Protection of ß-pancreatic cells from dysfunctionality of insulin using vitexin by apoptosis of INS-1 cells.

AIMS: This study was performed to explore the possible beneficial effects of vitexin on high glucose (HG)-induced cytotoxicity in pancreatic ß-cells. METHODS: INS-1 pancreatic ß-cell line has used this study. HG-induced (33 Mm) exposed INS-1 cell death; the apoptosis INS-1 cells treated vitexin 10, 20, 40, and 80 µg/mL for 24 hours. The anti-apoptosis properties were evaluated by MTT assay, glucose-stimulated insulin secretion assay, biochemical assay, annexin-V-FITC staining and western blot analysis. RESULTS: These findings demonstrate that vitexin treatment improved the HG-exposure, reduced the INS-1 cell viability and significantly enhanced glucose-stimulated insulin secretion in a dose-dependent manner. The antioxidant studies revealed that vitexin treatment significantly decreased lipid peroxidation and reactive oxygen species and increased antioxidant level of INS-1 cell line in 24 hrs. The findings of the study suggested that in the vitexin treatment group, pancreatic apoptosis and Bax protein expression reduced significantly. At the same time, Bcl-2 protein expression increased, and NF-κB protein in HG-induced INS-cells was inhibited. CONCLUSION: Therefore, our results suggest that vitexin can be successfully used to regulate the expression of Bcl-2 family proteins, reduce lipid peroxidation and to improve the secretion of antioxidants in pancreatic ß-cell lines.

Aptamer-17ß-estradiol-antibody sandwich ELISA for determination of gynecological endocrine function.

17ß-Estradiol-E2 (17ß-E2) is a steroid hormone that plays a major role in the reproductive endocrine system and is involved in various processes, such as pregnancy, fertility, and menopause. In this study, the performance of an enzyme-linked immunosorbent assay (ELISA) for 17ß-E2 quantification was enhanced by using a gold nanoparticle (GNP)-conjugated aptamer. An anti-17ß-E2-aptamer-GNP antibody was immobilized on an amine-modified ELISA surface. Then, 17ß-E2 was allowed to interact with and be sandwiched by antibodies. Aptamer-GNP conjugation was confirmed by colorimetric assays via the naked eye and UV-visible light spectroscopy. The detection limit based on a signal-to-noise ratio (S/N) of 3 was estimated to be 1.5 nM (400 pg/mL), and the linear range was 1.5-50 nM. Control experiments (without 17ß-E2/with a complementary aptamer sequence/with a nonimmune antibody) confirmed the specific detection of 17ß-E2. Moreover, 17ß-E2 spiking of human serum did not interrupt the interaction between 17ß-E2 and its antibody and aptamer. Thus, the developed ELISA can be used as an alternate assay for quantification of 17ß-E2 and assessment of endocrine-related gynecological problems.

The effect of Bertholletia excelsa on body weight, cholestrol, and c-reactive protein: A systematic review and meta-analysis of randomized controlled trials.

BACKGROUND & OBJECTIVE(S): Bertholletia excelsa is a rich herbal source of anti-oxidants and phenols. The goal of this study is to evaluation the effect of bertholletia excelsa nut on body weight, C-reactive protein (CRP) and lipid profile. METHODS: A literature search was conducted in PubMed, Scopus and Web of sciences databases by two reviewers up to October 2019. Random effect model used to combine results. RESULTS: Six studies included in analysis with 71 participants. The population was public population. Pooled results showed Bertholletia excelsa have reduction effect on triglyceride weighted mean difference (WMD: -8.23 mg/dl, 95 % CI -15.09, -1.38, I² = 0%), Cholesterol (WMD: -14.31 mg/dl, 95 % CI -23.38, -5.24, I² = 47 %), Low-density lipoprotein (LDL) (WMD: -9.27 mg/dl, 95 % CI -13.48, -5.06, I² = 0%). CONCLUSION: This study provided an evidence that Bertholletia excelsa nuts have reduction effect on triglyceride, cholesterol, and LDL levels.

An experimental study of exenatide effects on renal injury in diabetic rats1.

