Nondiabetic Subjects Research Articles

Vitamin D status in Type 2 Diabetes Mellitus in a Tertiary Level Hospital

Background: There is increasing evidence of a relationship between vitamin D status and type 2 diabetes. Diabetes has also been found to be associated with 25(OH)D (vitamin D) deficiency and the role of vitamin D has recently emerged, especially in preventing cardiovascular diseases and cancer. and insulin resistance. Objective: This study aimed to compare vitamin D deficiency between healthy and Type 2 Diabetes Mellitus (T2DM) patients. Methods: This cross-sectional study was conducted from July 2021 to June 2022 in the Department of Physiology, Rangpur Medical College, Rangpur. For this study, a total number of 100 subjects were selected among them 50 non-diabetic healthy subjects were included as control and 50 Type 2 Diabetes Mellitus patients were included as cases. The subjects of control were selected from the surrounding community of Rangpur district and subjects of cases were selected from Diabetic Association and from Outdoor of Endocrinology Department, Rangpur Medical College and Hospital, Rangpur. For statistical analysis, an independent sample t-test was performed by computer-based software SPSS-23.0 version for windows. Results: The mean vitamin D level was lower in the diabetic patients than in non-diabetic participants (14.1±8.3 ng/ml and 37.3±11.3, p<0.001). Conclusions: Early screening for serum vitamin D level is recommended for T2DM patients. Hence, it is crucial to promptly address any deficiencies in vitamin D levels. J Rang Med Col. March 2024; Vol. 9, No. 1: 77-81

Study of the Relationship Between Insulin Resistance, Iron Status Markers, and Body Weight in a Sample of Egyptian Population.

Iron plays a key role in the regulation of body iron homeostasis and is used as a clinical marker for iron deficiency (ID) and hemochromatosis. The idea that iron dysregulation may contribute to various metabolic diseases, such as obesity, insulin resistance, MetS, and T2DM, is a hot topic of discussion. The aim of this study is to investigate the relationship insulin resistance, iron status markers, and body weight in a sample of Egyptian population. A case control study was conducted on 90 subjects with age ranging from 18 to 70 years old from a diabetes outpatient clinic, and they were divided to three groups: Group I, non-obese- non-diabetic as the control group; Group II, obese-non-diabetic; and Group III, obese-diabetic. In our study, there was no statistically significant difference between the three studied groups regarding the different iron parameters. Similarly, we found that neither HOMA-IR nor body weight had a significant correlation with iron status markers. On the contrary, we detected significant positive correlations between the TIBC and the fasting blood glucose, between the serum iron and the LDL, between the TSAT and the systolic blood pressure, and between the HOMA-IR and hematocrit. Our study demonstrated no direct statistical significant relationship between the different iron parameters, obesity, and insulin resistance, either in the diabetic or non-diabetic subjects. This may be due to the complex metabolic dysregulation and the small number of the sample for future investigations.

Helicobacter pylori Infection and Insulin Resistance in Diabetic and Nondiabetic Subjects

Helicobacter pylori Infection and Insulin Resistance in Diabetic and Nondiabetic Subjects

Effects of hypertriglyceridemia with or without NEFA elevation on β-cell function and insulin clearance and sensitivity.

Hypertriglyceridemia is a risk factor for developing type 2 diabetes (T2D) and might contribute to its pathogenesis either directly or through elevation of non-esterified fatty acids (NEFAs). This study aimed at comparing the glucometabolic effects of acute hypertriglyceridemia alone or combined with NEFA elevation in non-diabetic subjects. Twenty-two healthy lean volunteers underwent two 5-h intravenous infusions of either saline or Intralipid, without (n=12) or with heparin (I+H; n=10) to activate the release of NEFAs. Oral glucose tolerance tests (OGTTs) were performed during the last 3h of infusion. Insulin sensitivity, insulin secretion rate (ISR), model-derived β-cell function, and insulin clearance were measured after 2h of lipid infusion and during the OGTTs. In fasting conditions, both lipid infusions increased plasma insulin and ISR and reduced insulin clearance, without affecting plasma glucose and insulin sensitivity. These effects on insulin and ISR were more pronounced for I+H than Intralipid alone. During the OGTT, the lipid infusions markedly impaired glucose tolerance, increased plasma insulin and ISR, and decreased insulin sensitivity and clearance, without significant group differences. Intralipid alone inhibited glucose-stimulated insulin secretion (i.e. β-cell glucose sensitivity) and increased β-cell potentiation, whereas I+H had neutral effects on these β-cell functions. In healthy non-obese subjects, mild acute hypertriglyceridemia directly reduces glucose tolerance, insulin sensitivity and clearance, and has selective and opposite effects on β-cell function that are neutralized by NEFAs. These findings provide new insight into plausible biological signals that generate and sustain insulin resistance and chronic hyperinsulinemia in the development of T2D.

