The Relationship between Red Blood Cell Distribution Width and Incident Diabetes in Chinese Adults: A Cohort StudyRead the full article
Journal of Diabetes Research publishes articles related to type 1 and type 2 diabetes. Topics include etiology, pathogenesis, management, and prevention of diabetes, as well as associated complications such as nephropathy.
Chief Editor Dr Mark Yorek, from the University of Iowa, is currently researching vascular and neural disease related to obesity and diabetes. His active research studies focus on etiology, treatment and prevention of nerve damage.
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Quantitative Analysis of Foveal Microvascular Differences in Diabetic Macular Edema with and without Subfoveal Neuroretinal Detachment
Purpose. This study is aimed at quantifying the difference of the foveal microvasculature in the eyes with diabetic macular edema (DME) with and without subfoveal neuroretinal detachment (SND+ and SND-, respectively). Methods. This retrospective, cross-sectional study included 48 eyes from 42 patients with DME (20 SND+ and 28 SND- eyes). Data collection included fundus color photographs, optical coherence tomography angiography (OCTA), and best-corrected visual acuity. The following parameters were evaluated with OCTA: foveal avascular zone (FAZ) parameters and vessel density in a width of 300 μm around the FAZ, superficial capillary plexus, deep capillary plexus (DCP), and choriocapillary plexus. The number of retinal hyperreflective spots (HRS) and the area of SND in the central 3 mm were evaluated at 0 degrees using B-scans. Results. Parafoveal vessel densities of DCP were significantly lower in SND+ than in SND- eyes (). The number of HRS was significantly higher in SND+ than in SND- eyes (). A statistically significant negative correlation between parafoveal vessel density in DCP and the number of HRS in all eyes was found (Spearman’s correlation, , ). Conclusion. DME with SND correlated with larger numbers of HRS and significant macular microvascular impairment in the DCP. The pathophysiology of decline of parafoveal vessel density in the DCP with an increase in the number of HRS in the eyes with DME with SND needs further investigation.
Effects of Nutritional Strategies on Glucose Homeostasis in Gestational Diabetes Mellitus: A Systematic Review and Network Meta-Analysis
Background. Gestational diabetes mellitus (GDM) is one of the most common complications of pregnancy, and nutritional therapy is the basis of GDM treatment. However, the effects of different forms of nutritional supplementation on improving gestational diabetes are uncertain. Objective. We conducted a network meta-analysis to evaluate the effects of supplementation with different nutrients on glucose metabolism in women with GDM. Methods. We conducted a literature search using PubMed, EMBASE, and the Cochrane Library to identify randomized controlled trials (RCTs) comparing the differences between different nutritional strategies in women with GDM. The Cochrane tool was used to assess the risk of bias. Pairwise meta-analysis and network meta-analysis were used to compare and rank the effects of nutritional strategies for the improvement of fasting plasma glucose (FPG), serum insulin, and homeostasis model assessment-insulin resistance (HOMA-IR). Results. We included thirteen RCTs with a total of 754 participants. Compared with placebo, omega-3, magnesium, vitamin D, zinc, and probiotics were more beneficial for improving FPG, serum insulin, and HOMA-IR. Network analysis showed that vitamin D supplementation was superior to omega-3 (-3.64 mg/dL, 95% CI: -5.77 to -1.51), zinc (-5.71 mg/dL, 95% CI: -10.19 to -1.23), probiotics (-6.76 mg/dL, 95% CI: -10.02 to -3.50), and placebo (-12.13 mg/dL, 95% CI: -14.55 to -9.70) for improving FPG. Magnesium supplementation was more beneficial for decreasing serum insulin compared with probiotics (-5.10 μIU/mL, 95% CI: -9.32 to -0.88) and placebo (-7.80 μIU/mL; 95% CI-11.95, -3.65). Vitamin D was more effective than probiotics (-0.99, 95% CI: -1.84 to -0.14) and placebo (-1.80, 95% CI: -2.45 to -1.16) for improving HOMA-IR. Conclusion. Vitamin D supplementation significantly reduced FPG and regulated HOMA-IR. Magnesium supplementation was superior in decreasing serum insulin than supplementation with other nutrients. Nutrient supplementation seemed to have an effect on glucose homeostasis maintenance in patients with GDM and may be considered an adjunctive therapy.
Glucose-Regulated Protein 78 in the Aqueous Humor of Patients with Diabetic Macular Edema
Purpose. We identified the associations between levels of aqueous glucose-regulated protein 78 (GRP78) and systemic or ocular factors in patients with center-involving diabetic macular edema (CIDME). Methods. We measured the aqueous concentrations of GRP78, interleukin- (IL-) 1β, IL-2, IL-8, IL-10, and IL-17, placental growth factor, and vascular endothelial growth factor (VEGF). We explored the associations between aqueous GRP78 levels and those of other aqueous factors, optical coherence tomography (OCT) findings, and systemic parameters in CIDME patients. Results. In multivariate regression analysis, aqueous GRP78 levels were associated with aqueous VEGF levels (), length of EZ disruption (), and duration of diabetes (). However, no significant relationship was observed between GRP78 levels and those of other systemic and ocular factors including inflammatory cytokines in the aqueous humor. In terms of responsiveness, the number of hyperreflective foci (≥8) was significantly associated with the responsiveness of three consecutive monthly intravitreal bevacizumab injections (, ), but not the aqueous GRP78 levels. Conclusions. Aqueous GRP78 levels correlated with VEGF levels in the aqueous humor and EZ disruption on OCT. However, GRP78 levels were not associated with those of inflammatory biomarkers in the aqueous humor or OCT findings. Additionally, GRP78 could not serve as a biomarker to predict short-term prognosis of anti-VEGF agent.
