Search

Ruoxi Zhen,1,2 Shuqi Wang,1,2 Shuchun Chen1– 3 1Graduate School of Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China; 2Department of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei, People’s Republic of China; 3Hebei Key Laboratory of Metabolic Diseases, Shijiazhuang, Hebei, People’s Republic of ChinaCorrespondence: Shuchun Chen, Department of Endocrinology, Hebei General Hospital, 348 Heping West Road, Shijiazhuang, Hebei, 050051, People’s Republic of China, Tel/Fax +86 31185988406, Email chenshuc2014@163.comPurpose: This study was designed to analyze correlations between the uric acid to high-density lipoprotein cholesterol ratio (UHR) and peripheral nerve conduction velocity (NCV) among type 2 diabetes mellitus (T2DM) patients.Patients and Methods: This was a single-center cross-sectional analysis of 324 T2DM patients. All patients were separated into a group with normal NCV (NCVN) and a group with abnormal NCV (NCVA). Patients were also classified into groups with low and high UHR values based on the median UHR in this study cohort. Neurophysiological data including motor and sensory conduction velocity (MCV and SCV, respectively) were measured for all patients.Results: Relative to patients with low UHR values, those in the high UHR group presented with greater NCVA prevalence (P = 0.002). UHR remained negatively correlated with bilateral superficial peroneal nerve SCV, bilateral common peroneal nerve MCV, bilateral ulnar nerve SCV, and bilateral right median nerve MCV even after adjustment for confounding factors. UHR was identified as an NCVA-related risk factor, with a 1.370-fold increase in NCVA prevalence for every unit rise in UHR (P < 0.001).Conclusion: These results identify UHR as a risk factor associated with NCVA that was independently negatively associated with NCV among T2DM patients.Keywords: type 2 diabetes mellitus, diabetic peripheral neuropathy, peripheral nerve conduction velocity, uric acid to

Ruoxi Zhen,1,2 Jiangli Ban,2,3 Zhuoya Jia,1,2 Yanhui Liu,2,3 Zelin Li,1,2 Shuchun Chen1,2,4 1Graduate School, Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China; 2Department of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei, People’s Republic of China; 3Graduate School, Hebei North University, Zhangjiakou, People’s Republic of China; 4Hebei Key Laboratory of Metabolic Diseases, Shijiazhuang, Hebei, People’s Republic of ChinaCorrespondence: Shuchun Chen, Department of Endocrinology, Hebei General Hospital, 348 Heping West Road, Shijiazhuang, Hebei, 050051, People’s Republic of China, Tel +86 31185988406, Fax +86 31185988406, Email chenshuc2014@163.comPurpose: The objective of this research was to examine the relationship between non-HDL cholesterol/HDL cholesterol ratio (NHHR) and vitamin D in type 2 diabetes mellitus (T2DM).Patients and Methods: This study enrolled 617 T2DM participants. Participants were separated into two groups: no vitamin D deficiency and vitamin D deficiency. Participants were split into two categories: individuals who had a high NHHR and those with a low NHHR, with the median NHHR serving as the cut-off. Eventually, the study participants were classified into two groups by gender, which were further classified into vitamin D deficient and non-vitamin D deficient groups.Results: NHHR values were substantially greater in vitamin D deficient group than in the non-deficient group in both male and female T2DM patients (P< 0.05). The high NHHR group displayed substantially lower vitamin D levels than the low NHHR group [16.21 (12.55,21.35) vs 19.05 (14.59,24.07), P< 0.001]. NHHR was discovered to be negatively and independently associated with vitamin D levels, and there was no sex difference.Conclusion: For the first time, our research revealed a negative relationship between NHHR and vitamin D in patients with T2DM.Keywords: vitamin D, diabetes, type 2 diabetes, lipid ratio, non-HDL-C /HDL-C

Shu Niu,1,&ast; Qingjuan Ren,1,&ast; Shuchun Chen,2 Xiaoyu Pan,2,3 Lin Yue,4 Xing Chen,2 Zelin Li,2 Ruoxi Zhen3 1Department of Endocrinology, Shijiazhuang People’s Hospital, Shijiazhuang, Hebei, People’s Republic of China; 2Department of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei, People’s Republic of China; 3Department of Internal Medicine, Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China; 4Department of Endocrinology, The Third Hospital of Shijiazhuang, Shijiazhuang, Hebei, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Shu Niu, Department of Endocrinology, Shijiazhuang People’s Hospital, Shijiazhuang, Hebei, People’s Republic of China, Email niushucccc@163.comPurpose: Among chronic liver diseases, non-alcoholic fatty liver disease (NAFLD) is one of the commonest. Although empagliflozin has several therapeutic uses in treating cardiovascular and renal disorders, its impacts and mechanisms on NAFLD are poorly understood. This research aimed to examine the metabolic regulatory mechanism through which empagliflozin protects against NAFLD.Methods: Equal grouping of twenty-seven male C57BL/6J mice into those fed a normal diet (NCD), those fed a high-fat diet (HFD), and those fed an HFD with empagliflozin (Empa) was approached. HE, oil red O staining, and Masson staining were utilized for evaluating the pathological damage to the liver and the mice’s liver and body weights. Lipids, blood glucose, and inflammation index were compared across the three groups. Liquid chromatography/mass spectrometry (LC-MS) has been employed for identifying liver metabolomics.Results: The findings suggested that empagliflozin mitigated the inflammatory and oxidative stress response associated with the buildup of lipids caused by HFD. Differentially expressed metabolites (DEMs) were identified by metabonomics analysis as present in both the HFD/NCD and Empa/HFD groups. These DE