Bone canonical Wnt signaling is downregulated in type 2 diabetes and associates with higher advanced glycation end-products (AGEs) content and reduced bone strength.

Type 2 diabetes (T2D) is associated with higher fracture risk, despite normal or high bone mineral density. We reported that bone formation genes (SOST and RUNX2) and advanced glycation end-products (AGEs) were impaired in T2D. We investigated Wnt signaling regulation and its association with AGEs accumulation and bone strength in T2D from bone tissue of 15 T2D and 21 non-diabetic postmenopausal women undergoing hip arthroplasty. Bone histomorphometry revealed a trend of low mineralized volume in T2D (T2D 0.249% [0.156-0.366]) vs non-diabetic subjects 0.352% [0.269-0.454]; p=0.053, as well as reduced bone strength (T2D 21.60 MPa [13.46-30.10] vs non-diabetic subjects 76.24 MPa [26.81-132.9]; p=0.002). We also showed that gene expression of Wnt agonists LEF-1 (p=0.0136) and WNT10B (p=0.0302) were lower in T2D. Conversely, gene expression of WNT5A (p=0.0232), SOST (p<0.0001), and GSK3B (p=0.0456) were higher, while collagen (COL1A1) was lower in T2D (p=0.0482). AGEs content was associated with SOST and WNT5A (r=0.9231, p<0.0001; r=0.6751, p=0.0322), but inversely correlated with LEF-1 and COL1A1 (r=-0.7500, p=0.0255; r=-0.9762, p=0.0004). SOST was associated with glycemic control and disease duration (r=0.4846, p=0.0043; r=0.7107, p=0.00174), whereas WNT5A and GSK3B were only correlated with glycemic control (r=0.5589, p=0.0037; r=0.4901, p=0.0051). Finally, Young's modulus was negatively correlated with SOST (r=-0.5675, p=0.0011), AXIN2 (r=-0.5523, p=0.0042), and SFRP5 (r=-0.4442, p=0.0437), while positively correlated with LEF-1 (r=0.4116, p=0.0295) and WNT10B (r=0.6697, p=0.0001). These findings suggest that Wnt signaling and AGEs could be the main determinants of bone fragility in T2D.

Bone canonical Wnt signaling is downregulated in type 2 diabetes and associates with higher advanced glycation end-products (AGEs) content and reduced bone strength

Type 2 diabetes (T2D) is associated with higher fracture risk, despite normal or high bone mineral density. We reported that bone formation genes (SOST and RUNX2) and advanced glycation end-products (AGEs) were impaired in T2D. We investigated Wnt signaling regulation and its association with AGEs accumulation and bone strength in T2D from bone tissue of 15 T2D and 21 non-diabetic postmenopausal women undergoing hip arthroplasty. Bone histomorphometry revealed a trend of low mineralized volume in T2D (T2D 0.249% [0.156–0.366]) vs non-diabetic subjects 0.352% [0.269–0.454]; p=0.053, as well as reduced bone strength (T2D 21.60 MPa [13.46–30.10] vs non-diabetic subjects 76.24 MPa [26.81–132.9]; p=0.002). We also showed that gene expression of Wnt agonists LEF-1 (p=0.0136) and WNT10B (p=0.0302) were lower in T2D. Conversely, gene expression of WNT5A (p=0.0232), SOST (p&lt;0.0001), and GSK3B (p=0.0456) were higher, while collagen (COL1A1) was lower in T2D (p=0.0482). AGEs content was associated with SOST and WNT5A (r=0.9231, p&lt;0.0001; r=0.6751, p=0.0322), but inversely correlated with LEF-1 and COL1A1 (r=–0.7500, p=0.0255; r=–0.9762, p=0.0004). SOST was associated with glycemic control and disease duration (r=0.4846, p=0.0043; r=0.7107, p=0.00174), whereas WNT5A and GSK3B were only correlated with glycemic control (r=0.5589, p=0.0037; r=0.4901, p=0.0051). Finally, Young’s modulus was negatively correlated with SOST (r=−0.5675, p=0.0011), AXIN2 (r=−0.5523, p=0.0042), and SFRP5 (r=−0.4442, p=0.0437), while positively correlated with LEF-1 (r=0.4116, p=0.0295) and WNT10B (r=0.6697, p=0.0001). These findings suggest that Wnt signaling and AGEs could be the main determinants of bone fragility in T2D.