High Glucose Induces Endothelial COX2 and iNOS Expression via Inhibition of Monomethyltransferase SETD8 Expression
Cyclooxygenase 2 (COX2) and inducible nitric oxide synthase (iNOS) overexpression results in endothelial apoptosis, thus mediating vascular endothelial injury in hyperglycaemia. E26 transformation-specific sequence transcription factor-1 (ESE-1), which belongs to the E26 transformation-specific family of transcription factors, has been demonstrated to be involved in COX2 and iNOS gene transcription. Our previous study indicated that SET domain-containing protein 8 (SETD8) downregulation is involved in high glucose-mediated endothelial inflammation in human umbilical vein endothelial cells (HUVECs). Here, we report that SETD8 plays a major role in hyperglycaemia-induced COX2 and iNOS expression. In HUVECs, upregulation of ESE-1 expression was related to high glucose-mediated apoptosis and COX2 and iNOS expression. High glucose inhibited SETD8 expression, and overexpression of SETD8 diminished the effects of high glucose treatment. Consistently, RNA silencing of SETD8 led to the opposite effect. Furthermore, SETD8 was found to interact with specificity protein 1 (SP1). Blockade of SP1 protected against high glucose-mediated endothelial injury. Mechanistically, we showed that H4K20me1, a downstream target of SETD8, and SP1 were enriched at the ESE-1 promoter region by ChIP assay. Luciferase reporter assays indicated that SETD8 overexpression attenuated ESE-1 promoter activity and augmented the inhibitory effect of siSP1 on ESE-1 promoter activity. In general, our data indicate that SETD8 interacts with SP1 to coregulate ESE-1 expression, which is involved in hyperglycaemia-mediated endothelial apoptosis in HUVECs.
The Usefulness of Genotyping of Celiac Disease-Specific HLA among Children with Type 1 Diabetes in Various Clinical Situations
Aim. The aim of the study was to determine the usefulness of HLA DQ2/DQ8 genotyping in children with T1D in various clinical situations: as a screening test at the diabetes onset, as a verification of the diagnosis in doubtful situations, and as a test estimating the risk of CD in the future. Materials and methods. Three groups of patients with T1D were included: newly diagnosed (), with CD and villous atrophy (), and with potential CD (). Genetic tests were performed (commercial test, PCR, and REX), and clinical data were collected. Results. The results of genetic tests confirmed the presence of DQ2/DQ8 in 94% of children with diabetes (group I) and in 100% of children with diabetes and CD (groups II and III, respectively). Comparative analysis of the HLA DQ2/DQ8 distribution did not show any differences. Allele (linked with HLA DQ8) was significantly less common in children with diabetes and CD (group I versus groups II and III, 56.5% vs. 24.5%; ). The probability of developing CD in -positive patients was 4 times lower (OR 0.25; 95% CI 0.118-0.529; ). was significantly less frequent in children with villous atrophy compared to potential CD (13% vs. 39%; ). Conclusions. Genotyping HLA DQ2/DQ8 as a negative screening has limited use in assessing the risk of CD at the diabetes onset and does not allow to verify the diagnosis of CD in doubtful situations. The presence of the allele modulates the risk of CD and significantly reduces it and can predict a potential form.
Impact of the Glycemic Control and Duration of Type 2 Diabetes on Vitamin D Level and Cardiovascular Disease Risk
Background and Aims. To investigate the impact of glycemic control and T2D duration on vitamin D status and cardiovascular disease (CVD) risk among Saudi patients. Methods. This case-control study was conducted in King Faisal Specialist Hospital, Saudi Arabia. A total of 25 nondiabetic controls and 92 patients with confirmed T2D, aged 20–60 years, were included. Patients with T2D were divided into the following groups based on disease duration (newly diagnosed: ≈6 months and long duration: ≥5 years) and glycemic control based on their glycated hemoglobin (HbA1C) level with a threshold of ≤0.053 mol/mol: newly diagnosed controlled (NC, ), newly diagnosed uncontrolled (NU, ), long duration controlled (LC, ), and long duration uncontrolled (LU, ). Blood levels of fasting blood glucose, HbA1C, lipid profile, and serum 25-hydroxyvitamin D (25(OH)D) were assessed and used to define the CVD risk score. Results. Our study showed that T2D duration was an independent predictor of vitamin D deficiency. The longer disease duration, the lower odds of being vitamin D deficient (odds ratio (OR) = 0.05, 95% CI: 0.01–0.29, ). No significant association was observed between vitamin D and HbA1C levels. In the NU group, CVD risk scores were directly correlated with serum 25(OH)D (, ). On the contrary, 25(OH)D was moderately inversely correlated with CVD risk score in the LU group (, ). Conclusion. Duration of diabetes rather than glycemic control is associated with vitamin D deficiency. Glycemic uncontrol may augment vitamin D deficiency-associated CVD risk in both newly diagnosed and old patients with type 2 diabetes.