Search Results
Search for other papers by Xue-Jiao Yang in
Google Scholar
PubMed
Search for other papers by Le-Yang Zhang in
Google Scholar
PubMed
Search for other papers by Qing-Hua Ma in
Google Scholar
PubMed
Search for other papers by Hong-Peng Sun in
Google Scholar
PubMed
Search for other papers by Yong Xu in
Google Scholar
PubMed
Search for other papers by Xing Chen in
Google Scholar
PubMed
Search for other papers by Chen-Wei Pan in
Google Scholar
PubMed
Purpose:
We aimed to examine the associations of platelet parameters with the presence of metabolic syndrome in community-dwelling older Chinese adults.
Methods:
Study sample was from the Weitang Geriatric Diseases Study, which included 4338 individuals aged 60 years or above. The mean age of the participants was 68 years. Metabolic syndrome was defined based on the Adult Treatment Panel III criteria. Platelet parameters were assessed using an automated hematology analyzer. Multiple logistic regression models were fitted to examine relationships between the platelet parameters and the presence of metabolic syndrome after adjusting for potential confounders.
Results:
The adjusted odds ratio (95% CI) of metabolic syndrome for the highest quartile of platelet parameters (platelet count, mean platelet volume, plateletcrit, platelet distribution width, platelet larger cell ratio) when compared to the lowest quartile were 1.32 (1.06, 1.64), 1.00 (0.81, 1.24), 1.37 (1.10, 1.71), 1.45 (1.14, 1.83), 1.11 (0.89, 1.39), respectively. Hypertension and diabetes modified the relationship between platelet distribution width and metabolic syndrome with the associations being significant in hypertensive and non-diabetic groups. The levels of platelet distribution width increased with the risk of metabolic syndrome in men but not in women.
Conclusion:
The levels of platelet count, plateletcrit and platelet distribution width increased in older adults with metabolic syndrome, suggesting that these parameters may be useful biomarkers for further risk appraisal of metabolic syndrome in aged population.
Search for other papers by Tao Yuan in
Google Scholar
PubMed
Search for other papers by Lanping Jiang in
Google Scholar
PubMed
Search for other papers by Chen Chen in
Google Scholar
PubMed
Search for other papers by Xiaoyan Peng in
Google Scholar
PubMed
Search for other papers by Min Nie in
Google Scholar
PubMed
Search for other papers by Xuemei Li in
Google Scholar
PubMed
Search for other papers by Xiaoping Xing in
Google Scholar
PubMed
Search for other papers by Xuewang Li in
Google Scholar
PubMed
Search for other papers by Limeng Chen in
Google Scholar
PubMed
Objective
Impaired glucose metabolism and insulin sensitivity have been reported in patients with Gitelman syndrome (GS), but insulin secretion and the related mechanisms are not well understood.
Design and methods
The serum glucose levels, insulin secretion and insulin sensitivity were evaluated in patients with GS (n = 28), patients with type 2 diabetes mellitus (DM) and healthy individuals (n = 20 in both groups) using an oral glucose tolerance test. Serum and urine sodium, potassium and creatinine levels were measured at 0, 30, 60, 120 and 180 min after an oral glucose load was administered.
Results
The areas under the serum glucose curves were higher in the GS patients than those in the healthy controls (17.4 ± 5.1 mmol·h/L vs 14.5 ± 2.8 mmol·h/L, P = 0.02) but lower than those in the DM patients (24.8 ± 5.3 mmol·h/L, P < 0.001). The areas under the serum insulin curves and the insulin secretion indexes in GS patients were higher than those in DM patients and lower than those in healthy subjects. The insulin secretion-sensitivity index of GS patients was between that of healthy subjects and DM patients, but the insulin sensitivity indices were not different among the three groups. After one hour of glucose administration, the serum potassium level significantly decreased from baseline, and the urinary potassium-to-creatinine ratio increased gradually and peaked at 2 h.
Conclusions
Glucose metabolism and insulin secretion were impaired in GS patients, but insulin sensitivity was comparable between GS patients and patients with type 2 DM. After administration of an oral glucose load, the plasma potassium level decreased in GS patients due to the increased excretion of potassium in the urine.
Department of Breast Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China
Search for other papers by Tian Zhou in
Google Scholar
PubMed
Department of Surgery, Second People's Hospital of Guizhou Province, Guiyang, Guizhou, China
Search for other papers by Dai-wei Zhao in
Google Scholar
PubMed
Search for other papers by Ning Ma in
Google Scholar
PubMed
Search for other papers by Xue-ying Zhu in
Google Scholar
PubMed
Search for other papers by Xing-hong Chen in
Google Scholar
PubMed
Search for other papers by Xue Luo in
Google Scholar
PubMed
Search for other papers by Song Chen in
Google Scholar
PubMed
Search for other papers by Qing-jun Gao in
Google Scholar
PubMed
Objective
Thyroid cancer (THCA) is the most common endocrine cancer in the world. Although most patients with THCA have a good prognosis, the prognosis of those with THCA who have an extra-glandular invasion, vascular invasion, and distant metastasis is poor. Therefore, it is very important to find potential biomarkers that can effectively predict the prognosis and progression of highly aggressive THCAs. It has been identified that forkhead box P4 (FOXP4) may be a new biomarker for the proliferation and prognosis for tumor diagnosis. However, the expression and function of FOXP4 in THCA remain to be determined.
Methods
In the present study, the function of FOXP4 in cells was investigated through the comprehensive analysis of data in The Cancer Genome Atlas and combined with experiments including immunohistochemistry (IHC), colony formation, Cell Counting Kit-8 assay, wound scratch healing, and transwell invasion assay.