Characterization of the gut bacterial and viral microbiota in latent autoimmune diabetes in adults

Latent autoimmune diabetes in adults (LADA) is a heterogeneous disease characterized by autoantibodies against insulin producing pancreatic beta cells and initial lack of need for insulin treatment. The aim of the present study was to investigate if individuals with LADA have an altered gut microbiota relative to non-diabetic control subjects, individuals with type 1 diabetes (T1D), and individuals with type 2 diabetes (T2D). Bacterial community profiling was performed with primers targeting the variable region 4 of the 16S rRNA gene and sequenced. Amplicon sequence variants (ASVs) were generated with DADA2 and annotated to the SILVA database. The gut virome was sequenced, using a viral particle enrichment and metagenomics approach, assembled, and quantified to describe the composition of the viral community. Comparison of the bacterial alpha- and beta-diversity measures revealed that the gut bacteriome of individuals with LADA resembled that of individuals with T2D. Yet, specific genera were found to differ in abundance in individuals with LADA compared with T1D and T2D, indicating that LADA has unique taxonomical features. The virome composition reflected the stability of the most dominant order Caudovirales and the families Siphoviridae, Podoviridae, and Inoviridae, and the dominant family Microviridae. Further studies are needed to confirm these findings.

Value of serum osteoprotegerin in the assessment of endothelial dysfunction in obesity

ObjectiveOsteoprotegerin is a member of the tumor necrosis factor receptor superfamily. The study aimed to assess serum osteoprotegerin and endothelial dysfunction relationship in obese non-diabetic subjects. Elucidating the association linking serum osteoprotegerin level to obesity and insulin resistance.Materials and methodsSixty obese non-diabetic subjects attending the outpatient endocrine clinic were compared with 20 controls. All subjects went through history taking, clinical examination, and anthropometric measuring. Laboratory tests included fasting blood glucose, HbA1c, HOMA-IR, lipid profile, and serum osteoprotegerin level—assessment of endothelial dysfunction measured by carotid intimal thickening and flow meter dilatation.ResultsObese subjects had significantly higher rates of insulin resistance and dyslipidemia compared with controls (P = 0.017 and 0.002, respectively). Serum osteoprotegerin levels were significantly lower in obese subjects compared with controls (P = 0.011). In obese subjects, there was a significant positive correlation between osteoprotegerin and HOMA-IR (r = 0.272; P = 0.035), whereas there was no significant correlation between OPG and endothelial dysfunction.ConclusionThe study showed that osteoprotegerin significantly decreased in obese non-diabetic individuals in comparison with control subjects. A significant positive correlation between osteoprotegerin and HOMA-IR has been reported in obese non-diabetic subjects. OPG can be considered a serum biomarker to predict insulin resistance in obese individuals.

Evaluation of a Lipid Profile in Normoglycemic and Pre-diabetic Saudi Office Employees in Makka Region: A Case-Control Study.

Diabetes mellitus (DM) poses a significant health challenge worldwide. The impact of a sedentary lifestyle in predicting and managing complications of diabetes represents an urgent need for health strategies. The objective of this study was to evaluate the lipid profile among normoglycemic and prediabetic Saudi office workers. The research was a case-control study carried out in Makkah al-Mukarramah (Kingdom of Saudi Arabia, KSA).Seventy-five office worker volunteers between the ages of 19 and 45 years were recruited for the study. The participants were divided into two groups: a control group of non-diabetic normal subjects (NGT) and prediabetic subjects with impaired fasting plasma glucose and/or impaired glucose tolerance (IGT), based on the American Diabetes Association recommendations. Measurements of glucose, hemoglobin A1C (HbA1C), total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), and low-density lipoprotein (LDL) were performed using standard procedures and commercial kits. Statistical analysis was performed to compare the lipid profile in the two groups, and a P-value of <0.05 was considered statistically significant. A proportion (58.7%) of the office workers are prediabetics; prediabetic office workers had higher total cholesterol compared to the controlgroup (p < 0.05). Triglyceride levels were higher in office workers with prediabetes compared to the normoglycemic group (p < 0.05). LDL levels were elevated in the prediabetic office workerscompared to the control group (p < 0.05). Office employees with prediabetes exhibit elevated levels of cholesterol, triglycerides, and LDL. The disturbance in lipid profile may be linked to impaired glucose tolerance in individuals with a sedentary lifestyle, such as office workers.

