Identification of co-expressed central genes and transcription factors in acute myocardial infarction and diabetic nephropathy.

BACKGROUND: Acute myocardial infarction (AMI) and diabetic nephropathy (DN) are common clinical co-morbidities, but they are challenging to manage and have poor prognoses. There is no research on the bioinformatics mechanisms of comorbidity, and this study aims to investigate such mechanisms. METHODS: We downloaded the AMI data (GSE66360) and DN datasets (GSE30528 and GSE30529) from the Gene Expression Omnibus (GEO) platform. The GSE66360 dataset was divided into two parts: the training set and the validation set, and GSE30529 was used as the training set and GSE30528 as the validation set. After identifying the common differentially expressed genes (DEGs) in AMI and DN in the training set, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses and protein-protein interaction (PPI) network construction were performed. A sub-network graph was constructed by MCODE, and 15 hub genes were screened by the Cytohubba plugin. The screened hub genes were validated, and the 15 screened hub genes were subjected to GO, KEGG, Gene MANIA analysis, and transcription factor (TF) prediction. Finally, we performed TF differential analysis, enrichment analysis, and TF and gene regulatory network construction. RESULTS: A total of 46 genes (43 up-regulated and 3 down-regulated) were identified for subsequent analysis. GO functional analysis emphasized the presence of genes mainly in the vesicle membrane and secretory granule membrane involved in antigen processing and presentation, lipopeptide binding, NAD + nucleosidase activity, and Toll-like receptor binding. The KEGG pathways analyzed were mainly in the phagosome, neutrophil extracellular trap formation, natural killer cell-mediated cytotoxicity, apoptosis, Fc gamma R-mediated phagocytosis, and Toll-like receptor signaling pathways. Eight co-expressed hub genes were identified and validated, namely TLR2, FCER1G, CD163, CTSS, CLEC4A, IGSF6, NCF2, and MS4A6A. Three transcription factors were identified and validated in AMI, namely NFKB1, HIF1A, and SPI1. CONCLUSIONS: Our study reveals the common pathogenesis of AMI and DN. These common pathways and hub genes may provide new ideas for further mechanistic studies.

Causal association of circulating metabolites with diabetic retinopathy: a bidirectional Mendelian randomization analysis.

Introduction: The retina is a highly metabolically active tissue, and there is a lack of clarity about the relationship between metabolites and diabetic retinopathy (DR). This study used two-sample bidirectional Mendelian randomization (MR) analyses to identify causal relationships between metabolites and DR. Methods: Genetic variants were selected from the open-access Genome-Wide Association Studies (GWAS) summary database as proxies for the 1400 most recently published metabolites. MR analysis was performed to examine associations between these metabolite traits and DR. Single nucleotide polymorphism (SNP) data that were significantly associated with exposure were screened through association analysis. Validated instrumental variables (IVs) were obtained by removing SNPs with linkage disequilibrium (LD) and F-statistic values below 10. MR analyses were performed using the inverse variance weighted (IVW) method as the primary approach. The robustness of the results was verified by sensitivity analyses, including assessments of heterogeneity, horizontal pleiotropy, and the leave-one-out method. Results: In the IVW approach and in the primary analysis of several sensitivity analyses, genetically determined glycolithocholate sulfate levels, androstenediol (3 beta, 17 beta) monosulfate (1) levels, 1-stearoyl-2-arachidonoyl-GPE (18:0/20:4) levels, 1-oleoyl-2-arachidonoyl-GPE (18:1/20:4) levels, 1-oleoyl-2-linoleoyl-GPE (18:1/18:2) levels, X-26109 levels, N6-methyllysine levels, (N6,N6-dimethyllysine levels), and (N2-acetyl,N6,N6-dimethyllysine levels) were negatively associated with the risk of DR. 5-hydroxymethyl-2-furoylcarnitine levels and the glutamate-to-alanine ratio were positively associated with the risk of DR. No reverse causal association was found between DR and metabolites. Discussion: This MR study suggests that nine metabolites may have a protective effect in DR, while two metabolites may be associated with an increased risk of DR. However, further research is needed to confirm these findings. Supplementation with beneficial metabolites may reduce DR risk and could potentially be a novel therapeutic approach to DR treatment.