Results
In the present study, relevant bioinformatic data showed that FOXP4 was highly expressed in THCA, which was consistent with the results of the IHC and cell experiments. Meanwhile, 10 FOXP4-related hub genes were identified as potential diagnostic genes for THCA. It was found in further experiments that FOXP4 was located in the nucleus of THCA cells, and the expression of FOXP4 in the nucleus was higher than that in the cytoplasm. FOXP4 knockdown inhibited in vitro proliferation of the THCA cells, whereas overexpression promoted the proliferation and migration of THCA cells. Furthermore, deficiency of FOXP4 induced cell-cycle arrest.
Conclusion
FOXP4 might be a potential target for diagnosing and treating THCA.
Department of Anatomy, Shanxi Medical University, Taiyuan, China
Search for other papers by Zhandong Lei in
Google Scholar
PubMed
Search for other papers by Yunfei Chen in
Google Scholar
PubMed
Search for other papers by Jin Wang in
Google Scholar
PubMed
Search for other papers by Yan Zhang in
Google Scholar
PubMed
Search for other papers by Wenjuan Shi in
Google Scholar
PubMed
Search for other papers by Xuejiao Wang in
Google Scholar
PubMed
Search for other papers by Dehai Xing in
Google Scholar
PubMed
Search for other papers by Dongxue Li in
Google Scholar
PubMed
Search for other papers by Xiangying Jiao in
Google Scholar
PubMed
Elucidating the mechanisms of regulation of β-cell proliferation is key to understanding the pathogenesis of diabetes mellitus. Txnip is a tumor suppressor that is upregulated in diabetes and plays an important role in the regulation of insulin sensitivity; however, its potential effect on pancreatic β-cell proliferation remains unclear. Here, we evaluated the role of Txnip in pancreatic β-cell compensatory proliferation by subjecting WT and Txnip knockout (KO) mice to a high-fat diet (HFD). Our results demonstrate that Txnip deficiency improves glucose tolerance and increases insulin sensitivity in HFD-induced obesity. The antidiabetogenic effect of Txnip deficiency was accompanied by increased β-cell proliferation and enhanced β-cell mass expansion. Furthermore, Txnip deficiency modulated the expression of a set of transcription factors with key roles in β-cell proliferation and cell cycle regulation. Txnip KO in HFD mice also led to activated levels of p-PI3K, p-AKT, p-mTOR and p-GSK3β, suggesting that Txnip may act via PI3K/AKT signaling to suppress β-cell proliferation. Thus, our work provides a theoretical basis for Txnip as a new therapeutic target for the treatment of diabetes mellitus.
Search for other papers by Shi-en Fu in
Google Scholar
PubMed
Search for other papers by Rou-mei Wang in
Google Scholar
PubMed
Search for other papers by Xing-huan Liang in
Google Scholar
PubMed
Search for other papers by Jing Xian in
Google Scholar
PubMed
Search for other papers by Jie Pan in
Google Scholar
PubMed
Search for other papers by Xue-lan Chen in
Google Scholar
PubMed
Search for other papers by Cheng-cheng Qiu in
Google Scholar
PubMed
Search for other papers by Zhi-ping Tang in
Google Scholar
PubMed
Search for other papers by Ying-fen Qin in
Google Scholar
PubMed
Search for other papers by Hai-yan Yang in
Google Scholar
PubMed
Department of Endocrinology, The Affiliated Hospital of Guilin Medical University, Guilin, China
Search for other papers by Li-li Huang in
Google Scholar
PubMed
Search for other papers by Ya-qi Kuang in
Google Scholar
PubMed
Search for other papers by Yan Ma in
Google Scholar
PubMed
Search for other papers by Zuo-jie Luo in
Google Scholar
PubMed
Introduction
Chronic thyrotoxic myopathy (CTM) is a common, easily neglected complication of hyperthyroidism. There are currently no standard diagnostic criteria for CTM, and the ultrasonic characteristics of CTM-affected skeletal muscle remain unclear. Herein, we aimed to evaluate hyperthyroid patients for CTM by ultrasound and identify ultrasonic muscle parameter cutoffs for CTM diagnosis.
Materials and methods
Each participant underwent ultrasonography. The original (muscle thickness (MT), pennation angle (PA), and cross-sectional area (CSA)) and corrected (MT/height (HT), MT/body mass index (BMI), CSA/HT, and CSA/BMI) parameters of the vastus lateralis and vastus medialis (VM) were evaluated. The diagnostic effectiveness of ultrasound for predicting CTM was determined using receiver operating characteristic (ROC) curve analysis. Our study included 203 participants: 67 CTM patients (18 males, 49 females), 67 non-CTM patients (28 males, 39 females) and 69 healthy controls (20 males, 49 females).
Results
The CTM group had lower muscular ultrasonic and anthropometric parameters, higher thyroid hormone and thyroid-stimulating hormone receptor antibody (TRAb) levels, and a longer duration of hyperthyroidism than the non-CTM group (P < 0.05). The VM-PA, VM-CSA, VM-CSA/HT, and VM-CSA/BMI were lower in females than in males (P < 0.05). Free thyroxine (FT4) and TRAb both showed significant negative correlations with VM-MT, VM-MT/HT, VM-CSA, and VM-CSA/HT (P < 0.05). VM-MT/BMI and VM-CSA/HT, respectively, best predicted male and female CTM (AUC = 0.84, 0.85; cutoff ≤ 0.07, < 4.01).
Conclusion
Ultrasound measurement of muscular parameters, especially in the VM, is a valid and feasible way of diagnosing and characterizing possible CTM in hyperthyroidism.