Jiangli Ban,1,2 Xiaoyu Pan,2,3 Liqun Yang,2 Zhuoya Jia,2,3 Ruoxi Zhen,2,3 Xueqing Zhang,2,4 Shuchun Chen2,3 1Graduate School of Hebei North University, Zhangjiakou, People’s Republic of China; 2Department of Endocrinology, Hebei General Hospital, Shijiazhuang, People’s Republic of China; 3Graduate School of Hebei Medical University, Shijiazhuang, People’s Republic of China; 4Graduate School of North China University of Science and Technology, Tangshan, People’s Republic of ChinaCorrespondence: Shuchun Chen, Department of Endocrinology, Hebei General Hospital, 348 Heping West Road, Shijiazhuang, 050051, People’s Republic of China, Tel/Fax +86 31185988406, Email chenshuc2014@163.comPurpose: This study aimed to examine the correlation between fibrinogen/albumin (FAR) and diabetic peripheral neuropathy (DPN).Patients and Methods: A total of 342 patients were included and categorized into either the DPN group or the Non-DPN (NDPN) group based on their DPN status. The FAR index was determined by calculating the ratio of fibrinogen (FIB) to serum albumin (ALB), multiplied by 100. The participants were then divided into a High-FAR group and a Low-FAR group using the median FAR value as the threshold. Neurophysiological data were collected from the participants, which included motor conduction velocity (MCV) and sensory conduction velocity (SCV).Results: The DPN group displayed higher FAR levels [(DPN vs NDPN:6.72 (5.89,7.74) vs 5.94± 1.14], in addition to slower SCV and MCV data compared to the NDPN group. The high FAR group had a higher prevalence of DPN (78.9% vs 55.6%) (P< 0.05). There was a negative correlation between FAR and NCV, including bilateral median nerve SCV, left ulnar nerve SCV, bilateral median nerve MCV, bilateral common peroneal nerve MCV, bilateral tibial nerve MCV, and left ulnar nerve MCV. FAR was revealed to be an independent risk factor for the development of DPN in patients and demonstrated a greater predictive value for DPN developmen

Niu S, Ren Q, Chen S, et al. Diabetes Metab Syndr Obes. 2023;16:2549–2560. The authors have advised the correspondence section on page 2549 is incorrect. The correct correspondence details are as follows. Correspondence: Shuchun Chen, Department of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei, People’s Republic of China, Email chenshuc2014@163.com The authors apologize for this error.

Xiaoyu Pan,1,2 Zhuoya Jia,1,2 Ruoxi Zhen,1,2 Lin Yue,3 Shu Niu,1,4 Jiangli Ban,2 Shuchun Chen1,2 1Department of Internal Medicine, Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China; 2Department of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei, People’s Republic of China; 3Department of Endocrinology, The Third Hospital of Shijiazhuang, Shijiazhuang, Hebei, People’s Republic of China; 4Department of Endocrinology, Shijiazhuang People’s Hospital, Shijiazhuang, Hebei, People’s Republic of ChinaCorrespondence: Shuchun Chen, Department of Endocrinology, Hebei General Hospital, Shijiazhuang, People’s Republic of China, Tel/Fax +86 31185988406, Email chenshuc2014@163.comPurpose: Studies have shown that atherosclerotic plaques are associated with changes in the microbial composition of the intestinal flora and obesity, and that the small intestine plays an irreplaceable role in regulating intestinal flora homeostasis, but the role of the small intestine in the development of obesity-related atherosclerosis remains understudied. Therefore, this study explores the role of the small intestine in obesity-induced atherosclerosis and its molecular mechanisms.Methods: In the GSE59054 data, small intestine tissue samples from 3 normal and 3 obese mice were analyzed using bioinformatics methods. Screening for differentially expressed genes (DEGs) using the GEO2R tool. The DEGs were next processed for bioinformatics analysis. We constructed an obese mouse model and measured aortic arch pulse wave velocity (PWV). Aortic and small intestine tissues were stained with hematoxylin-eosin (HE) to observe pathological changes. Finally, immunohistochemistry was performed to verify the expression of small intestinal proteins.Results: We identified a total of 122 DEGs. Pathway analysis revealed that BMP4, CDH5, IL1A, NQO1, GSTM1, GSTA3, CAV1 and MGST2 were mainly enriched in the Fluid shear stress and atherosclerosis pathway. In addition, BMP4, N

