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Objective: We aimed to examine the relationship between osteocalcin (OC) and the risk of incident diabetes and the risk of incident diabetic kidney disease (DKD).Research Design and Methods: We followed 5,396 participants without diabetes (nondiabetes subcohort) and 1,174 participants with diabetes and normal kidney function (diabetes subcohort) at baseline. Logistic regression and modified Poisson regression models were used to estimate the relative risk (RR) of baseline OC levels with incident diabetes and DKD.Results: During a mean 4.6-year follow-up period, 296 cases of incident diabetes and 184 cases of incident DKD were identified. In the nondiabetes subcohort, higher OC levels were linearly associated with a decreased risk of diabetes (RR for 1-unit increase of loge-transformed OC 0.51 [95% CI 0.35-0.76]; RR for highest vs. lowest quartile 0.65 [95% CI 0.44-0.95]; P for trend < 0.05). In the diabetes subcohort, OC levels were linearly inversely associated with incident DKD (RR for 1-unit increase of loge-transformed OC 0.49 [95% CI 0.33-0.74]; RR for highest vs. lowest quartile 0.56 [95% CI 0.38-0.83]; P for trend < 0.05), even independent of baseline estimated glomerular filtration rate and urinary albumin-to-creatinine ratio. No significant interactions between OC and various subgroups on incident diabetes or DKD were observed.Conclusions: Lower OC levels were associated with an increased risk of incident diabetes and DKD. [ABSTRACT FROM AUTHOR]

Aim. To investigate the effects of alcohol on serum glycated albumin (GA) levels in Chinese men. Methods. A total of 2314 male subjects from the Jinuo ethnic group in China were enrolled. Of these, 986 subjects drank alcohol frequently and 404 subjects did not. Lifestyle information was gathered by using a questionnaire, and measurements of blood pressure, body mass index, blood glucose level, liver function, and kidney function were collected. GA was measured by using an enzymatic method. Frequent drinking was defined as a history of drinking ethanol > 80 g/d within the past two weeks. Nondrinking was defined as no alcohol consumption in the past three months. Subjects with an alcohol intake between 0 and 80 g/d in the past two weeks were included in the drinking-occasionally group. Analysis of variance (ANOVA), correlation analysis, and linear regression were used to evaluate the effects of drinking on serum GA levels. Decision tree regression (DTR) algorithm was used to evaluate the effect of features (variables) on GA levels. Results. We found that male subjects who drank frequently had significantly lower serum GA levels than subjects who did not drink (13.0 ± 1.7 vs. 14.1 ± 3.7, p < 0.05). Spearman's correlation analysis calculated a coefficient of −0.152 between drinking and GA (p < 0.005). Linear regression established that drinking was an independent predictor for GA levels with a standardized regression coefficient of −0.144 (p < 0.05). Decision tree regression showed that the effect of drinking on GA levels (0.0283) is five times higher than that of smoking (0.0057). Conclusions. Frequent alcohol consumption could result in decreased GA levels in men of the Jinuo ethnic group in China. [ABSTRACT FROM AUTHOR]

Type 2 diabetes mellitus (T2DM) accounts for approximately 90% of all diabetic patients, and osteoporosis is one of the complications during T2DM process. ATP6V1H (V-type proton ATPase subunit H) displays crucial roles in inhibiting bone loss, but its role in osteogenic differentiation remains unknown. Therefore in this study, we aimed to explore the biological role of ATP6V1H in osteogenic differentiation. OM (osteogenic medium) and HG (high glucose and free fatty acids) were used to induce the MC3T3-E1 cells into osteogenic differentiation in a T2DM simulating environment. CCK8 assay was used to detect cell viability. Alizarin Red staining was used to detect the influence of ATP6V1H on osteogenic differentiation. ATP6V1H expression increased in OM-MC3T3-E1 cells, while decreased in OM+HG-MC3T3-E1 cells. ATP6V1H promoted osteogenic differentiation of OM+HG-MC3T3-E1 cells. Overexpression of ATP6V1H inhibited Akt/GSK3β signaling pathway, while knockdown of ATP6V1H promoted Akt/GSK3β signaling pathway. ATP6V1H overexpression promoted osteogenic differentiation of OM+HG-MC3T3-E1 cells. The role of ATP6V1H in osteogenic differentiation in a T2DM simulating environment involved in Akt/GSK3β signaling pathway. These data demonstrated that ATP6V1H could serve as a potential target for osteogenic differentiation in a T2DM simulating environment. [ABSTRACT FROM AUTHOR]

