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Men and women with diabetes show significant differences in adherence to nutritional recommendations, but sex differences in plasma lipid profile are unlikely to be explained by nutritional factors. Adherence to the nutritional recommendations is associated with a better plasma lipid profile regardless of sex, thus reinforcing the importance of substituting saturated for unsaturated fat sources, increasing fiber and reducing added sugar intake.

Context. We previously developed and validated an inexpensive and parsimonious prediction model of 2-year all-cause mortality in real-life type 2 diabetic patients. Objective. This model, now named ENFORCE, was now investigated in terms of i) prediction performance at 6 years, a more clinically useful time-horizon; ii) further validation in an independent sample; iii) performance comparison in real-life versus clinical trial setting. Design. Observational prospective. Randomized clinical trial. Setting. White patients with type 2 diabetes. Patients. Gargano Mortality Study (GMS; n=1019), Foggia Mortality Study (FMS; n=1045), Pisa Mortality Study (PMS; n=972) as real-life samples and the standard glycemic arm of the ACCORD clinical trial (n=3150). Main Outcome Measure. The endpoint was all-cause mortality. Prediction accuracy and calibration were estimated to assess model's performances.Results. ENFORCE yielded a 6-year mortality C-statistics of 0.79, 0.78 and 0.75 in GMS, FMS and PMS, respectively (P heterogeneity=0.71). Pooling the three cohorts, a 6-year mortality C-statistic of 0.80 was observed. In the ACCORD trial, ENFORCE achieved a Cstatistic of 0.68, a value which is significantly lower than that obtained in the pooled real-life samples (P<0.0001). This difference resembles that observed with other models when comparing real-life vs. clinical trial settings, thus suggesting it is a true, replicable phenomenon.Conclusions. Time horizon of ENFORCE has been extended to 6 years and validated in three independent samples. ENFORCE is a free (http://www.operapadrepio.it/enforce/enforce.php) and user-friendly risk calculator of all-cause mortality in White type 2 diabetic patients from real-life setting.We extended and validated an inexpensive and parsimonious prediction model of 6-year all-cause mortality in White patients with type 2 diabetes from both real-life and clinical trial settings.

The improvement in albuminuria associated with DPP-4i suggests that these agents may provide renal benefits beyond their glucose-lowering effects, thus offering direct protection from DKD. These promising results must be interpreted with caution and need to be confirmed in forthcoming studies.

BackgroundMicrovascular complications (MC) have been claimed to increase the risk for cardiovascular disease in diabetic subjects. However, the effect of MC burden on the risk of major vascular outcomes and all-cause mortality in type 1 diabetes is still poorly explored. We evaluated the relationship between microvascular complications burden and incidence of major cardiovascular events and all-cause mortality in subjects with type 1 diabetes.MethodsWe recruited 774 participants with type 1 diabetes in a single-center observational study over a follow-up of 10.8 ± 2.5 years. Hazard ratios (HR) for cardiovascular outcomes and all-cause death associated with microvascular complications were determined by unadjusted and adjusted Cox regression analysis.ResultsOut of 774 individuals, 54.9% had no-MC, 32.3% 1 MC, 9.7% 2 MC and 3.1% 3 MC. A total of 54 deaths (7.0%) occurred. Death rate increased from no-MC 2.1% (Ref) to 1 MC 7.2% (HR 3.54 [95% CI 1.59–7.87]), 2 MC 14.7% (HR 6.41 [95% CI 2.65–15.49]) and 3 MC 66.7% (HR 41.73 [95% CI 18.42–94.57], p < 0.0001). After adjustments, HRs were: 1 MC 2.05 (95% CI 0.88–4.76), 2 MC 1.98 (95% CI 0.75–5.21), 3 MC 7.02 (95% CI 2.44–20.20, p = 0.002). Forty-nine subjects (6.7%) had at least one cardiovascular event, and cumulative incidence went from no-MC 2.2% (Ref) to 1 MC 5.0%; (HR 2.27 [95% CI 0.96–5.38]), 2 MC 26.8% (HR 12.88 [95% CI 5.82–28.50]) and 3 MC 40.9% (HR 29.34 [95% CI 11.59–74.25], p < 0.0001). Upon adjustments, HRs were: 1 MC 1.59 (95% CI 0.65–3.88), 2 MC 4.33 (95% CI 1.75–10.74), 3 MC 9.31 (95% CI 3.18–27.25, p < 0.0001). Thirty-five individuals (4.8%) had at least one coronary event, which cumulative incidence increased with MC burden (p < 0.0001).ConclusionsIn type 1 diabetes, microvascular complications burden increases in an independent dose-dependent manner the risk of major cardiovascular outcomes and all-cause mortality. The presence and number of microvascular complications should be considered in stratifying overall cardiovascular risk in type 1 diabetes.