Comparative assessment of the corneal endothelium following phacoemulsification surgery in patients with type II diabetes and nondiabetes

Abstract: PURPOSE: The purpose is to assess the corneal endothelial changes after phacoemulsification surgery in diabetic patients and compare with those of nondiabetic subjects. METHODS: The study compared the corneal endothelial changes in diabetics and nondiabetics after phacoemulsification surgery. The study population included 40 patients with diabetes mellitus with good glycemic control and 40 nondiabetic patients who underwent uneventful phacoemulsification surgery. Central corneal endothelial cell density (ECD), central corneal thickness (CCT), and percentage of hexagonality percentage coefficient of variation (%CV) were measured preoperatively and postoperatively (at 4 and 12 weeks) using a specular microscope. RESULTS: Mean ECD loss (%) was measured as 9.85% and 8.41% at 4 weeks and 12 weeks postoperatively in the diabetic group while ECD loss percentage was 7.09% and 5.74% in the control group at the same time intervals, respectively. Furthermore, a significant difference was noted on comparing mean ECD measurements between the two groups at the postsurgical visits (4 weeks and 12 weeks). While the CCT was found to be similar in both diabetic and nondiabetic patients, increase was observed in the values of (%CV in both the groups at postoperative 4 weeks’ and 12 weeks’ follow-up. The values of both %CV and percentage hexagonality showed statistically significant differences between the diabetic and nondiabetic group before surgery and at 4 weeks’ and 12 weeks’ postoperative examinations. CONCLUSION: The patients with diabetes suffered greater endothelial damage despite good glycemic control as compared to nondiabetic patients which indicates the necessity of far more care to protect cornea endothelium in patients with diabetes.

Ultrasound Assessment of Carotid Intima-Media Thickness: Comparison between Diabetes and Nondiabetes Subjects, and Correlation with Serum Vitamin D.

This multicenter cross-sectional study was performed on two groups of adults (nondiabetes and type 2 diabetes) of various ages, sexes, and body mass index (BMI). CIMT for each side was measured at three segments using high-resolution ultrasound, and the mean of both sides was determined. Comparison was made between each group, and the association of CIMT with each of age, sex, BMI, serum vitamin D status, smoking, and physical activity status was studied. The chi-square test was used to compare categorical data, and binary logistic regression was utilized to ascertain the relationship between CIMT and the study variables. A significant difference was observed between the CIMT of the diabetes and nondiabetes group, average CIMT was 0.82 ± 0.23 mm vs. 1.12 ± 0.24 mm for the nondiabetes and diabetes group, respectively, with P value <0.005. No significant correlation was observed between serum vitamin D level and CIMT neither in the study group as a whole nor in either subgroup; however, a significant association was observed between CIMT with each of age, sex, BMI, smoking, and physical activity status. Ultrasound is a sensitive tool for CIMT evaluation. Diabetes has a 5.4-fold higher risk of having high CIMT. Serum vitamin D level showed no significant influence on CIMT. Smoking, BMI, and physical activity are among the modifiable risk factors with significant influence on CIMT.

Efficacy of 1-hour postload plasma glucose as a suitable measurement in predicting type 2 diabetes and diabetes-related complications: A post hoc analysis of the 30-year follow-up of the Da Qing IGT and Diabetes Study.