PURPOSE: To investigate the effects of exenatide on renal injury in streptozotocin-induced diabetic rats. METHODS: Fifty SD rats were randomly divided into normal control, model, exenatide-1, exenatide-2 and exenatide-3 groups, 10 rats in each group. The diabetic nephropathy model was constructed in later 4 groups. Then, the later 3 groups were treated with 2, 4 and 8 µg/kg exenatide for 8 weeks, respectively. The serum and urine biochemical indexes and oxidative stress and inflammatory indexes in renal tissue were determined. RESULTS: Compared to the model group, in exenatide-3 group the serum fasting plasma glucose and hemoglobin A1c levels were significantly decreased, the fasting insulin level was significantly increased, the renal index and blood urea nitrogen, serum creatinine and 24 h urine protein levels were significantly decreased, the renal tissue superoxide dismutase and glutathione peroxidase levels were significantly increased, the malondialdehyde level was significantly decreased, and the renal tissue tumor necrosis factor alpha, interleukin 6, hypersensitive C-reactive protein and chemokine (C-C motif) ligand 5 levels were significantly decreased P<0.05). CONCLUSIONS: Exenatide can mitigate the renal injury in diabetic rats. The mechanisms may be related to its resistance of oxidative stress and inflammatory response in renal tissue.

An experimental study of exenatide effects on renal injury in diabetic rats

Abstract Purpose: To investigate the effects of exenatide on renal injury in streptozotocin-induced diabetic rats. Methods: Fifty SD rats were randomly divided into normal control, model, exenatide-1, exenatide-2 and exenatide-3 groups, 10 rats in each group. The diabetic nephropathy model was constructed in later 4 groups. Then, the later 3 groups were treated with 2, 4 and 8 μg/kg exenatide for 8 weeks, respectively. The serum and urine biochemical indexes and oxidative stress and inflammatory indexes in renal tissue were determined. Results: Compared to the model group, in exenatide-3 group the serum fasting plasma glucose and hemoglobin A1c levels were significantly decreased, the fasting insulin level was significantly increased, the renal index and blood urea nitrogen, serum creatinine and 24 h urine protein levels were significantly decreased, the renal tissue superoxide dismutase and glutathione peroxidase levels were significantly increased, the malondialdehyde level was significantly decreased, and the renal tissue tumor necrosis factor alpha, interleukin 6, hypersensitive C-reactive protein and chemokine (C-C motif) ligand 5 levels were significantly decreased P<0.05). Conclusions: Exenatide can mitigate the renal injury in diabetic rats. The mechanisms may be related to its resistance of oxidative stress and inflammatory response in renal tissue.

An insight into the key genes and biological functions associated with insulin resistance in adipose tissue with microarray technology.

In the present study, the key genes and biological functions associated with insulin resistance were investigated by comparing the gene expression profiles of adipose tissue obtained from insulin­sensitive and insulin­resistant patients. The gene expression data set GSE20950 was downloaded from the Gene Expression Omnibus, including 39 adipose tissue samples obtained from insulin­sensitive and insulin­resistant patients undergoing gastric bypass surgery. Adipose samples were divided into two groups (the insulin­sensitive and insulin­resistant groups) and the differentially expressed genes (DEGs) were screened out with packages of R. The interactions among DEGs were retrieved with Osprey and functional enrichment analysis was performed with the WebGestalt system. Information regarding the interaction network and enriched biological functions was combined to construct a functional interaction network. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was then conducted using the Database for Annotation, Visualization and Integrated Discovery. A total of 170 DEGs were detected in the insulin­sensitive group, 8 downregulated and 162 upregulated. Response to glucose stimulus was the most significantly over­represented functional term. The focal adhesion pathway was identified to be significant in the genes of the functional interaction network. The present study revealed key biological functions and DEGs in adipose tissues associated with insulin resistance, which may facilitate the development of novel therapies for insulin resistance and diabetes.

Longitudinal study of diffusion tensor imaging properties of affected cortical spinal tracts in acute and chronic hemorrhagic stroke.