Circulating immune cell phenotyping is potentially relevant for diabetic retinopathy risk assessment.

BACKGROUND: Inflammation is believed to play a central role in the development of diabetes mellitus and is a common feature of type 2 diabetes mellitus (T2DM). However, the association with diabetic retinopathy (DR) remains a topic of debate. METHODS: This study employed two-sample bidirectional Mendelian randomization (MR) analyses to establish causal associations between immune cell characteristics and DR. Using publicly available GWAS genetic data, we investigated the causal relationship between 731 immune cell characteristics and the risk of DR. A total of four types of immune features, including relative cell (RC), absolute cell (AC), median fluorescence intensities (MFI), and morphological parameters (MP), were included. Sensitivity analysis was conducted to assess the robustness, heterogeneity, and potential horizontal pleiotropy of the results. RESULTS: Thirty-five immune cell phenotypes were correlated with the risk of developing DR among four immune traits (MFI, RC, AC, and MP), and DR resulted in altered expression of twenty-six immune cells. CONCLUSION: We have demonstrated a strong correlation between immune cell traits and DR using a genetic approach. This finding offers valuable insights for early DR prevention and future clinical research and treatment.

Influence of glucagon-like peptide-1 receptor agonists on fat accumulation in patients with diabetes mellitus and non-alcoholic fatty liver disease or obesity: A systematic review and meta-analysis of randomized control trials.

AIM: This systematic review and meta-analysis aimed to comprehensively evaluate the impact of glucagon-like peptide 1 receptor agonists (GLP-1RAs) on visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) in individuals with diabetes mellitus and non-alcoholic fatty liver disease (NAFLD) or obesity. METHODS: A search of PubMed, Embase, and Web of Science until October 2023 identified 13 Randomized Controlled Trials (RCTs) meeting the inclusion criteria. Bias risk was assessed using the Cochrane risk-of-bias instrument. Statistical analysis utilized standard mean differences (SMD) in Review Manager 5.4. Heterogeneity and publication bias were assessed. This study used the protocol registered with the Platform of Registered Systematic Review and Meta-analysis Protocols (INPLASY2023110020). RESULTS: GLP-1RA treatment significantly reduced VAT (SMD -0.55, 95 % CI [-0.90, -0.19]), SAT (SMD -0.59, 95 % CI [-0.99, -0.19]), body weight (SMD -1.07, 95 % CI [-1.67, -0.47]), and body mass index (BMI) (SMD -1.10, 95 % CI [-1.74, -0.47]) compared to controls. Heterogeneity was observed for VAT (I2 = 79 %, P < 0.01), SAT (I2 = 73 %, P < 0.01), body weight (I2 = 82 %, P < 0.01), and BMI (I2 = 82 %, P < 0.01). No publication bias was detected for VAT (P = 0.57) and SAT (P = 0.18). GLP-1RA treatment improved fasting blood glucose (FBG), postprandial glucose (PPG), hemoglobin A1c (HbA1c), Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), and fibrosis-4 (FIB-4). CONCLUSIONS: This meta-analysis highlights GLP-1RAs' potential to reduce fat accumulation, body weight, and BMI and improve glycemic control in individuals with diabetes mellitus and NAFLD or obesity. These findings supported using GLP-1RAs as promising therapeutic agents to address abnormal adipose tissue distribution and metabolic dysfunction.

Influence of age on static postural control in adults with type 2 diabetes mellitus: a cross-sectional study.