Background: This study investigated the performance of the A1CNow(+®) test (Bayer Diabetes Care, Sunnyvale, CA) in a large population of Chinese patients with diabetes.Subjects and Methods: Hemoglobin A1c (HbA1c) levels in 1,618 Chinese patients with diabetes 10-94 years of age were measured with both the A1CNow(+) test, from a fingerstick blood sample, and the high-performance liquid chromatography (HPLC) test, using a venous blood sample, within 24 h. The reportable ranges of the HbA1c values were 4.0-13.0% (A1CNow(+)) and 4.1-16.8% (HPLC). An error grid analysis (EGA) method was developed to quantify the accuracy of the A1CNow(+) results against the HPLC reference results.Results: The A1CNow(+) results were highly correlated with the HPLC reference results (r=0.945, P<0.01). Passing-Bablok regression analysis showed a good linear agreement between the two variables, and the linear regression equation fitted as y=-0.10+1.00x (P=0.21). The Bland-Altman difference plot presented that the mean bias of the A1CNow(+) results minus the HPLC reference results was -0.09% (P<0.001); the 95% confidence intervals for the limits of agreement were -1.28% to 1.09%, with 96.5% of the data points lying within this zone. The results of the EGA showed that 80.2% of the A1CNow(+) results were accurate, 17.7% were acceptable, 1.9% may lead to inappropriate treatment, and 0.3% may lead to severe clinical consequence.Conclusions: The A1CNow(+) test values demonstrated a slight negative bias from the HPLC values. The majority of A1CNow(+) test values were accurate when compared with results from the reference method. [ABSTRACT FROM AUTHOR]

Background. Fibroblast growth factor (FGF)-21 has been recently characterized as a potent metabolic regulator, but the physiological role of FGF-21 remains poorly understood. This study was designed to investigate serum FGF-21 levels in type 2 diabetes mellitus (T2DM) patients and explore the correlations between its serum levels and various cardiometabolic parameters in humans. Methods. Fifty-four newly diagnosed patients with T2DM (NDDM), 54 subjects with long duration of T2DM (LDDM), that is, more than 5 years, and 35 normal controls participated in this study. Fasting serum FGF-21 levels were measured using ELISA kits. The anthropometric parameters, glucose, glycosylated hemoglobin A1c, lipids, insulin, and high-sensitive C-reactive protein (hsCRP) levels were also measured in fasting status. Results. Serum FGF-21 levels were significantly higher in patients with NDDM and LDDM than in controls (361.80 ± 140.28 pg//mL and 351.17 ± 133.44 pg//mL vs. 185.89 ± 59.29 pg//mL, both p < 0.01), but there was no difference in serum FGF-21 levels between NDDM and LDDM. Fasting serum FGF-21 was found to correlate positively and significantly with age, waist-to-hip ratio, systolic blood pressure, fasting plasma glucose, glycosylated hemoglobin A1c, homeostasis model assessment (HOMA) of insulin resistance, and hsCRP, but negatively with HOMA of β-cell insulin secretion. Furthermore, multiple regression analyses showed that fasting insulin, HOMA of insulin resistance, low-density lipoprotein cholesterol, and hsCRP were independent factors influencing serum FGF-21 levels. Logistic regression analyses demonstrated that serum FGF-21 was significantly associated with T2DM. Conclusions. Serum FGF-21 levels were significantly increased in patients with T2DM. They may play a role in the pathogenesis of T2DM. [ABSTRACT FROM AUTHOR]

The article presents a study on the photoisomerization behavior and synthesis of thiazolylazo polyimide (PI). It states that post azocoupling reaction scheme was used to prepare the PI with thiazolylazo side chain. Results of the study show that thermal stability of the polymer is quite good from glass-transition temperature and temperature at 10% of weight loss under nitrogen gas of the polymer is 138.9 celsius and 510.6 celsius.

Objective. The aim of this study was to identify the candidate genes in type 2 diabetes mellitus (T2DM) and explore their potential mechanisms. Methods. The gene expression profile GSE26168 was downloaded from the Gene Expression Omnibus (GEO) database. The online tool GEO2R was used to obtain differentially expressed genes (DEGs). Gene Ontology (GO) term enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed by using Metascape for annotation, visualization, and comprehensive discovery. The protein-protein interaction (PPI) network of DEGs was constructed by using Cytoscape software to find the candidate genes and key pathways. Results. A total of 981 DEGs were found in T2DM, including 301 upregulated genes and 680 downregulated genes. GO analyses from Metascape revealed that DEGs were significantly enriched in cell differentiation, cell adhesion, intracellular signal transduction, and regulation of protein kinase activity. KEGG pathway analysis revealed that DEGs were mainly enriched in the cAMP signaling pathway, Rap1 signaling pathway, regulation of lipolysis in adipocytes, PI3K-Akt signaling pathway, MAPK signaling pathway, and so on. On the basis of the PPI network of the DEGs, the following 6 candidate genes were identified: PIK3R1, RAC1, GNG3, GNAI1, CDC42, and ITGB1. Conclusion. Our data provide a comprehensive bioinformatics analysis of genes, functions, and pathways, which may be related to the pathogenesis of T2DM. [ABSTRACT FROM AUTHOR]

