The International Journal of Romanian Society of Endocrinology / Registered in 1938

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  • Perspectives

    Zhu FF, Yang LZ

    Bioinformatic Analysis Identifies Potentially Key Differentially Expressed Genes and Pathways in Orbital Adipose Tissues of Patients with Thyroid Eye Disease

    Acta Endo (Buc) 2019 15(1): 1-8 doi: 10.4183/aeb.2019.1

    Context. Thyroid eye disease (TED), an orbital inflammatory status, generally occurred in Graves’ disease. Objective. This study aimed to acquire further insight into molecular mechanisms of TED, especially several key involved genes and pathways. Design. The microarray dataset GSE58331 including expression data for orbital adipose tissue samples, isolated from TED patients and normal controls, was downloaded from a publicly accessible Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified from 23 adipose tissues of TED patients versus 20 samples from normal controls. Subjects and Methods. A protein-protein interaction network of DEGs was constructed by using Search Tool for the Retrieval of Interacting Genes and Cytoscape 3.6.0. Several hub genes/proteins were extracted from the proteinprotein interaction network based on connectivity degree. Furthermore, we used the iRegulon plugin of Cytoscape3.6.0 to predict the transcription factors (TFs). Results. A total of 678 DEGs (538 up- and 140 down-regulated genes) were identified in TED patients. Proopiomelanocortin (POMC), interleukin 2 (IL-2), G protein subunit gamma 3 (GNG3), CXC motif chemokine receptor 4 (CXCR4), toll like receptor 4 (TLR4), colony stimulating factor 1 receptor (CSF1R), lysophosphatidic acid receptor 3 (LPAR3), CXC motif chemokine ligand-8 (CXCL8), etc., were considered as the hub genes among the DEGs. There were 6 TFs predicted to be differentially expressed in regulating the DEGs related to TED. A total of 71 DEGs had been reported to be associated with TED in the Comparative Toxicogenomics Database. Conclusions. Through this analysis, we have identified plenty of potential biomarkers and pathways which may have an important role in the pathogenesis of TED. However, these findings require verification by more detailed future experimental studies.
  • General Endocrinology

    Lu YL, L. Ye, H. Wu, F.Z. Xia, J. Yu, Yang LZ

    The up-regulated expression of both phospholipase A2 and cyclooxygenase-2 is involved in renal injury in streptozotocin-induced diabetic rats

    Acta Endo (Buc) 2013 9(1): 23-32 doi: 10.4183/aeb.2013.23

    Context. Recent evidence has stressed that many proinflammatory factors are particularly conducive to the progression of diabetic nephropathy, but the mechanisms underlying the changes are poorly understood. Objective. The purpose of this study was to investigate if up-regulated expression of both phospholipase A2 (PLA2) and cyclooxygenase-2 (COX-2) is involved in renal damage and micro-inflammatory state in streptozotocin-induced diabetic rats. Animals and methods. Sixteen Sprague Dawley rats were randomly divided into 2 groups: control group and diabetes group. Animals in diabetes group were treated with intraperitoneal injection of streptozotocin. Eight weeks later, rat renal tissue was studied with light and transmission electron microscopes, and PLA2 and COX-2 and their mRNA expression were examined by immunohistochemistry and reverse transcription polymerase chain reaction, respectively. Results. The renal pathological lesions in diabetes group were obvious, including increased amounts of mesangial matrix, thickening of the glomerular and tubular basement membranes and fusion and effacement of the adjacent podocyte foot processes. Infiltrating inflammatory cells were observed in the tubules. Compared with control group, the expression of cytosolic PLA2 and COX-2 was significantly increased in diabetes group. Conclusions. It uncovers that the PLA2-COX-2 pathway may lead to renal inflammation associated with renal damage in streptozotocin- induced diabetic rats.
  • General Endocrinology

    Wen F, Yang Y, Sun C, Fang H, Nie L, Li L, Liu Y, Yang Z

    Resistin Inhibits Glucose-Stimulated Insulin Secretion through miR-494 by Target on STXBP5