Aim: It was the aim of this study to assess static postural control characteristics in people with type 2 diabetes mellitus (T2D) of different ages using a force platform. A relationship was also established between static postural control parameters and age in this study. Methods: A total of 706 participants with T2D were included in this study. The participants were stratified into three age groups: Group 1 (<60 years old), Group 2 (60-70 years old), and Group 3 (>70 years old). Static postural control assessment during two-leg stance was performed on a force platform by all participants. The center of pressure (CoP)-related parameters were measured under two stance conditions (eyes open and closed). Kruskal-Wallis tests were applied to explore the difference among the different age groups. Multivariate regression analysis was performed to determine the relation between age and static postural control parameters. Results: Group 1 (<60 years old) had significantly less CoP total tracking length (TTL), sway area (SA), and CoP velocity along the Y direction (V-Y) under both eyes-open and eyes-closed conditions compared with Group 2 (60-70 years old) and Group 3 (>70 years old). Group 1 (<60 years old) had significantly less CoP maximum sway length along the X direction (MSL_X) and longer tracking length each area unit (TTL/SA) under the eyes-open condition compared with Group 2 (60-70 years old) and Group 3 (>70 years old). There was a significantly positive correlation between age and the most static postural parameters such as CoP TTL, SA, MSL-X, MSL-Y, and V-Y. There was a significantly negative correlation between age and TTL/SA. Conclusion: This study suggested that older T2D participants had worse static postural control ability than younger ones. Most static postural parameters presented a significant correlation with age; the higher the age, the worse the static postural control.

Integrative analyses of biomarkers and pathways for diabetic nephropathy.

Background: Diabetic nephropathy (DN) is a widespread diabetic complication and a major cause of terminal kidney disease. There is no doubt that DN is a chronic disease that imposes substantial health and economic burdens on the world's populations. By now, several important and exciting advances have been made in research on etiopathogenesis. Therefore, the genetic mechanisms underlying these effects remain unknown. Methods: The GSE30122, GSE30528, and GSE30529 microarray datasets were downloaded from the Gene Expression Omnibus database (GEO). Analyses of differentially expressed genes (DEGs), enrichment of gene ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA) were performed. Protein-protein interaction (PPI) network construction was completed by the STRING database. Hub genes were identified by Cytoscape software, and common hub genes were identified by taking intersection sets. The diagnostic value of common hub genes was then predicted in the GSE30529 and GSE30528 datasets. Further analysis was carried out on the modules to identify transcription factors and miRNA networks. As well, a comparative toxicogenomics database was used to assess interactions between potential key genes and diseases associated upstream of DN. Results: Samples from 19 DNs and 50 normal controls were identified in the GSE30122 dataset. 86 upregulated genes and 34 downregulated genes (a total of 120 DEGs). GO analysis showed significant enrichment in humoral immune response, protein activation cascade, complement activation, extracellular matrix, glycosaminoglycan binding, and antigen binding. KEGG analysis showed significant enrichment in complement and coagulation cascades, phagosomes, the Rap1 signaling pathway, the PI3K-Akt signaling pathway, and infection. GSEA was mainly enriched in the TYROBP causal network, the inflammatory response pathway, chemokine receptor binding, the interferon signaling pathway, ECM receptor interaction, and the integrin 1 pathway. Meanwhile, mRNA-miRNA and mRNA-TF networks were constructed for common hub genes. Nine pivotal genes were identified by taking the intersection. After validating the expression differences and diagnostic values of the GSE30528 and GSE30529 datasets, eight pivotal genes (TYROBP, ITGB2, CD53, IL10RA, LAPTM5, CD48, C1QA, and IRF8) were finally identified as having diagnostic values. Conclusion: Pathway enrichment analysis scores provide insight into the genetic phenotype and may propose molecular mechanisms of DN. The target genes TYROBP, ITGB2, CD53, IL10RA, LAPTM5, CD48, C1QA, and IRF8 are promising new targets for DN. SPI1, HIF1A, STAT1, KLF5, RUNX1, MBD1, SP1, and WT1 may be involved in the regulatory mechanisms of DN development. Our study may provide a potential biomarker or therapeutic locus for the study of DN.

CircRNA expression profiles and functional analysis in a mouse model of chronic intermittent hypoxia-induced renal injury: new insight into pathogenesis.