Aims To assess the effects of lockdown due to COVID-19 pandemic on glucose metrics, measured by glucose monitoring systems, in adult individuals with type 1 diabetes. Methods We conducted a systematic literature search for English language articles from MEDLINE, Scopus and Web of Science up to February 28, 2021, using “diabetes”, “lockdown”, and “glucose” as key search terms. Time in range (TIR) was the main outcome; other metrics were time above range (TAR), time below range (TBR), mean blood glucose (MBG) and its variability (%CV), estimated HbA1c (eA1c) or glucose management indicator (GMI). Results Seventeen studies for a total of 3,441 individuals with type 1 diabetes were included in the analysis. In the lockdown period, TIR 70-180 mg/dl increased by 3.05% (95% CI 1.67-4.43%; p < 0.0001) while TAR (>180 mg/dL and >250 mg/dL) declined by 3.39% (-5.14 to -1.63%) and 1.96% (-2.51 to -1.42%), respectively ( p < 0.0001 for both). Both TBR <70 and <54 mg/dL remained unchanged. MBG slightly decreased by 5.40 mg/dL (-7.29 to – 3.51 mg/dL; p < 0.0001) along with a reduction in %CV. Pooled eA1c and GMI decreased by 0.18% (-0.24 to -0.11%; p < 0.0001) and a similar reduction was observed when GMI alone was considered (0.15%, -0.23 to -0.07%; p < 0.0001). Sensor use was only slightly but not significantly reduced during lockdown. Conclusions This meta-analysis shows that well-controlled people with type 1 diabetes on both MDI and CSII with continuous or flash glucose monitoring did not experience a deterioration in glucose control throughout the COVID-19 lockdown, showing a modest, though statistically significant improvement in many glucose control parameters.

The Alb CKD phenotype is present in a significant proportion of individuals with type 1 diabetes supporting the hypothesis of two distinct pathways (Alb and Alb) of progression towards advanced kidney disease in type 1 diabetes. These are probably distinct pathways as suggested by different sets of covariates associated with the two CKD phenotypes.

Endogenous and exogenous signals derived by the gut microbiota such as lipopolysaccharides (LPS) orchestrate inflammatory responses contributing to development of the endothelial dysfunction associated with atherosclerosis in obesity, metabolic syndrome, and diabetes. Endothelial progenitor cells (EPCs), bone marrow derived stem cells, promote recovery of damaged endothelium playing a pivotal role in cardiovascular repair. Since healthy nutrition improves EPCs functions, we evaluated the effect of a fermented grain, Lisosan G (LG), on early EPCs exposed to LPS. The potential protective effect of LG against LPS-induced alterations was evaluated as cell viability, adhesiveness, ROS production, gene expression, and NF-kB signaling pathway activation. Our results showed that LPS treatment did not affect EPCs viability and adhesiveness but induced endothelial alterations via activation of NF-kB signaling. LG protects EPCs from inflammation as well as from LPS-induced oxidative and endoplasmic reticulum (ER) stress reducing ROS levels, downregulating proinflammatory and proapoptotic factors, and strengthening antioxidant defense. Moreover, LG pretreatment prevented NF-kB translocation from the cytoplasm into the nucleus caused by LPS exposure. In human EPCs, LPS increases ROS and upregulates proinflammatory tone, proapoptotic factors, and antioxidants. LG protects EPCs exposed to LPS reducing ROS, downregulating proinflammatory and proapoptotic factors, and strengthening antioxidant defenses possibly by inhibiting NF-κB nuclear translocation.