    Acta Endo (Buc) 2017 13(1): 32-39 doi: 10.4183/aeb.2017.32

    Aims. Resistin has been reported to impair the pancreatic beta cells and associated with insulin resistance. MicroRNAs (miRNAs) are short, endogenously produced non-coding ribonucleotides that bind mRNAs and function mainly as negative regulators in mammals. MiRNAs have been implicated in many diseases, including insulin resistance and diabetes. A considerable body of evidence has indicated an important function for miRNAs in insulin secretion. The current study was designed to investigate the effects of miR-494 in the reductions in insulin secretion attributable to resistin. Methods. Insulin secretion was determined by ELISA, and expressions of genes were identified using quantitative RT-PCR (qRT-PCR) or Western blot analysis. Results. Insulin secretion was significantly reduced by resistin. Overexpression of miR-494 inhibited insulin secretion both in diet culture and high glucose medium in MIN6 cell lines. MiR-494 down-regulated the protein level of STXBP5 by pairing with sites in the 3′UTR. Conclusion. miR-494 is involved in the insulin secretion regulated by resistin via its effects on STXBP5 in MIN6 cells.
  • Endocrine Care

    Li Q, Yang LZ

    Hemoglobin A1c Level Higher Than 9.05% Causes a Significant Impairment of Erythrocyte Deformability in Diabetes Mellitus

    Acta Endo (Buc) 2018 14(1): 66-75 doi: 10.4183/aeb.2018.66

    Context. Clinical studies demonstrated erythrocyte deformability (ED) is impaired in diabetic patients and described the correlations between HbA1c and ED. Few studies further investigated what an exact elevated HbA1c level linked to the impairment of ED in diabetes. Objective. This study was to determine a cut-off point of HbA1c level leading to the impairment of ED in patients with diabetes. Design. This was a retrospective observational study. ROC curve analysis was used to determine an optimal cut-off value of HbA1c for the increasing HSRV. Subjects and Methods. In this study, 300 type 2 diabetic patients were enrolled. The whole blood viscosity was measured. High shear reductive viscosity (HSRV) was used to indirectly estimate ED. Based on the obtained cut-off value and glycemic control criteria for HbA1c, we divided all the cases into different groups to further confirm the accuracy of the cut-off value. Results. In 300 patients, ROC curve illustrated that 9.05% was the optimal cut-off value as a predictor of the increasing HSRV. And higher odds ratio (OR) for significant decrease in ED was seen in the patients with HbA1c >9.05% compared to those with HbA1c≤9.05% (OR: 3.78, 95% CI: 2.08-6.87). HSRV increased significantly in patients with HbA1c level >9.05% in comparison to patients with HbA1c levels <6.5% between 6.5 and 8.0% and between 8.0 and 9.05%. Conclusion. ED decreased significantly in diabetic patients as soon as HbA1c level was higher than 9.05%.
  • General Endocrinology

    Yang YS, Chan KC, Wang CJ, Peng CH, Huang CN

    Vascular Smooth Muscle Cell Proliferation and Migration Induced by Oleic Acid, a Mechanism Involving Connective Tissue Growth Factor Signals

    Acta Endo (Buc) 2015 11(2): 162-169 doi: 10.4183/aeb.2015.162

    The aim of this study was to examine the highglucose and high fatty acid status effect on the development of atherosclerosis. Materials and Methods. We used rat thoracic aorta smooth muscle cell line A7r5. We investigated mechanisms underlying high-glucose and high fatty acid (oleic acid) conditions on vascular smooth muscle cell (VSMC) mimicking concurrent status of diabetes and dyslipidemia. Results. Glucose-oleic acid stimulated cell proliferation and migration while the proliferating cell nuclear antigen (PCNA) level and matrix metalloproteinase (MMP)-2 were activated. In addition, the expressions of connective tissue growth factor (CTGF) and fatty acid synthase (FASN) enhanced by glucose-oleic acid were increased. The proliferation signal mediated by glucoseoleic acid condition was demonstrated via CTGF/FASN, while MMP-2 was regulated by CTGF but not FASN. Conclusion. Oleic acid in the presence of high glucose level can induce VSMC proliferation and migration leading to diabetes-associated vascular atherosclerosis. Furthermore, via activation of CTGF, increased expression of FASN suggested a possibility of lipogenesis in VSMC which may also contribute to diabetes-associated vascular atherosclerosis.
  • General Endocrinology