Increasing evidence has demonstrated that circular RNAs (circRNAs) play crucial roles in the pathogenesis of multiple diseases. However, the functions of circRNAs in renal injury induced by obstructive sleep apnea (OSA) are poorly understood. The aim of this current study is to identify the global changes of circRNAs expression in OSA-induced renal damage. The mouse model of OSA treated by chronic intermittent hypoxia (CIH) was established. We assessed the expression profiles of circRNAs in CIH caused renal injury by microarray analysis. Bioinformatic analyses were further performed by us to assess those differentially expressed circRNAs. Quantitative realtime PCR (qRT-PCR) were then conducted to assure the data of microarray. Finally, a circRNA-miRNA -mRNA competing endogenous RNA (ceRNA) regulatory network was constructed. We found 11 upregulated and 13 downregulated circRNAs in CIH-induced renal injury. The qRT-PCR validated that the six selected circRNAs were identical to the results of microarray. Both Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were further employed to annotate the potential functions of dysregulated circRNAs. Finally, we established a ceRNA network to predict the target genes of circRNAs. In general, our results first illustrate that circRNAs are aberrantly expressed in OSA-induced renal injury, which might aid in offering novel genetic insights into this disease and potential therapeutic targets for OSA-associated chronic kidney disease.

Full-Length Transcriptomes and Sex-Based Differentially Expressed Genes in the Brain and Ganglia of Giant River Prawn Macrobrachium rosenbergii.

Macrobrachium rosenbergii is an important aquaculture prawn that exhibits sexual dimorphism in growth, with males growing much faster than females. However, the mechanisms controlling these complex traits are not well understood. The nervous system plays an important role in regulating life functions. In the present work, we applied PacBio RNA-seq to obtain and characterize the full-length transcriptomes of the brains and thoracic ganglia of female and male prawns, and we performed comparative transcriptome analysis of female and male prawns. A total of 159.1-Gb of subreads were obtained with an average length of 2175 bp and 93.2% completeness. A total of 84,627 high-quality unigenes were generated and annotated with functional databases. A total of 6367 transcript factors and 6287 LncRNAs were predicted. In total, 5287 and 6211 significantly differentially expressed genes (DEGs) were found in the brain and thoracic ganglion, respectively, and confirmed by qRT-PCR. Of the 435 genes associated with protein processing pathways in the endoplasmic reticula, 42 DEGs were detected, and 21/26 DEGs with upregulated expression in the male brain/thoracic ganglion. The DEGs in this pathway are regulated by multiple LncRNAs in polypeptide folding and misfolded protein degradation in the different organs and sexes of the prawn. Our results provide novel theories and insights for studying the nervous system, sexual control, and growth dimorphism.

Structural, antioxidant, and immunomodulatory activities of an acidic exopolysaccharide from Lactiplantibacillus plantarum DMDL 9010.

This study investigated the structural, antioxidant, and immunomodulatory activities of acidic exopolysaccharide (EPS-LP2) isolated from Lactiplantibacillus plantarum DMDL 9010. EPS-LP2 is composed of fucose (Fuc), arabinose (Ara), galactose (Gal), glucose (Glc), mannose (Man), and D-fructose (Fru) with a molar ratio of 0.13: 0.69: 8.32: 27.57: 62.07: 0.58: 0.46, respectively. Structural analysis of EPS-LP2 exhibited a smooth irregular lamellar surface, rod-like structure with swollen ends and slippery surfaces, and good thermal stability. Based on the methylation and NMR analysis, sugar residues including t-Manp, t-Glcp, 2-Manp, 6-Galp, 6-Glcp, and 4-Glcp were found to exist in EPS-LP2. In the 50∼400 µg/ml range, EPS-LP2 showed negligible neurotoxicity to RAW264.7 cells. Moreover, EPS-LP2 could protect RAW264.7 cells from oxidative injury by lowering the generation of reactive oxygen species (ROS), malondialdehyde (MDA), and the secretion of lactate dehydrogenase (LDH). In contrast, an increase in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and the concentrations of glutathione (GSH) were observed. Immunoreactivity assays showed that EPS-LP2 could suppress the expression of NO, tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6) and inhibit the activation of the mitogen-activated protein kinase (MAPK)/nuclear factor-κB-gene binding (NF-κB) cell pathway. Conclusively, EPS-LP2 could be a potential natural antioxidant and immunomodulatory agent in functional foods and medicines.