Xing Chen,1 Shuchun Chen,2,3 Qingjuan Ren,3 Shu Niu,3 Xiaoyu Pan,3 Lin Yue,3 Zelin Li,3 Ruiyi Zhu,3 Zhuoya Jia,3 Xiaoyi Chen,3 Ruoxi Zhen,3 Jiangli Ban3 1Department of Nephrology, Hebei General Hospital, Shijiazhuang, 050051, People’s Republic of China; 2Department of Endocrinology, Hebei General Hospital, Shijiazhuang, 050051, People’s Republic of China; 3Department of Internal Medicine, Hebei Medical University, Shijiazhuang, 050017, People’s Republic of ChinaCorrespondence: Shuchun Chen, Department of Endocrinology, Hebei General Hospital, 348 Heping West Road, Shijiazhuang, Hebei, 050051, People’s Republic of China, Tel/Fax +86 311 85988406, Email chenshuchunwork88@163.comPurpose: Semaglutide, a new long-acting glucagon-like peptide-1 analogue, has shown benefits for renal diseases, but its direct role on kidney metabolism under obesity remains unclear. The study aims to elucidate the protective effect and metabolic modulation mechanism of semaglutide on obesity-related kidney injury.Methods: Male C57BL/6J mice were divided into control and obesity groups. Mice in the obesity group had a high-fat diet and were treated with or without semaglutide (30nmol/kg/day). The study assayed blood biochemistry and then evaluated renal pathological injury through Periodic Acid-Schiff staining and electron microscopy. Metabolomics was utilized to analyze obesity-related metabolites in kidney samples.Results: Semaglutide significantly improved glucose homeostasis, insulin resistance, and kidney injury in obese mice. We successfully identified 377 altered metabolites (P< 0.05). It was suggested that semaglutide directly improved oxidative stress and inflammation-related metabolites such as nicotinamide adenine dinucleotide (NAD+) and adenosine in the kidney of obese mice, which have not been documented in obesity-related kidney injury. Relevant enriched pathways were included phospholipids and lysophospholipids metabolism, purine metabolism, NAD+ metabolism, and insu

Zelin Li,1,2 Cuijuan Qi,1 Zhuoya Jia,1,2 Ruoxi Zhen,1,2 Lin Ren,1,3 Yujiao Jia,1,2 Shuchun Chen1,2,4 1Graduate School of Hebei Medical University, People’s Republic of China; 2Department of Endocrinology, Hebei General Hospital, People’s Republic of China; 3North China University of Science and Technology, People’s Republic of China; 4Hebei Key Laboratory of Metabolic Diseases, People’s Republic of ChinaCorrespondence: Shuchun Chen, Department of Endocrinology, Hebei General Hospital, 348 Heping West Road, 050051, People’s Republic of China, Tel +86 031185988406, Fax +86 031185988406, Email chenshuc2014@163.comPurpose: To study the correlation between estimated glucose disposition rate (eGDR) and coagulation parameters in type 2 diabetes patients (T2DM).Materials and Methods: A total of 948 patients suffering from T2DM were enrolled for this research. Various blood coagulation parameters including prothrombin time (PT), activated partial thromboplastin time (APTT), and fibrinogen (FIB) were assessed. Body mass index (BMI), hypertension, and the levels of glycated hemoglobin (HbA1c) were used to calculate the patients’ eGDRs. All patients were sorted into two groups: those with high eGDRs (eGDR≥ 7.5) and those with low eGDRs (eGDR< 7.5). The patients were then separated into groups of men and women. The connection between eGDR and coagulation indexes was examined using Spearman correlation, Pearson correlation, and multiple linear regression analysis.Results: In comparison to the high-eGDR group, reduced PT and APTT levels with increased FIB levels were observed in the low-eGDR group (P =0.006, P < 0.001, and P = 0.035, respectively). The eGDR showed a positive relation with APTT (r = 0.142, P < 0.001), a negative relation with FIB (r = − 0.082, P = 0.012), and no correlation with PT (r =0.064, P =0.050) in the all patients. As well as, the eGDR demonstrated a positive relation with APTT (r = 0.173, P < 0.001), a negative relation with FIB