBG was conducted in patients in good control.

Dipeptidyl peptidase 4 (DPP-4) is an enzyme that is produced by endothelial cells in different districts and circulates in plasma. Patients with type 2 diabetes show a reduction in active Glucagon-Like Peptide-1 (GLP-1) that could be due to impairment of secretion or its degradation or both. GLP-1 is rapidly inactivated in vivo, mainly by the DPP-4. Some authors suggest that Metformin has no direct inhibitory effect on DPP-4 activity and that Metformin and the other biguanides enhance GLP-1 secretion; others suggest a possible role of Metformin in the inhibition of the DPP-4 activity. In order to better elucidate the role of insulin sensitizers on the modulation of GLP-1 circulating levels, DPP-4 activity and mRNA expression were measured in cultured human aortic endothelial cells (HAEC) and human microvascular dermal endothelial cells (HMVEC) exposed to high glucose, Metformin and Rosiglitazone. Present data show that hyperglycemia is capable of increasing in a significant manner the DPP-4 activity only in microvascular endothelial cells. Rosiglitazone is able to modulate in a negative manner the expression of DPP-4 but not its activity in macrovascular endothelial cells, while at 24 h of exposure it is able to increase significantly DPP-4 activity but not its expression in microvascular endothelial cells. Metformin at 48 h only in microvascular endothelial cells is able to reduce in a significant manner (p = 0.01) the activity of DPP-4 but not its expression. The modulation of DPP-4 is site specific.

Diabetic cardiomyopathy has been defined as "a distinct entity characterized by the presence of abnormal myocardial performance or structure in the absence of epicardial coronary artery disease, hypertension, and significant valvular disease". The diagnosis stems from the detection of myocardial abnormalities and the exclusion of other contributory causes of cardiomyopathy. It rests on non-invasive imaging techniques which can demonstrate myocardial dysfunction across the spectra of clinical presentation. The presence of diabetes is associated with an increased risk of developing heart failure, and the 75% of patients with unexplained idiopathic dilated cardiomyopathy were found to be diabetic. Diabetic patients with microvascular complications show the strongest association between diabetes and cardiomyopathy, an association that parallels the duration and severity of hyperglycemia. Metabolic abnormalities (that is hyperglycemia, hyperinsulinemia, and hyperlipemia) can lead to the cellular alterations characterizing diabetic cardiomyopathy (that is myocardial fibrosis and/or myocardial hypertrophy) directly or indirectly (that is by means of renin-angiotensin system activation, cardiac autonomic neuropathy, alterations in calcium homeostasis). Moreover, metabolic abnormalities represent, on a clinical ground, the main therapeutic target in the patients with diabetes since the diagnosis of diabetes is made. Since diabetic cardiomyopathy is highly prevalent in the asymptomatic type 2 diabetic patients, screening for its presence at the earliest stage of development can lead to prevent the progression to chronic heart failure. The most sensitive test is standard echocardiogram, while a less expensive pre-screening method is the detection of microalbuminuria.

The aim of this study was to assess the feasibility and efficacy of an Interactive Educational and Support Group programme (IESG) for patients with type 1 diabetes. A sample of 96 type 1 diabetic outpatients was studied measuring the effects of participation in IEGS on metabolic control and diabetes-related quality of life (QoL). Those refusing to participate (n = 48) and a sample of 37 patients who were not invited to IESG (control) where studied for comparison. After one year, participants showed a significant (p0.05) improvement of HbA(1c) from 7.7+/-1.6 to 7.2+/-1.5%, whereas no variation of HbA(1c) was observed in non-participants and controls. No significant variation of QoL was observed in any of the three groups. At two-years follow-up, HbA(1c) of the patients attending IESG was not significantly different from that at one-year follow-up, and it was significantly lower than that observed at enrolment. QoL showed a significant improvement at 2 years with respect to baseline and one-year follow-up. In conclusion, this programme appears to be effective in the improvement of medium term metabolic control and QoL.

The aim of the present cohort study is the assessment of treatment failure rates in patients on monotherapy with metformin or insulin secretagogues, observed in a routine clinical setting. A cohort of patients without any pharmacological treatment was also observed. A retrospective observational cohort study was performed on a consecutive series of 2,020 type 2 diabetic patients receiving monotherapy with an oral agent (metformin or insulin secretagogue, n = 1,126) or drug-naive (n = 894). HbA1c and prescribed hypoglycemic therapy were recorded yearly. Patients were followed until death, change of residence, failure to treatment, or up to 48 months. The mean duration of follow up was 34.8 ± 18.0 months. In a Cox regression analysis, metformin was associated with a significant reduction, and insulin secretagogues with a significant increase, in the risk of failure to therapy during follow up. When duration of diabetes and baseline BMI were added to the model, insulin secretagogues, but not metformin, were still associated with increased risk of failure. In conclusion, insulin secretagogues are associated with increased failure rate in comparison with metformin. This difference could be due to detrimental effect of secretagogues, rather than to a beneficial action of metformin.

The prevalence of obesity has been increasing dramatically in the last decades; the major metabolic complication of obesity is insulin resistance and type-2 diabetes because there are pathogenetic mechanisms linking obesity and type-2 diabetes. Diabetes is also rapidly increasing worldwide; such a description of the key stages in the evolution of type-2 diabetes may be of great interest for implementing antidiabetes treatment. In recent times, type-2 diabetes therapy has been based on drugs, which improve insulin sensibility or stimulate insulin secretion or slow down glucose absorption. Recently, an ADA and EASD consensus has been released to develop a common approach for the management of hyperglycaemia in adults. The development of new classes of blood-glucose-lowering medications to supplement the older therapies, such as lifestyle-directed interventions, insulin, sulfonylureas, and metformin, has increased the different possible options for the treatment of type-2 diabetes. Therapeutic approaches aiming to potentiate the biological effects of incretins include degradation-resistant GLP-1 receptor agonists (incretin mimetics), and inhibitors of dipeptidyl peptidase-IV (DPP-IV) activity (incretin enhancers) will be very useful to slow down type-2 diabetes progression. Weight-loss interventions, such as a hypocaloric diet and physical exercise, in addition to agents such as orlistat, sibutramine and cannabinoid receptor antagonists, may have favourable effects upon fat storage, nutrient metabolism and ultimately glucose tolerance or type-2 diabetes. When the therapeutic target is not achieved, insulin with metformin could be suggested, but is this approach the ideal one for all patients? Perhaps it is possible to delay the initiation of insulin therapy, therefore, the actual and future therapeutical options are considered in the present review.