The degeneration of retinal neurons and glial cells has recently been postulated in the pathogenesis of diabetic retinopathy. Optical coherence tomography (OCT) allows to perform qualitative and quantitative measurements of retinal thickness (RT) with identification of individual retinal layers. We compared RT, retinal nerve fiber layer (RNFL) thickness, and ganglion cell layer (GCL) thickness obtained by OCT in type 1 diabetic patients with and without clinically diagnosed retinopathy. The study included 77 consecutive patients with type 1 diabetes (39 men, 38 women; median age, 35 years [interquartile range (IQR), 29-42]; median disease duration, 10 years [IQR, 9-14]) and 31 age- and sex-matched controls. We measured RT in the fovea, parafovea, and perifovea, as well as RNFL and GCL thickness. We divided diabetic patients into 2 subgroups, i.e., those with diabetic retinopathy and without retinopathy. We observed thicker perifoveal retina (P = 0.05), mean RNFL (P = 0.002), inferior RNFL (P <0.0001), and superior and inferior GCL (P = 0.05 and P = 0.04, respectively) in diabetic subjects compared with the control group. We detected retinopathy in 23 diabetic patients (29%). Compared with patients without retinopathy, subjects with retinopathy had thinner parafoveal retina (P = 0.05), mean RNFL (P = 0.002), inferior and nasal RNFL (P = 0.002, P = 0.03), superior (P = 0.05) and inferior GCL (P = 0.006). Significant correlations were found between duration of diabetes and nasal RNFL thickness (r = -0.32, P = 0.004) and parafoveal RT (r = -0.47, P <0.001). The results might suggest the loss of intraretinal neural tissue in type 1 diabetic patients with retinopathy. Neurodegeneration in diabetic retinopathy is closly associated with disease duration.

Background: Skin autofluorescence (AF) measured with an AF reader device is a noninvasive tool to measure the tissue accumulation of advanced glycation end products (AGEs). The aim of the study was to assess the association between AF and microvascular complications in type 1 diabetes mellitus (DM1). Methods: The study population consisted of 140 DM1 patients, 28 years old (interquartile range [IQR], 23–35), 76 of whom were women, with disease duration of 13 years (IQR, 8–19). We used the AGE Reader (DiagnOptics, Groningen, The Netherlands) to measure the AF phenomenon, which occurs because of fluorescent properties of AGEs. The patients were divided according to the presence or absence of diabetes-associated microvascular complications: retinopathy, nephropathy, and neuropathy and any microangiopathy. Results: The median AF was 2.0 (IQR, 1.7–2.4). In the univariate logistic regression AF was significantly associated with retinopathy (odds ratio [OR] 2.47, 95% confidence interval [CI] 1.26–4.84, P = 0.008), nephropathy (OR 3.15, 95% CI 1.34–7.39, P = 0.008), neuropathy (OR 3.17, 95% CI 1.46–6.90, P = 0.003), and any microvascular complication (OR 2.94, 95% CI 1.46–5.92, P = 0.002). Multivariate logistic regression showed that skin AF was independently associated only with diabetic neuropathy (OR 2.98, 95% CI 0.99–8.90, P = 0.05). Conclusions: The tissue accumulation of AGE is significantly associated with microvascular complications in DM1.

There are scarce data about the effect of metformin on lipid profile in patients with type 1 diabetes. The present study is the first prospective clinical trial evaluating the effect of combined therapy of metformin and insulin on the pool of oxidized and glycated low‑density lipoproteins (LDL) in young patients with type 1 diabetes and concomitant obesity. A total of 33 obese patients with type 1 diabetes treated with intensive insulin therapy were randomized into a group where metformin was added. The remaining 19 patients continued to receive intensive insulin therapy (control group). In all patients, lipid profile and glycemia were assessed using routine laboratory tests. Oxidized and glycated LDL were measured using commercially available kits. Laboratory tests were performed at baseline and at a control visit after 6 months of treatment. A significant decrease in the levels of glycated hemoglobin, fasting plasma glucose, postprandial glucose, average glucose, triglycerides, glycated LDL, and body mass index was observed in the group receiving combined therapy. A similar decrease was not observed in the control group. The remaining lipid parameters were not changed during follow‑up in any of the groups. Addition of metformin to intensive insulin therapy in young obese patients with type 1 diabetes results in a significant reduction of glycated LDL levels. This can be possibly explained by better glucose control, which improved insulin sensitivity of the peripheral tissues and reduced body mass in this patient group.

The purpose of this study was to evaluate the impact of high intensity exercise on glucose levels and risk of metabolic decompensation in males with type 1 diabetes (T1D), depending on the method of insulin administration. The study comprised 29 males (aged 25.3±5.1 years; duration of diabetes 10.3±3.2 years) treated with continuous subcutaneous insulin infusion (CSII) or multiple daily insulin injections (MDI). Treadmill exercise test was performed twice in each patient until subjective exhaustion as maximum according to the Borg scale. All the patients achieved ≥85% of the maximal heart rate. Distance during the test was 4 500±1 400 m and 4 473±1 559 m in the MDI and CSII groups, respectively, which was achieved in 31±8 min. During the test and in the 6 h after, no clinically significant episodes of hypoglycemia occurred. Mean glucose levels did not exceed 10 mmol/L in most patients. The risk of the composite endpoint (hypoglycemia2.2 mmol/L) was higher in patients treated with MDI than CSII (OR3.75, 95%CI:1.22–11.52, p=0.02). In conclusion, planned high intensity physical effort in men with well-controlled T1D is metabolically safe. CSII shows greater metabolic advantage over MDI during and after high intensity exercise in men with T1D.