    Wen F, Zhou L, Wu X, Xia S, Sun C, Yang Z

    Characterization of mIRNA and mRNA Expression Profiles in Normal and Resistin-Treated Mouse Liver by Microarray

    Acta Endo (Buc) 2015 11(3): 284-293 doi: 10.4183/aeb.2015.284

    Aims. To investigate the changes in the miRNAs and mRNAs expressed in the liver upon induction of “hyperresistinemia”. Methods. We identified mRNA and miRNAs that were differentially expressed between normal and resistin-treated liver tissue using microarrays. Expression was validated using quantitative RT-PCR (qRT-PCR). The putative targets and pathways of the differentially expressed miRNAs and mRNAs were investigated, respectively, using various computational algorithms. In addition, the interactions between differentially expressed miRNAs and mRNAs were analyzed. Results. After the filtration of the signals below the threshold level, we identified 34 miRNAs and 875 genes with expression levels different by more than 1.5-fold and 2.0-fold, respectively, between the two groups. These observations were confirmed by qRT-PCR. Bidirectional prediction analyses showed that the differentially expressed miRNAs may be inversely regulated by their predicted targets. Conclusion. Hyperresistinemia results in changes in the miRNAs and mRNAs expressed in the liver.
  • General Endocrinology

    Chen L, Gu T, Yang LZ

    A Novel Intragenic Deletion Related to the Arginine Vasopressin V2 Receptor Causes Nephrogenic Diabetes Insipidus

    Acta Endo (Buc) 2020 16(3): 295-297 doi: 10.4183/aeb.2020.295

    Background. Nephrogenic diabetes insipidus (NDI) is a disease characterized by a defective response to the antidiuretic hormone (ADH) of the renal collecting duct leading to a decline in the ability of the pro-urine concentration. Case presentation. A 23-year-old man presented with an over 20-year history of polyuria concomitant with hydronephrosis. The diagnosis of NDI was established by gene analysis as well as a water-deprivation and vasopressin test. All exons of arginine vasopressin V2 receptor (AVPR2) gene were amplified and sequenced. A novel hemizygous intragenic inframe deletion, cDNA 255th bp to 263th bp in exon 2 of AVPR2, was identified. These relevant translations from the 85th amino acid Asp to 88th amino acid Val were missed and replaced by amino acid Glu. After treating the patient with hydrochlorothiazide, his symptoms improved significantly. Conclusion. The genetic analysis revealed a novel X-linked intragenic inframe deletion, AVPR2 gene cDNA 255th bp to 263th bp, causing NDI.
  • Endocrine Care

    Li Q, Zhao Y, Wang YP, Yang Y, He SM, Zhang X, Wang Z, Luo LY

    Correlation between Serum 25(OH)D and Abdominal Visceral Fat Area in Patients with Type 2 Diabetes Mellitus in the Context of Different Bone Mass

    Acta Endo (Buc) 2021 17(3): 351-357 doi: 10.4183/aeb.2021.351

    Objective. To investigate the correlation between serum levels of 25-hydroxy vitamin D [25(OH)D] and the visceral fat area of patients with type 2 diabetes mellitus (T2DM) in the context of different bone mass. Materials and Methods. A total of 180 patients with T2DM were randomly selected for bone mineral density (BMD) examination. According to the results, they were divided into three groups: T2DM normal bone group (group A); T2DM bone mass reduction group (group B); T2DM osteoporosis group (group C). Result. Serum 25(OH)D levels in NC group, A group, B group and C group decreased in turn, and Visceral fat area (VFA) in group B and group C were significantly higher than those in group A and NC [(29.41±4.87) vs. (22.76±4.23) vs. (17.78±3.61) vs. (9.70±3.01), P<0.05], [(117.76±38.79), (125.08±37.90) vs. (89.79±26.51), (97.53±28.61), P<0.05]. Pearson correlation analysis showed that L1-L4 lumbar vertebrae bone density was positively correlated with 25(OH)D and VFA; left femoral neck bone density was positively correlated with 25(OH)D, and negatively correlated with VFA. Conclusion. Serum 25(OH)D and VFA may be associated with the development of T2DM combined with OP.
  • Case Report