Vitamin D and iodine status was associated with the risk and complication of type 2 diabetes mellitus in China.

The purpose of this study was to assess the relationship between 25-hydroxyvitamin D (25(OH)D), urinary iodine concentration (UIC), and type 2 diabetes mellitus (T2DM) risk and complications and to establish a model to predict T2DM in the general population. A total of 567 adults (389 T2DM patients and 178 controls) were enrolled, and the levels of 25(OH)D, iodine, and blood biochemical parameters were measured. Pearson's correlation analysis showed an inverse correlation between 25(OH)D level, UIC, and T2DM risk. Low 25(OH)D level was a risk factor for developing T2DM (OR, 0.81; 95% CI, 1.90-2.63; P = 0.043) after adjustment for multiple risk factors. 25(OH)D level and UIC were inversely correlated with short-term and long-term glucose levels. 25(OH)D deficiency was also associated with a high incidence of T2DM complicated with thyroid dysfunction. A prediction model based on 25(OH)D, iodine status, and other risk factors was established and recommended to screen high-risk T2DM in the general population and provide early screening and timely treatment for them.

LncRNA RNCR3 promotes endothelial cell proliferation and inflammatory cytokine secretion via regulating miR-185-5p/cyclin D2 axis.

Endothelial cell is one critical structure of blood vessels, and irregular migration and proliferation of endothelial cell might cause progression of several vascular diseases such as atherosclerosis and restenosis. We showed that TNF-α, PDGF-bb, and IL-1ß promote RNCR3 expression in a dose-dependent manner inhuman endothelial cell. RNCR3 level is higher in serum of atherosclerosis patients compared with those in control volunteers. Overexpression of RNCR3 promotes cell proliferation and three inflammatory cytokine secretion including IL-6, IL-1ß, and TNF-α in endothelial cell. We illustrated that overexpression of RNCR3 inhibits miR-185-5p expression in endothelial cell. Furthermore, we indicated that miR-185-5p level is lower in the serum of patients with atherosclerosis compared with those in control volunteers. There is a negative correlation between miR-185-5p and RNCR3 expression in serum of patients with atherosclerosis. Using Targetscan, it predicted that miR-185-5p may bind to cyclin D2 and miR-185-5p is one potential target of miR-185-5p. Luciferase reporter data indicated that miR-185-5p suppresses luciferase value of wild-type cyclin D2 while it has no influence of cyclin D2 mutant. Overexpression of RNCR3 enhances cyclin D2 expression in endothelial cell. Moreover, RNCR3 induces cell growth and enhances inflammatory cytokine secretion through modulating cyclin D2 expression in endothelial cell. These results suggested that RNCR3 may serve as one new target for the treatment of atherosclerosis.

Novel talc encapsulated lanthanum alginate hydrogel for efficient phosphate adsorption and fixation.

In the present work, talc (a low-cost clay) encapsulated salts alginate (TAL) beads were synthesized by cross-linking with lanthanum ion and tested for phosphate adsorption. Multiple methods were applied for the characterization of composites. The combined effect of talc and lanthanum improved phosphate removal performance of TAL beads. Factors such as talc content, La3+ concentration, adsorbent dosage, pH, co-existing ions (Cl-, NO3- and SO42-) were studied in batch experiments. The optimized TAL-7 beads exhibited satisfactory selectivity towards phosphate in the coexistence of competing anions and could remain efficient phosphate removal in the pH range of 4-6. The phosphate removal efficiency reached to 95% with a maximum uptake of 16.4 mg P/g obtained at the optimal pH 4. Further experiments suggested that Langmuir isotherm model and the pseudo-second-order kinetic model could well describe the phosphate adsorption process of TAL-7 beads. Moreover, TAL-7 beads exhibited superior phosphate fixation performance in the long-term experiment. The results from adsorption experiment and characterization analysis demonstrated that TAL-7 beads could be a cost-effective and promising biosorbent for phosphate adsorption and fixation in the aqueous environment.