Abstract: Ordered mesoporous carbon (OMC)–SnO2 nanocomposite was prepared by a melt injection method using SnCl2·2H2O as the tin source. The results of X-ray diffraction (XRD) indicated that tin dioxide in the nanocomposite was crystalline. The BJH adsorption average pore size was greatly reduced from 5.1nm for OMC to 2.9nm for the mesoporous OMC–SnO2 composite which is due to the partial occupation of the pores by the tin species incorporated into the mesoporous carbon. The OMC–SnO2 electrode exhibits excellent cycle stability: the retentive capacity (472.1mAh/g) up to 30 cycles is 62.2% of the initial capacity (758.2mAh/g) which is much better than that for commercial SnO2. These results suggest that OMC–SnO2 nanocomposite would be a promising anode material for lithium ion battery. [Copyright &y& Elsevier]

Objective: We aimed to examine the relationship between osteocalcin (OC) and the risk of incident diabetes and the risk of incident diabetic kidney disease (DKD)., Research Design and Methods: We followed 5,396 participants without diabetes (nondiabetes subcohort) and 1,174 participants with diabetes and normal kidney function (diabetes subcohort) at baseline. Logistic regression and modified Poisson regression models were used to estimate the relative risk (RR) of baseline OC levels with incident diabetes and DKD., Results: During a mean 4.6-year follow-up period, 296 cases of incident diabetes and 184 cases of incident DKD were identified. In the nondiabetes subcohort, higher OC levels were linearly associated with a decreased risk of diabetes (RR for 1-unit increase of loge-transformed OC 0.51 [95% CI 0.35-0.76]; RR for highest vs. lowest quartile 0.65 [95% CI 0.44-0.95]; P for trend < 0.05). In the diabetes subcohort, OC levels were linearly inversely associated with incident DKD (RR for 1-unit increase of loge-transformed OC 0.49 [95% CI 0.33-0.74]; RR for highest vs. lowest quartile 0.56 [95% CI 0.38-0.83]; P for trend < 0.05), even independent of baseline estimated glomerular filtration rate and urinary albumin-to-creatinine ratio. No significant interactions between OC and various subgroups on incident diabetes or DKD were observed., Conclusions: Lower OC levels were associated with an increased risk of incident diabetes and DKD., (© 2022 by the American Diabetes Association.)

Diabetes mellitus is a prevalent disease result in several complications, including bone problems. Previous studies have shown that microRNA (miR)-26a regulates glucose metabolism and plays a protective role in diabetes. However, whether miR-26a also affects bone quality in diabetes remains unknown. In the present study, we evaluated the potential effects of miR-26a on bone in diabetic mice. We administrated miR-26a in streptozotocin-induced diabetic mice. The metabolic parameters, bone quality, osteoblast and osteoclast markers, and insulin signaling activation were measured. miR-26a ameliorated insulin resistance and glucose tolerance, improved bone microarchitecture and quality, increased osteoblasts and bone formation, decreased osteoclasts, and promoted the insulin signaling pathway in diabetic mice. These effects were abolished in insulin receptor-compromised Col1a1-Insr +/- mice. In conclusion, miR-26a could ameliorate bone-specific insulin resistance and bone quality in diabetic mice, which depended on the insulin receptors on osteoblasts. Our findings highlight the potential of miR-26a as a therapeutic target for diabetes mellitus-related bone metabolism and diseases., (Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.)