To evaluate whether 1-hour plasma glucose (1hPG) can be a comparable measurement to 2-hour plasma glucose (2hPG) in identifying individuals at high risk of developing diabetes. A total of 1026 non-diabetic subjects in the Da Qing IGT and Diabetes Study were included and classified according to baseline postload 1hPG. The participants were followed up and assessed at 6-, 20- and 30year follow-up for outcomes including diabetes, all-cause and cardiovascular mortality, cardiovascular disease (CVD) events, and microvascular disease. We then conducted a proportional hazards analysis in this post hoc study to determine the risks of developing type 2 diabetes and its complications in a '1hPG-normal' group (1hPG <8.6 mmol/L) and a '1hPG-high' group (≥8.6 mmol/L). The predictive values of 1hPG and 2hPG were evaluated using a time-dependent receiver-operating characteristic (ROC) curve. Compared with the 1hPG-normal group, the 1hPG-high group had increased risk of diabetes (hazard ratio [HR] 4.45, 95% CI 3.43-5.79), all-cause mortality (HR 1.46, 95% CI 1.07-2.01), CVD mortality (HR 1.84, 95% CI 1.16-2.95), CVD events (HR 1.39, 95% CI 1.03-1.86) and microvascular disease (HR 1.70, 95% CI: 1.03-2.79) after adjusting for confounders. 1hPG exhibited a higher area under the ROC curve (AUC) for predicting diabetes than 2hPG during the long-term follow-up (AUC [1hPG vs. 2hPG]: 10 years: 0.86 vs. 0.84, p = 0.08; 20 years: 0.88 vs. 0.87, p = 0.04; 30 years: 0.85 vs. 0.82, p = 0.009). Elevated 1hPG level (≥8.6 mmol/L) was associated with increased risk of developing type 2 diabetes and its long-term complications, and could be considered as a suitable measurement for identifying individuals at high risk of type 2 diabetes.

Assessment of Serum Lipoprotein(a) Status in Type 2 Diabetes Mellitus

Introduction: Lipoprotein (a) is made up of an atherogenic LDL lipoparticle and a potentially thrombogenic apoprotein a and is therefore responsible for cardiovascular disease. The objective of this study is to evaluate serum lipoprotein (a) status and to investigate the correlation of elevated serum lipoprotein (a) levels with other cardiovascular risk factors in type 2 diabetics.&#x0D; Materials and Methods: This is a case-control study involving 82 patients, 37 type 2 diabetic patients and 45 non-diabetic control subjects. Sociodemographic data were collected and each patient underwent routine lipid assessment and lipoprotein (a) testing.&#x0D; Results: The prevalence of hyperlipoproteinemia (a) is 17.8% in control subjects and 29.7% in type 2 diabetics. HDL cholesterolemia is significantly higher in controls than in type 2 diabetics (p =0.028) while LDL cholesterol and serum lipoprotein (a) levels are higher in type 2 diabetics than in controls with a statistically significant difference (p=0.025 and p=0.026 respectively). The mean lipoprotein (a) values ​​of 0.36±0.34 g/l in women are higher than those of male subjects which are 0.28±0.20 g/l (p=0.171). Mean serum lipoprotein (a) levels of 0.39±0.32 g/l in type 2 diabetics are significantly higher than those of controls which are 0.25±0.21 g/l (p= 0.026). Plasma concentrations of lipoprotein (a) vary with age and appear to be increased beyond the age of 45. There is no correlation between lipoprotein (a) and other cardiovascular risk factors.&#x0D; Conclusion: Hyperlipoproteinemia (a) is common in type 2 diabetics and women have the highest plasma levels. Serum lipoprotein (a) concentrations are not correlated with other cardiovascular risk factors and therefore constitute an independent risk factor.

A Prospective 1-Year Follow-up of Glycemic Status and C-Peptide Levels of COVID-19 Survivors with Dysglycemia in Acute COVID-19 Infection.

We evaluated changes in glycemic status, over 1 year, of coronavirus disease 2019 (COVID-19) survivors with dysglycemia in acute COVID-19. COVID-19 survivors who had dysglycemia (defined by glycosylated hemoglobin [HbA1c] 5.7% to 6.4% or random glucose ≥10.0 mmol/L) in acute COVID-19 were recruited from a major COVID-19 treatment center from September to October 2020. Matched non-COVID controls were recruited from community. The 75-g oral glucose tolerance test (OGTT) were performed at baseline (6 weeks after acute COVID-19) and 1 year after acute COVID-19, with HbA1c, insulin and C-peptide measurements. Progression in glycemic status was defined by progression from normoglycemia to prediabetes/diabetes, or prediabetes to diabetes. Fifty-two COVID-19 survivors were recruited. Compared with non-COVID controls, they had higher C-peptide (P< 0.001) and trend towards higher homeostasis model assessment of insulin resistance (P=0.065). Forty-three COVID-19 survivors attended 1-year reassessment. HbA1c increased from 5.5%±0.3% to 5.7%±0.2% (P<0.001), with increases in glucose on OGTT at fasting (P=0.089), 30-minute (P=0.126), 1-hour (P=0.014), and 2-hour (P=0.165). At baseline, 19 subjects had normoglycemia, 23 had prediabetes, and one had diabetes. Over 1 year, 10 subjects (23.8%; of 42 non-diabetes subjects at baseline) had progression in glycemic status. C-peptide levels remained unchanged (P=0.835). Matsuda index decreased (P=0.007) and there was a trend of body mass index increase from 24.4±2.7 kg/m2 to 25.6±5.2 (P=0.083). Subjects with progression in glycemic status had more severe COVID-19 illness than non-progressors (P=0.030). Reassessment was not performed in the control group. Subjects who had dysglycemia in acute COVID-19 were characterized by insulin resistance. Over 1 year, a quarter had progression in glycemic status, especially those with more severe COVID-19. Importantly, there was no significant deterioration in insulin secretory capacity.