MiR-27a promotes insulin resistance and mediates glucose metabolism by targeting PPAR-γ-mediated PI3K/AKT signaling.

This study aimed to establish a high-fat diet (HFD)-fed obese mouse model and a cell culture model of insulin resistance (IR) in mature 3T3-L1 adipocytes. A dual-luciferase reporter assay (DLRA) was confirmed interaction between miR-27a and the 3'-untranslated region (UTR) of Peroxisome proliferator-activated receptor (PPAR)-γ. The inhibition of PPAR-γ expression by microRNA (miR)-27a in IR cells at both the protein and mRNA levels was confirmed by a mechanistic investigation. Moreover, the 3'-UTR of PPAR-γ was found to be a direct target of miR-27a, based on the DLRA. Furthermore, antagomiR-27a upregulated the activation of PI3K/Akt signaling and glucose transporter type 4 (GLUT4) expression at the protein and mRNA levels. Additionally, the PPAR inhibitor T0070907 repressed the insulin sensitivity upregulated by antagomiR-27a, which was accompanied by the inhibition of PPAR-γ expression and increased levels of AKT phosphorylation and GLUT4. The PI3K inhibitor wortmannin reduced miR-27a-induced increases in AKT phosphorylation, glucose uptake, and GLUT4. miR-27a is considered to be involved in the PPAR-γ-PI3K/AKT-GLUT4 signaling axis, thus leading to increased glucose uptake and decreased IR in HFD-fed mice and 3T3-L1 adipocytes. Therefore, miR-27a is a novel target for the treatment of IR in obesity and diabetes.

Reduced Serum Levels of Brain-Derived Neurotrophic Factor Are Related to Mild Cognitive Impairment in Chinese Patients with Type 2 Diabetes Mellitus.

BACKGROUND: Brain-derived neurotrophic factor (BDNF) is involved in obesity, type 2 diabetes mellitus (T2DM), and cognitive dysfunction. The present study sought to assess the role of serum levels of BDNF in the pathophysiological process of mild cognitive impairment (MCI), a preclinical phase of dementia in 715 Chinese patients with T2DM. METHODS: Cross-sectional data were obtained from 715 patients with T2DM recruited from a Chinese diabetes center. Serum levels of BDNF were measured with sandwich enzyme-linked immunosorbent assay. The influence of BDNF on MCI was examined using univariate and multivariate binary logistic regression analyses. RESULTS: In univariate and multivariate logistic regression analyses, for each one-unit increase of BDNF, the unadjusted and adjusted risk of MCI decreased by 9% (OR 0.91; 95% CI 0.88-0.93, p < 0.001) and 6% (0.94; 0.87-0.98, p < 0.001) respectively. In multivariate models comparing the first (Q1), second and third quartiles against the fourth quartile of BDNF, BDNF in Q1 and Q2 were associated with MCI, and increased risk of MCI by 275% (OR 3.75; 95% CI 2.38-6.03) and 155% (2.55; 1.32-4.02). These results suggested that for each 1 ng/mL increase of serum level of BDNF, the association became stronger among obese diabetic patients (OR 0.91, 95% CI 0.85-0.96; p < 0.001) versus nonobese diabetic patients (OR 0.95, 95% CI 0.86-0.98; p = 0.001). CONCLUSION: The present data demonstrated that reduced serum levels of BDNF were associated with increased risk of MCI and might be useful for identifying diabetic patients at risk of dementia for early prevention strategies.

[Correlation between ectopic fat accumulation and insulin sensitivity in obese individuals with different glucose tolerance levels].