This study investigated the clinical value of diffusion tensor imaging (DTI) in predicting the motor outcome in patients with basal ganglia hemorrhage. This prospective study included 23 patients assessed with DTI to measure the fractional anisotropy (FA) value in affected cortical spinal tract (CST) at three time points: day 0, day 30 and day 90 after onset. The motor function score (MFS) was applied to evaluate motor function and patients were divided into good and poor outcome groups according to the MFS on day 90. The mean FA value on day 0 was significantly lower in the poor outcome group than in the good outcome group (p<0.01). FA value gradually decreased in the poor outcome group until day 90 after onset, while it continuously increased in the good outcome group. The MFS obtained at day 90 after onset was significantly correlated with the initial FA value in the affected cerebral peduncle (r=-0.926, p<0.01). Receiver operating characteristic curve analysis showed that the FA value on day 0 could predict motor function outcome with a sensitivity of 88.89% and specificity of 92.86% at the initial FA value of 0.45. The FA value of affected CST in acute cerebral hemorrhage may valuably predict the motor function outcome and its dynamic change may represent the Wallerian degeneration in motor tracts after hemorrhagic stroke.

Serum lycopene levels in patients with diabetic retinopathy.

PURPOSE: Accumulating evidence indicates that oxidative stress may play an important role in the pathogenesis of type 2 diabetes and its complications. Lycopene, a very potent antioxidant of carotenoids, has received considerable scientific interest in recent years for its potential role in the prevention of oxidative stress-related chronic diseases. This study was undertaken to investigate whether the serum levels of lycopene are altered between type 2 diabetic patients with and without diabetic retinopathy. METHODS: A total of 71 patients with type 2 diabetes were analyzed and compared with 23 nondiabetic healthy controls. Serum lycopene concentrations were assayed using high-performance liquid chromatography. RESULTS: Lycopene level was found to be significantly lower in diabetic patients than in controls (p = 0.021). In the diabetic group, subjects with proliferative diabetic retinopathy had significantly lower lycopene levels than subjects without diabetic retinopathy or with nonproliferative diabetic retinopathy. In the analysis of correlations, hemoglobin A1c were negatively correlated with lycopene (r = -0.345, p = 0.007) after multivariate adjustment. A stepwise linear multiple regression model revealed that age and hemoglobin A1c were significant determinants of lycopene. CONCLUSIONS: Our findings show that measuring serum lycopene is a novel convenient method for evaluating oxidative damage. Diabetic patients, especially those with advanced diabetic retinopathy, had significantly lower serum lycopene levels; this suggests that lycopene may be helpful for the diagnosis, severity, and therapeutic evaluation of diabetic retinopathy.

Intensive therapy for diabetes through influence on innate immune system.

Steno-2 Study has previously shown that original intensive therapy reduced the risk of cardiovascular and microvascular events to about 50% of that of conventional treatment in type 2 diabetic patients. Further, in the subsequent follow-up study, intensive therapy was found to have sustained beneficial effects on cardiovascular events and death rate in this population. Another clinical trial, China Da Qing Diabetes Prevention Study, has recently reported that group-based lifestyle interventions over six years could prevent or delay the development of diabetes in patients with impaired glucose tolerance (IGT). The two famous intervention trials have demonstrated a consistent salutary effect of intensive therapy on the development and progression of diabetes and its complications. However, the exact mechanisms of the sustained beneficial effects remain to be elusive. There is a growing body of evidence to suggest that type 2 diabetes is associated with a general activation of the innate immune system, in which there is a chronic, cytokine-mediated state of low-grade inflammation. Some diabetic treatment agents with anti-inflammatory properties may lower both acute-phase reactants which are components of the innate immune system independent of their anti-hyperglycemic actions or lipid-lowering effects. The immunomodulatory effects of regular exercise, and in particular resistance training, may have positive effects on innate immunity and so may provide benefits for the profile of type 2 diabetes in addition to improving strength and functional abilities. Therefore, we speculate that the effects on the innate immune system through pharmacologic therapy or lifestyle modification such as exercise training are able to account - at least amongst others - for carry-over beneficial effects of multifactorial intervention on insulin resistance and type 2 diabetes. This hypothesis, if proved to be valid, might provide a new therapeutic option for the management of type 2 diabetes.