Fei Hua

INPLASY202190097 Association between Lipocalin-2 levels and Gestational Diabetes Mellitus: A Systematic Review and Meta-Analysis Keywords: Gestational diabetes mellitus; lipocalin-2; association. D…

Relationship of Bone Status with Serum Uric Acid and Bilirubin in Men with Type 2 Diabetes: A Cross-Sectional Study - Article abstract #930410

Background: The microRNA-30 family plays a critical role in the pathogenesis of podocyte injury. Cx43 plays an essential role in intercellular communication, which is essential for coordinated kidney function. This study was conducted to explore the function of microRNA-30s/Cx43 in podocyte injury in diabetic nephropathy (DN), both in vivo and in vitro. Methods: SD rats were given streptozotocin (STZ) injections to induce DN. Podocytes were incubated in the medium in the presence or absence of high glucose (HG). The effects of the microRNA-30/Cx43 axis on DN and its underlying mechanisms were investigated by TUNEL assay, PAS, immunohistochemical staining, immunofluorescence staining, Western blot, RT-qPCR, RNA interference, and luciferase reporter assay. Podocytes were transfected with microRNA-30 family mimics, microRNA-30 family inhibitors, Cx43 siRNA, and negative controls to detect the effect of the microRNA-30/Cx43 axis. MicroRNA-30 family mimic AAVs, and microRNA-30 family inhibitor AAVs applied to regulate microRNA-30 family expression in the kidneys of the STZ-induced DN model rats to reveal the underlying mechanisms of the microRNA-30/Cx43 axis in DN. Results: MicroRNA-30 family member expression was downregulated in HG-treated podocytes and the glomeruli of STZ-induced DN rats. Luciferase reporter assays confirmed Cx43 is a directed target of microRNA-30s. The overexpression of microRNA-30 family members attenuated the HG-induced podocyte injury and protected against podocyte apoptosis and endoplasmic reticulum stress (ERS) both in vivo and in vitro. Also, silencing Cx43 expression eased podocyte apoptosis, injury, and ERS induced by a HG+microRNA-30 family inhibitor. Double-immunofluorescence staining assays proved the co-localization of caspase12 and Cx43. Conclusions: The overexpression of microRNA-30 family members prevents HG-induced podocyte injury and attenuates ERS by modulating Cx43 expression. The microRNA-30/Cx43/ERS axis might be a potential therapeutic target to treat DN.

Diabetes is a metabolic disorder accompanied by complications of multiple organs and systems. Diabetic nephropathy (DN) is one of the most prevalent lethal complications of diabetes. Although numerous biomarkers have be clarified for early diagnosis of DN, renal biopsy is still the gold standard. As a noninvasive imaging diagnostic method, blood oxygen level-dependent (BOLD) MRI can help understand the kidney oxygenation status and fibrosis process and monitor the efficacy of new drugs for DN via monitoring renal blood oxygen levels. Recent studies have shown that noncoding RNAs including microRNAs (miRNAs), long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) were all involved in the development of DN, which could be exploited as therapeutic strategy to control DN. Dyslipidemia is also a common complication of diabetes. Apolipoprotein M (apoM), as a novel apolipoprotein, may be related to the development and progression of diabetes, which need to further investigation. Obstructive sleep apnea (OSA) is another common complication of diabetes and is an independent risk factor for cardiovascular disease (CVD). At present, there is no simple, effective and rapid diagnostic method to early identification of OSA in patients with diabetes. A nomogram consisted of waist-to-hip ratio, smoking status, body mass index, serum uric acid, HOMA-IR and history of fatty liver might be an alternative method to early assess the risk of OSA.

Background: Obstructive sleep apnea (OSA) is highly prevalent among patients with type 2 diabetes mellitus (T2DM) in China, but few patients with clinical symptoms of OSA are referred for diagnostic polysomnography (PSG). Thus, this study aimed to develop and validate an easy-to-use nomogram that predicts the severity of OSA in patients with T2DM. Methods: This retrospective study included consecutive patients with T2DM admitted to the Endocrinology Department, Third Affiliated Hospital of Soochow University between January 1, 2016 and December 31, 2019. OSA was diagnosed with PSG. Participants were randomly assigned to a training cohort (70%) and a validation cohort (30%). Demographic, anthropometric, and biochemical data were collected. A least absolute shrinkage and selection operator (LASSO) regression model was used to reduce data dimensionality and identify factors for inclusion in the nomogram (training cohort). Nomogram validation was performed in the validation cohort. Results: The study included 280 participants in the training group and 118 participants in the validation group. OSA prevalence was 58.5%. LASSO regression identified waist-to-hip ratio (WHR), smoking status, body mass index (BMI), serum uric acid (UA), the homeostasis model assessment insulin resistance index (HOMA-IR), and history of fatty liver disease as predictive factors for inclusion in the nomogram. Discrimination and calibration in the training group (C-index =0.88) and validation group (C-index =0.881) were good. The nomogram identified patients with T2DM at risk for OSA with an area under the curve of 0.851 [95% confidence interval (CI), 0.788–0.900]. Conclusions: Our nomogram could be used to facilitate individualized prediction of OSA risk in patients with T2DM and help prioritize patients for diagnostic PSG.

Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disease that affects 1 in every 200 people in the general population, leading to cardiac ischemia, heart failure and increased risk of sudden death. Recently, accumulating evidence has suggested that long noncoding RNAs (lncRNAs) may serve specific roles in various biological processes and participate in the pathology of various diseases, including HCM. Although a large number of lncRNAs have been detected, the functions of lncRNAs in HCM are still unknown. In the present study, a global triple network based on competitive endogenous RNA (ceRNA) theory was constructed using data from the National Center for Biotechnology Information Gene Expression Omnibus. Furthermore, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses of mRNAs in the lncRNA‑microRNA (miRNA)‑mRNA network were performed using the Cytoscape plugins, BiNGO and Database. The lncRNA‑miRNA‑mRNA network was composed of 30 lncRNA nodes, 94 mRNA nodes and 8 miRNA nodes. Subsequently, hub nodes and the number of relationship pairs were analyzed and showed that 5 lncRNAs (ENST00000597346.1, ENST00000458178.1, ENST00000544461.1, ENST00000567093.1 and ENST00000571219.1) were closely related to HCM. Cluster module analysis and Random Walk with Restart of the ceRNA network further confirmed the potential role of two lncRNAs (ENST00000458178.1 and ENST00000567093.1) in HCM. The present study provides a new strategy for identifying potential pathways associated with HCM or other diseases. Furthermore, lncRNA‑miRNA pairs may be regarded as candidate diagnostic biomarkers or potential therapeutic targets for HCM.

BACKGROUND Cystatin C is a protease inhibitor that is increased in the serum of patients with chronic kidney disease (CKD) and is associated with an increased risk of developing cardiovascular disease (CVD). This study aimed to evaluate the association between serum levels of cystatin C and arterial stiffness, associated with dyslipidemia, obesity, and increased pulse pressure, in middle-aged and elderly individuals without CKD in a population in China. MATERIAL AND METHODS A cross-sectional population-based study included 1,138 patients aged ≥40 years without CKD, defined as an estimated glomerular filtration rate measured by serum creatinine (eGFRSCr) ≥60 ml/min/1.73 m². Study participants provided clinical details, including height and weight, and blood samples for serum measurements of cystatin C and lipid profiles and completed a clinical questionnaire. Pulse pressure was calculated as the mean systolic pressure (SBP) minus the diastolic pressure (DBP). Data underwent multivariate logistic regression analysis. RESULTS An increase in serum levels of cystatin C was associated with an increased risk of arterial stiffness. Each standard deviation in the increase of cystatin C resulted in a 22% increased risk of dyslipidemia, a 27% increased risk of obesity, and a 24% increased risk of increased pulse pressure, after adjusting for confounders. These associations were further confirmed in a sensitivity analysis by excluding participants with hypertension, diabetes, and patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). CONCLUSIONS In middle-aged and elderly individuals without CKD, arterial stiffness determined by obesity, dyslipidemia and increased pulse pressure, was significantly associated with increased serum levels of cystatin C.

Background: The role of body fat distribution in uric acid metabolism is still ambiguity. We aimed to investigate the independent contribution of visceral adipose measured by visceral adiposity index and lipid accumulation product and liver fat assessed by fatty liver index to the risk of hyperuricemia. Methods: We conducted a cross-sectional study involving 1284 participants aged ≥ 40 years old recruited from communities in Zhonglou district, Changzhou. Each participant completed a standard questionnaire, and provided blood samples for biochemical measurements. Visceral adiposity index, fatty liver index and lipid accumulation product were calculated by simple anthropometric and functional parameters. Hyperuricemia was defined as serum uric acid ≥ 420 μmol/l for males and ≥ 360 μmol/l for females. Results: The prevalence of hyperuricemia was 15.9% and gradually increased across tertiles of adiposity-based indices. The visceral adipose-based measurements (visceral adiposity index, fatty liver index, lipid accumulation product) had better power to discriminate hyperuricemia than body mass index (BMI), waist circumference and neck circumference, and visceral adiposity index exhibited the highest power, with the area under the receiver operating characteristics curve (AUROC) of 0.662 (0.636–0.688). Multivariate logistic regression found 1.49-fold, 2.21-fold and 2.12-fold increased risk of hyperuricemia with 1-unit increment of visceral adiposity index, fatty liver index, and lipid accumulation product, respectively. Compared to tertile 1, the odds ratios of hyperuricemia for the second tertile and the third tertile of visceral adiposity index were 1.57 (1.00–2.50) and 3.11 (1.96–4.94), those of fatty liver index were 1.64 (1.05–2.68) and 3.58 (1.94–6.01), and those of lipid accumulation product were 1.93 (1.19–3.15) and 3.53 (2.05–6.09), respectively. However, no significant associations of BMI, waist circumference and neck circumference with hyperuricemia were observed. Conclusions: Visceral adipose accumulation increased the risk of hyperuricemia, independently of BMI, waist circumference and neck circumference, among middle-aged and elderly Chinese adults.