    Zhou TC, Yang Y, Zhang L, Liu YY, Lai X, Li Y, Li X, Xiong YX, Yang YL, Irwin DM

    Novel Genetic Findings in a Chinese Family with Early-Onset Female-Related Type 2 Diabetes

    Acta Endo (Buc) 2017 13(3): 364-369 doi: 10.4183/aeb.2017.364

    No inheritance of early-onset female-related type 2 diabetes was reported within Chinese families. In this study, we aim to describe the inheritance pattern of type 2 diabetes in a 3-generation family and identify the gene responsible for type 2 diabetes. Genome-wide multipoint parametric linkage analysis revealed a maximum multipoint logarithm of odds (lod) score of 2.1 for a locus being associated with type 2 diabetes in this family on chromosome 20p11.2-12 between 23.5~30.8cM. Type 2 diabetes may be transmitted as an autosomal dominant trait with a high female-related penetrance in this family. Here we describe the first genetic locus for type 2 diabetes at chromosome 20p11.2-12. This region contains 8 known or predicted genes (PLCB1, PLCB4, LAMP5, PAK7, ANKEF1, SNAP25, SLX4IP, and JAG1). Gene SNAP25 which linked to energy or glucose homeostasis associated phenotypes may play a role in the development of type 2 diabetes in this family.
  • General Endocrinology

    Yang G, Chen S, Ding P, Jiang G, Fu C, Hu G, Feng X, Zhu W

    Pioglitazone Improves Insulin Sensitivity in Insulinresistant KKAy Mice: Involvement of a PPAR?-Dependent Signaling Pathway

    Acta Endo (Buc) 2013 9(4): 515-524 doi: 10.4183/aeb.2013.515

    Aim. To explore the effects and underlying mechanisms of pioglitazone (pio) on insulin sensitivity in insulin-resistant KKAy mice. Methods. Sixteen eight-week-old male KKAy mice were randomly assigned to two groups based on body weight: an insulin resistance model group and a pioglitazone treatment group (hereafter referred to as the pio-group). Eight male C57BL/6J mice were used as an insulin resistance control group. Mice in all three groups were fed an AIN-93G diet, and pio was added to the diet in the pio-group. After twelve weeks of treatment, blood glucose, serum insulin, glucose tolerance, and insulin tolerance were measured. ELISA was used to determine adiponectin and leptin in serum. A real time PCR assay was used to detect the mRNA of adiponectin and leptin in epididymal adipose tissue. A Western blot assay was used to analyze protein expression and/ or phosphorylation levels of peroxisome proliferator activated receptor γ (PPARγ), insulin receptor substrate 1 (IRS1), and protein kinase B (PKB/AKT) in the liver and epididymal adipose tissue.Results. The results showed that Pio treatment may effectively reduce levels of blood glucose and serum insulin, improve insulin tolerance and glucose tolerance, increase serum adiponectin, decrease serum leptin, and enhance mRNA expression of adiponectin in epididymal adipose tissue. Furthermore, with pio treatment, protein expression of PPARγ and phosphorylation levels of IRS1 and AKT were increased in the liver and epididymal adipose tissue. Conclusion. These results suggested that Pio intervention may ameliorate insulin resistance and improve insulin sensitivity in KKAy mice, which may be due to an increase of PPARγ and further activation of the insulin signaling transduction pathway (IRS1 and AKT) in the liver and epididymal adipose tissue of KKAy mice.