Background: Diabetes mellitus is characterized by hyperglycemia which displays insufficiency or resistance to insulin. One of the complications of diabetes is the increased risk of fracture and the impairment of bone repair and regulation. There have been evidences from previous studies that mesenchymal stem cells (MSCs) from bone marrow promote cartilage and callous formation. In addition, IL-10, an anti-inflammatory cytokine, has been observed to relieve inflammation-related complications in diabetes., Methods: In this study, the role of IL-10-overexpressing bone marrow-derived MSCs (BM-MSCs) was examined in the diabetic mice model with femur fracture. MSCs were isolated from the BALB/c mice and IL-10 over expression was conducted with lentivirus transduction. The streptozotocin (STZ)-induced diabetes model with femoral fracture was established. BM-MSCs with IL-10 over expression were transplanted into the fracture area. The expressions of inflammatory factors IL-6, TNF-α and INF-γ were examined by qPCR and immunoblot; the biomechanical strength of the fracture site of the mice was examined and evaluated., Results: Data showed that IL-10 overexpressed BM-MSCs transplantation decreased inflammatory response, promoted bone formation, and increased the strength of the fracture site in STZ-induced diabetic mice with femoral fracture., Conclusion: IL-10 overexpressed BM-MSCs transplantation accelerated fracture repair in STZ-induced diabetic mice, which in turn provides potential clinical application prospects., (© Biomedical Engineering Society 2019.)

Adropin has been identified as potent regulatory hormone implicated in insulin sensitivity and the maintenance of energy homeostasis. The aim of current study was to investigate serum adropin concentrations of type 2 diabetes mellitus (T2DM) patients in the fasting status, especially those overweight/obese and evaluate the relationships between adropin levels and metabolic parameters. A total of 116 T2DM patients and 60 controls with normal glucose tolerance (NGT) were recruited to the study. Adropin concentration was determined using commercial ELISA kits. Anthropometric characteristics were collected and biochemistry, glycosylated hemoglobin A 1 c (HbA 1 c) and fasting insulin (FIns) were detected by clinical laboratory. Insulin resistance was estimated by homeostasis model 2 assessment of insulin resistance (HOMA2-IR). Serum adropin levels in Chinese T2DM patients were decreased compared with the controls [3.8 (3.0-5.5) vs. 5.5 (3.7-7.9) ng/mL, p < 0.01]. Meanwhile, overweight/obese patients had more considerably reduced levels of adropin. Adropin level was negatively correlated with body mass index (BMI), high-sensitive C reactive protein (hs-CRP), triglycerides (TG), fasting plasma glucose (FPG), FIns, HOMA2-IR and HbA 1 c, while positively with high-density lipoprotein cholesterol (HDL-C) in study participants (p < 0.01). The correlations of adropin with glucolipid variables (TG, HDL-C, FPG, FIns, HOMA2-IR, HbA 1 c) still existed after adjusting the effect of BMI. Besides, HOMA2-IR and HbA 1 c were independent factors associated with serum adropin levels. Binary logistic regression analyses showed that adropin was significantly associated with T2DM after removing confounding factors (p < 0.01). Receiver operating characteristic (ROC) curve demonstrated adropin concentration of 5.8 ng/mL could be used as a possible optimal cut-off value to identify T2DM from non-T2DM with sensitivity of 81.9% and specificity of 46.7%. Serum adropin concentrations are decreased in Chinese T2DM patients, especially those overweight/obese. Adropin, associated with glucolipid homeostasis and insulin sensitivity, may implicate in the pathogenesis of T2DM.

Objectives: This study aimed to detect α- and β-thalassaemia mutations in the Jino ethnic minority population of Yunnan Province, Southwest China., Design: A total of 1613 Jino adults were continuously recruited from February 2012 to April 2012. Fasting venous blood samples were obtained to determine haematological variables. Haemoglobin analysis was conducted using high-performance liquid chromatography. Participants with hypochromic microcytic anaemia or positive haemoglobin analysis profiles were confirmed by α- and β-globin genetic testing, including DNA microarray analysis, direct sequencing methods and multiplex gap-PCR assays., Setting: Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Jiao Tong University Affiliated Sixth People's Hospital., Results: We found 363 suspected cases by primary screening of haematological variables and haemoglobin analysis. After further genetic testing, four types of α- and β-thalassaemia mutation were detected in 203 out of 363 individuals. Both α(0)- and α(+)-thalassaemia mutations, --(SEA) and -α(3.7), were identified. β-Thalassaemia mutations included CD17 (HBB:c.52A>T) and CD26 (HbE or HBB:c.79G>A). In addition, 13 HbE carriers had coexisting α(0)- or α(+)-thalassaemia deletions. Clinical haematological variables indicated that, in this study, carriers of all thalassaemic genotypes had more severe hypochromic microcytic anaemia than non-thalassaemic individuals., Conclusions: Our results provide information on the Jino ethnic minority that may be useful for further genetic counselling, prenatal screening and clinical diagnosis of thalassaemia in this region., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/)