ANGPTL3 is a novel HDL component that regulates HDL function

BackgroundAngiopoietin-like protein 3 (ANGPTL3) is secreted by hepatocytes and inhibits lipoprotein lipase and endothelial lipase activity. Previous studies reported the correlation between plasma ANGPTL3 levels and high-density lipoprotein (HDL). Recently ANGPTL3 was found to preferentially bind to HDL in healthy human circulation. Here, we examined whether ANGPTL3, as a component of HDL, modulates HDL function and affects HDL other components in human and mice with non-diabetes or type 2 diabetes mellitus.MethodsHDL was isolated from the plasma of female non-diabetic subjects and type-2 diabetic mellitus (T2DM) patients. Immunoprecipitation, western blot, and ELISA assays were used to examine ANGPTL3 levels in HDL. Db/m and db/db mice, AAV virus mediated ANGPTL3 overexpression and knockdown models and ANGPTL3 knockout mice were used. The cholesterol efflux capacity induced by HDL was analyzed in macrophages preloaded with fluorescent cholesterol. The anti-inflammation capacity of HDL was assessed using flow cytometry to measure VCAM-1 and ICAM-1 expression levels in TNF-α-stimulated endothelial cells pretreated with HDL.ResultsANGPTL3 was found to bind to HDL and be a component of HDL in both non-diabetic subjects and T2DM patients. Flag-ANGPTL3 was found in the HDL of transgenic mice overexpressing Flag-ANGPTL3. ANGPLT3 of HDL was positively associated with cholesterol efflux in female non-diabetic controls (r = 0.4102, p = 0.0117) but not in female T2DM patients (r = − 0.1725, p = 0.3224). Lower ANGPTL3 levels of HDL were found in diabetic (db/db) mice compared to control (db/m) mice and were associated with reduced cholesterol efflux and inhibition of VCAM-1 and ICAM-1 expression in endothelial cells (p < 0.05 for all). Following AAV-mediated ANGPTL3 cDNA transfer in db/db mice, ANGPTL3 levels were found to be increased in HDL, and corresponded to increased cholesterol efflux and decreased ICAM-1 expression. In contrast, knockdown of ANGPTL3 levels in HDL by AAV-mediated shRNA transfer led to a reduction in HDL function (p < 0.05 for both). Plasma total cholesterol, total triglycerides, HDL-c, protein components of HDL and the cholesterol efflux function of HDL were lower in ANGPTL3−/− mice than ANGPTL3+/+ mice, suggesting that ANGPTL3 in HDL may regulate HDL function by disrupting the balance of protein components in HDL.ConclusionANGPTL3 was identified as a component of HDL in humans and mice. ANGPTL3 of HDL regulated cholesterol efflux and the anti-inflammatory functions of HDL in T2DM mice. Both the protein components of HDL and cholesterol efflux capacity of HDL were decreased in ANGPTL3−/− mice. Our findings suggest that ANGPTL3 in HDL may regulate HDL function by disrupting the balance of protein components in HDL. Our study contributes to a more comprehensive understanding of the role of ANGPTL3 in lipid metabolism.

Oral Lesions and Oral Health-Related Quality of Life in Adult Patients with Psoriasis: A Retrospective Chart Review.