OBJECTIVE: To investigate the correlation between liver and skeletal muscle fat contents and insulin resistance in obese individuals with different levels of glucose tolerance. METHODS: RESULTS: Ten non-obese individuals with normal glucose tolerance (NGT), 9 obese individuals with NGT, and 7 obese individuals with impaired glucose tolerance (IGT) were enrolled in this study. All the participants were examined for insulin sensitivity by hyperinsulinemic-euglycemic clamp and for liver and skeletal muscle fat accumulation quantified by proton magnetic resonance spectroscopy (1H MRS). The data were collected from the subjects including somatometric measurements, fasting plasma glucose, 2-h plasma glucose (2hPG), fasting insulin, and blood biochemistry. Linear correlation analysis and multiple linear stepwise regression analysis were used to analyze the relationship between ectopic fat accumulation and insulin resistance. RESULTS: The glucose infusion rates (GIR, presented as the M value) differed significantly among IGT-obese (3.95∓1.66 mg·kg-1·min-1), NGT-obese (6.14∓1.90 mg·kg-1·min-1) and NGT-non-obese (8.78∓2.46 mg·kg-1·min-1) groups (P<0.05). The 3 groups also showed significant differences in liver fat contents [(15.23∓3.09)%, (6.25∓0.38)%, and (1.89∓0.90)%, respectively, P<0.05] and intramyocellular lipids in the tibialis anterior (2.69∓0.95, 2.61∓1.45, and 1.54∓0.66 mmol/kg, respectively, P<0.05). Linear analysis revealed that liver fat content, but not skeletal muscle fat content, was significantly correlated with the M value. Multiple linear stepwise regression analysis using M value as the dependent variable (Y) revealed that liver fat content (X) was an independent factor inversely correlated with the M value (regression equation: Y=-30.562X+9.007, R2=0.717, P<0.01). CONCLUSIONS: Liver fat accumulation, but not skeletal muscle fat accumulation, is correlated with insulin resistance and impaired glucose metabolism.

Elevated circulating level of a cytokine, pancreatic-derived factor, is associated with metabolic syndrome components in a Chinese population.

AIMS/INTRODUCTION: Pancreatic-derived factor (PANDER) is an important factor involved in obesity, glucose intolerance and abnormal lipid metabolism in animals. Nevertheless, the relationship between PANDER and metabolic syndrome (MetS) in humans has not yet been reported. MATERIALS AND METHODS: To determinate the relationship between PANDER and MetS components, 212 individuals aged between 40 and 65 years were recruited. Fasting plasma PANDER and other variables were measured. Correlations of plasma PANDER and other variables were carried out. Plasma PANDER level was compared in participants with no metabolic components and those with any metabolic components, as well as in normal glucose tolerance, impaired glucose tolerance and diabetes mellitus participants. RESULTS: In all the participants, there were 65 participants in the no metabolic components group and 147 participants in the any metabolic components group. Plasma PANDER level was increased with the number of MetS components (P < 0.05) and correlated with metabolic score (r = 0. 529, P < 0.001). In addition, plasma PANDER significantly correlated with fasting plasma glucose (r = 0.187, P = 0.046), 2-h plasma glucose (r = 0.195, P = 0.035), homeostasis model assessment of ß-cell function (r = -0.191, P = 0.039), triglyceride (r = 0.305, P = 0.001) and high-density lipoprotein cholesterol (r = -0.333, P < 0.001). Using multivariable logistic regression analysis, circulating PANDER was associated with an increased risk ratio of impaired glucose tolerance or diabetes mellitus (odds ratio 2.22, 95% confidence interval 1.15-4.42, P = 0.018) after adjustment of the other possible confounders. CONCLUSIONS: Circulating level of PANDER in relation to the accumulation in MetS suggested that persons with elevated levels of PANDER were associated with an increased risk of metabolic syndrome.

Predictability of 1-h postload plasma glucose concentration: A 10-year retrospective cohort study.