Psoriasis is a widespread chronic inflammatory skin disease, that negatively affects physical and emotional well-being and quality of life, as shown by the generally low Dermatology Life Quality Index (DLQI). Psoriasis is burdened by associated comorbidities and some patients manifest concurrent oral lesions, although the existence of oral psoriasis remains controversial. Psoriasis-specific and nonspecific oral lesions and Oral Health-Related Quality of Life (OHRQoL), self-assessed using the Oral Health Impact Profile-14 (OHIP-14) questionnaire, were retrospectively reviewed in adult untreated psoriasis patients with ≥15 teeth, who were non-smokers and had no dental or periodontal infections. Sample (age, gender, comorbidities) and descriptive variables (Body Surface Area-BSA, Psoriasis Area and Severity Index-PASI, Dermatology Life Quality Index-DLQI, severity of psoriasis, distribution of lesions and predominant involvement, years since diagnosis) were correlated with DLQI and OHIP-14 and compared by baseline DLQI and OHRQoL classes. Charts from 90 participants were included. No oral lesions were detected, and excellent/good OHRQoL was found in 94% of the participants. DLQI scores displayed positive significant associations with PASI and BSA, while OHIP-14 with hypertension and IMID, and age. PASI and BSA were significantly higher in participants with DLQI > 10 and also differed significantly among OHQRoL ranks, as well as mucosal involvement and comorbidities. Specifically, among subjects revealing an Excellent OHQRoL, 92.6% were non-IMID, 75% non-hypertensive, 89.7% non-diabetic subjects, 86.8% of non CVD-subjects.

The role of telomerase reverse transcriptase in the mitochondrial protective functions of Angiotensin-(1–7) in diabetic CD34+ cells

Angiotensin (Ang)-(1–7) stimulates vasoprotective functions of diabetic (DB) CD34+ hematopoietic stem/progenitor cells partly by decreasing reactive oxygen species (ROS), increasing nitric oxide (NO) levels and decreasing TGFβ1 secretion. Telomerase reverse transcriptase (TERT) translocates to mitochondria and regulates ROS generation. Alternative splicing of TERT results in variants α-, β- and α-β-TERT, which may oppose functions of full-length (FL) TERT. This study tested if the protective functions of Ang-(1–7) or TGFβ1-silencing are mediated by mitoTERT and that diabetes decreases FL-TERT expression by inducing splicing.CD34+ cells were isolated from the peripheral blood mononuclear cells of nondiabetic (ND, n = 68) or DB (n = 74) subjects. NO and mitoROS levels were evaluated by flow cytometry. TERT splice variants and mitoDNA-lesions were characterized by qPCR. TRAP assay was used for telomerase activity. Decoy peptide was used to block mitochondrial translocation (mitoXTERT).TERT inhibitor or mitoXTERT prevented the effects of Ang-(1–7) on NO or mitoROS levels in DB-CD34+ cells. FL-TERT expression and telomerase activity were lower and mitoDNA-lesions were higher in DB cells compared to ND and were reversed by Ang-(1–7) or TGFβ1-silencing. The prevalence of TERT splice variants, with predominant β-TERT expression, was higher and the expression of FL-TERT was lower in DB cells (n = 25) compared to ND (n = 30). Ang-(1–7) or TGFβ1-silencing decreased TERT-splicing and increased FL-TERT. Blocking of β-splicing increased FL-TERT and protected mitoDNA in DB-cells.The findings suggest that diabetes induces TERT-splicing in CD34+ cells and that β-TERT splice variant largely contributes to the mitoDNA oxidative damage.

Assessment of hepatic fibrosis with non-invasive indices in subjects with diabetes before and after liver transplantation.

One of the most common complications of cirrhosis is diabetes, which prevalence is strictly related to severity of hepatopathy. Actually, there are no data on the persistence of post-transplant glucose abnormalities and on a potential impact of diabetes on development of fibrosis in the transplanted liver. To this aim, we evaluated liver fibrosis in cirrhotic subjects before and after being transplanted. The study included 111 individuals who had liver transplantation. The assessment was performed before and two years after surgery to investigate a potential impact of the persistence of diabetes on developing de novo fibrosis in the transplanted liver. The degree of fibrosis was assessed using the Fibrosis Index Based on 4 Factors (FIB-4) and the Aspartate to Platelet Ratio Index (APRI). At pre-transplant evaluation, 63 out of 111 (56.8%) subjects were diabetic. Diabetic subjects had higher FIB-4 (Geometric mean, 95% confidence interval: 9.74, 8.32-11.41 vs 5.93, 4.71-7.46, P<0.001) and APRI (2.04, 1.69-2.47 vs 1.18, 0.90-1.55, P<0.001) compared to non-diabetic subjects. Two years after transplantation, 39 out of 111 (35.1%) subjects remained with diabetes and continued to show significantly higher FIB-4 (3.14, 2.57-3.82 vs 1.87, 1.55-2.27, P<0.001) and APRI (0.52, 0.39-0.69 vs 0.26, 0.21-0.32, P<0.001) compared to subjects without diabetes. Thus, persistence of diabetes after surgery is a possible risk factor for an evolution to fibrosis in the transplanted liver, potentially leading to worsened long-term outcomes in this population.

High-protein, low glycemic index snack from optimized blend of three wholegrains exhibits nutraceutical quality and elicits low glycemic response in diabetic human subjects

Snack products are evolving as new carriers of functional ingredients with nutritional and health-promoting benefits. A blend of whole grains is increasingly being utilized to harness the functional potential of the grain mix. Amaranth, acha, and pearl millet grains flours were optimized using response surface methodology (RSM), to obtain optimum blends (90:5:5 and 47.98:26.68:25.34) with high protein content and low glycemic index. Snack bar products from the blends were labelled MBY and MBZ. A total of 40 diabetic and 10 non-diabetic subjects were recruited. Of the diabetic, about 42% were overweight while 40% were obese, the non-diabetic had normal weights. Each was allowed to consume snacks containing the equivalent of 50 g of carbohydrates. Finger prick was employed to evaluate the postprandial glucose response of snack products while venous blood was evaluated for antioxidant enzymes, carbohydrate-hydrolyzing activities, and insulin using standard methods. Consumption of the multigrain snacks elicited a stable postprandial response (133–141 mg/dL) with 16 and 24% postprandial decline. In addition, snacks had low to intermediate glycemic index (52 and 56) in diabetic and low glycemic index (43 and 45) in non-diabetics; likewise reduced α-amylase/α-glucosidase activities compared to control snacks. Similarly, glutathione level, glutathione peroxidase, superoxide dismutase, and catalase activities in serum from subjects that consumed multigrain snacks were upregulated compared to control and market sample groups. Moreso, snack products promoted a reduction in serum insulin levels in diabetic subjects (45 and 17% for MBY and MBZ respectively). Following the nutraceutical properties displayed by the formulated snack especially MBY, it can be promoted as a functional snack for the management of diabetes while solving the limited snack product choice of diabetes sufferers.Graphical

Determinants of Vitamin D deficiency among type 2 diabetes mellitus patients: A retrospective study.

Recent studies have shown an association between vitamin D deficiency (VDD) and type 2 diabetes mellitus patients (T2DM), but the precise relationship between these conditions has yet to be clarified. In this study, we aimed to estimate the incidence of VDD among diabetic patients and identify any relationship between diabetes and the determinants of VDD among T2DM individuals. A retrospective cross-sectional study was conducted at King Abdulaziz University Hospital, Jeddah, Saudi Arabia. Patients of either gender were selected from electronic records and checked for vitamin D levels, glycosylated hemoglobin (HbA1c), and other parameters. A total of 864 subjects were enrolled. Subjects were grouped according to HbA1c levels, with < 5.7%, 5.7% to 6.49%, and > 6.5% considered normal, impaired, and diabetic, respectively. VDD was common, with an incidence of 723 (83.7%) subjects. A significantly lower vitamin D level was found in diabetic subjects than in nondiabetic subjects (29.1 ± 12.0 vs 44.0 ± 28.3, P < .001). A total of 207/209 (99%) subjects with impaired HbA1c and 179/183 (97.8%) people with diabetes had VDD. Interestingly, none of the diabetic or impaired HbA1c subjects had normal vitamin D levels. A significant association was found between VDD and being > 50 years old, overweight, or obese, as well as HbA1c, fasting plasma glucose, calcium, and total cholesterol (TC) levels. A high rate of VDD and significantly lower vitamin D levels were found in diabetic subjects. Age, being overweight, obesity, HbA1c, and fasting plasma glucose were the few determinants of VDD among T2DM patients. These findings highlight the importance of addressing vitamin D status in managing and preventing T2DM, particularly in those over the age of 50, those who have higher body weight, and those with raised HbA1c and fasting plasma glucose levels.