AIMS/INTRODUCTION: Elevated 1-h postload plasma glucose concentration (1hPG) during oral glucose tolerance test has been linked to an increased risk of type 2 diabetes and a poorer cardiometabolic risk profile. The present study analyzed the predictability and cut-off point of 1hPG in predicting type 2 diabetes in normal glucose regulation (NGR) subjects, and evaluated the long-term prognosis of NGR subjects with elevated 1hPG in glucose metabolism, kidney function, metabolic states and atherosclerosis. MATERIALS AND METHODS: A total of 116 Han Chinese classified as NGR in 2002 at the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China, were investigated. Follow-up was carried out in 2012 to evaluate the progression of glucose metabolism, kidney function, metabolic syndrome and carotid atherosclerosis. RESULTS: The areas under receiver operating characteristic curves were higher for 1hPG than FPG or 2hPG (0.858 vs 0.806 vs 0.746). The cut-off value of 1hPG with the maximal sum of sensitivity and specificity in predicting type 2 diabetes in NGR subjects was 8.85 mmol/L. The accumulative incidence of type 2 diabetes in subjects with 1hPG ≥8.85 mmol/L was higher than those <8.85 mmol/L (46.2% vs 3.3%, P = 0.000; relative risk 13.846, 95% confidence interval 4.223-45.400). On follow up, the prevalence of metabolic syndrome and abnormal carotid intima-media thickness in the subjects with 1hPG ≥8.85 mmol/L tended to be higher compared with those <8.85 mmol/L. CONCLUSIONS: 1hPG is a good predictor of type 2 diabetes in NGR subjects, and the best cut-off point is 8.85 mmol/L. Some tendency indicates that NGR subjects with 1hPG ≥8.85 mmol/L are more prone to metabolic syndrome and carotid atherosclerosis.

Characteristics of morphology, electrophysiology, and central projections of two sensilla styloconica in Helicoverpa assulta larvae.

The medial and lateral styloconic sensilla, constituting the main taste organs of lepidopterous caterpillars, were investigated in the oligophagous species, Helicoverpa assulta (Guenée) (Lepidoptera: Noctuidae). In this paper, the two sensilla were morphologically and physiologically characterized by scanning electron microscopy and tip recordings, respectively. The central projections of their respective sensory neurons were mapped by anterograde staining experiments combined with confocal laser scanning microscopy. The results showed that the two sensilla are in general morphologically similar. However, the size of the peg on the medial sensillum is significantly greater than that of the lateral. Tobacco leaf saps, sinigrin, and nicotine elicited strong responses from neurons housed by the medial sensillum, whereas sucrose activated primarily the lateral sensillum. All stained neurons in either sensillum showed a projection pattern involving axons entering the subesophageal ganglion through the ipsilateral maxillary and passing further on through the ipsilateral circumesophageal connective to the tritocerebrum of the brain. In the subesophageal ganglion, the axons targeted two areas: the ventrolateral section and the region near the neuromere midline. One distinction between the staining patterns originating from the two sensilla, however, is that axons arising from the medial sensillum, and not the lateral, give off some additional neural branches in the subesophageal ganglion including a few arborizations surrounding a tract, plus a long process extending posteriorly along the midline. Differences in the central projections derived from the two sensilla styloconica have not been reported previously.

[Expression of matrix metalloproteinase 2 in oral verruvous carcinoma and squamous cell carcinoma].

OBJECTIVE: To determine the expression of MMP2 mRNA in oral verruvous carcinoma and squamous cell carcinoma. METHODS: Thirty cases were divided into 3 groups: verruvous carcinoma (n = 10), well-differentiated squamous cell carcinoma (n = 15) and moderately or poorly differentiated squamous cell carcinoma (n = 5). Reverse transcription polymerase chain reaction (RT-PCR) was used to test the expression of MMP2 mRNA in the carcinoma tissues and matched normal tissues from 3 groups above. RESULTS: The expression of MMP2 mRNA in the carcinoma tissues was significantly higher than that in their matched normal tissues (P < 0.05). The expression of MMP2 mRNA in verruvous carcinoma was significantly higher than that in well-differentiated and moderately or poorly differentiated squamous cell carcinoma (P < 0.05). However, the expression of MMP2 mRNA was not obviously different between well-differentiated and moderately or poorly differentiated squamous cell carcinoma (P > 0.05). CONCLUSION: The expression of MMP2 mRNA in oral verruvous carcinoma and squamous cell carcinoma tissues was significantly higher than that in their matched normal tissues. The expression of MMP2 mRNA in verruvous carcinoma was significantly higher than that in squamous cell carcinoma.