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Type 1 diabetes mellitus (T1DM) is characterized by hyperglycemia manifesting as insufficient insulin. Toll-like receptor-4 (TLR4) has been implicated in diabetic osteoporosis. We established streptozotocin (STZ)-induced diabetic mouse model and examined the relevant osteoporosis factors in different experimental groups, the WT-CON group, WT-STZ group, KO-CON group and KO-STZ group, respectively. No obvious protection of TLR4 deletion was shown in mice with diabetes. There was no obvious difference in the body weight or blood glucose concentration between WT-STZ group and KO-STZ group. However, TLR4 deletion reduced the receptor activator of NF-κB ligand (RANKL)-induced osteoclast differentiation. Furthermore, TLR4 knockout attenuated STZ-induced diabetic osteoporosis via inhibiting osteoblasts and pre-inflammation factors mediated by the NF-κB pathway. TLR4 deletion ameliorated STZ-induced diabetic osteoporosis in mice, and TLR4 may be used as a potential therapeutic target for the treatment of diabetic osteoporosis.

Background and aim Circular RNAs (circRNAs) have been highlighted to exert essential biological functions in papillary thyroid cancer (PTC). The purpose of this study was explore diagnostic utility of circRNAs in PTC patients. Patients and methods The distinctive expression profile of serum circRNAs was determined by individual quantitative real-time PCR (qRT-PCR) in two independent cohorts of 113 PTC patients, 80 thyroid nodules, and 111 healthy controls (HCs). A combination of circRNAs (circRNA-based combination index) was constructed by logistic regression. Results Individual qRT-PCR identification showed that two circRNAs (circRAPGEF5 and hsa_circ_0058124) were significantly up-regulated in PTC patients compared with HCs and thyroid nodules. Receiver-operating characteristic (ROC) curve analysis suggested that a combination of circRNAs was superior to individual circRNA in distinguishing PTC patients from HCs and thyroid nodules with area under ROC curve of more than 0.80. Furthermore, the combination of circRNAs increased significantly after systematic treatment, suggesting that it could monitor PTC dynamics. Additionally, the combination of circRNAs was independently correlated with PTC presence. Conclusion The combination of these altered circRNAs was correlated with PTC and may serve as a novel diagnostic approach.

Castleman’s disease is a rare disease which is difficult to diagnose early due to its lack of specific manifestations, and also is easily confused with lymphoma or other solid tumors. Castleman’s disease can occur in any part of the body containing lymph nodes and is most common in the chest, followed by the neck, abdomen, and axillae. A 37-year-old woman was admitted to our hospital because of a tumor near the adrenal gland found by computed tomography. Positron emission tomography-computed tomography revealed that the retroperitoneal tumor may be a malignant disease. However, the pathological diagnosis after laparoscopic resection was retroperitoneal Castleman’s disease, hyaline vascular type.

Diabetic nephropathy (DN) is a major cause of end-stage renal disease and one of the most severe diabetic complications. However, there is lack of effective treatments for DN and the underlying mechanisms of the renal injury remain unclear. In current study, we evaluated the effects of silibinin on DN and further explored the underlying mechanisms. We administrated silibinin to db/db mice for 10 weeks. Then we monitored the diabetic metabolic parameters, kidney function, oxidative stress and AKT signaling pathway in db/db mice. Administration of silibinin to db/db mice improved diabetic condition, as evidenced by the decrease of body weight, HbAc1level and serum insulin level in db/db mice. Silibinin prevented kidney injury and attenuated oxidative stress in db/db mice. Silibinin activated AKT signaling pathway and decreased the levels of p-GSK-3β, Bax and cleaved caspase-3. Silibinin ameliorates diabetic nephropathy by activating the AKT signaling pathway.

Background Previous literatures have implied that the liver fat deposition plays a crucial role in the development and progression of insulin resistance. In the present study, we aimed to investigate the association of liver fat content (LFC) with glucose metabolism status in the population of newly diagnosed type 2 diabetes mellitus (nT2DM), prediabetes mellitus (PDM) and normal controls (NC), and assessing if the LFC could as an indicator for the prediction of T2DM. Methods A total of 242 subjects (including 141 nT2DM patients, 48 PDM subjects and 53 NC) were enrolled. The levels of LFC were quantified by using the proton magnetic resonance spectroscopy ([1H]-MRS) technique. Clinical and laboratory parameters of study subjects were collected by medical records and biochemical detection. One-way ANOVA or nonparametric test (Kruskal–Wallis) was applied for intergroup comparisons; intergroup comparison was performed in using of Bonferroni multiple-significance-test correction. Results There were significantly increased LFC levels in nT2DM (14.72% ± 6.37%) than in PDM (9.62% ± 4.41%) and that of NC groups (5.11% ± 3.66%) (all p AUC, CP30/G30 AUC, Ins AUC/G AUC, CP AUC/G AUC, homeostatic model assessment for β-cell function index (HOMA-β) and matsuda insulin sensitivity index (Matsuda ISI). Multilinear regression analysis showed that LFC, body mass index (BMI) and diastolic blood pressure (DBP) contributed for the prediction of HOMA-IR, and total cholesterol (TC), age, waist circumference (WC) and low-density lipoprotein cholesterol (LDL-C) were the significant contributors for HOMA-β. Conclusions Our study revealed an increased LFC level and prevalence of NAFLD in nT2DM than in PDM and that of NC groups, the increase of LFC was closely associated with insulin resistance and impaired glucose metabolism status, may be regarded as potential indicator contributing to the development and progression of T2DM.

Introduction To investigate the serum retinol binding protein (RBP)-4, cystatin C (Cys C), homocysteine (HCY) and high-sensitivity C-reactive protein (hs-CRP) levels in newly diagnosed type 2 diabetes mellitus (NT2DM) patients, prediabetes mellitus (PDM) subjects and normal controls, as well as their correlation with clinical and laboratory indexes, such as blood pressure and lipoprotein. Material and methods A total of 242 subjects, including 141 NT2DM patients, 48 PDM subjects and 53 healthy controls, were recruited in the present study. Serum RBP-4, Cys C and hs-CRP concentrations were measured by enzyme-linked immunosorbent assay (ELISA). HCY concentration was determined by the chemical luminescence method. Results There were significant differences in Cys C and hs-CRP among NT2DM patients, PDM subjects and normal controls. In comparison to controls, there were significantly elevated Cys C and hs-CRP levels in PDM (both p < 0.001), and a significantly increased Cys C level in NT2DM (p < 0.001); however, there were no significant differences in Cys C and hs-CRP levels between NT2DM and PDM, and no significant differences of hs-CRP levels between NT2DM and normal controls. No significant differences of RBP-4 and HCY levels among NT2DM, PDM and normal control groups were observed. Conclusions Aberrant Cys C expression and its clinical associations in NT2DM suggest their important role in this disease.

Objectives Fibroblast growth factor-21 (FGF-21) plays an important role in glucose and lipid metabolism. This study aims to systemically review the evidence regarding the relationship between the FGF-21 levels and type 2 diabetes mellitus (T2DM), as well as the related influential factors. Methods Research related to plasma/serum FGF-21 levels in patients with T2DM and healthy controls were searched in PubMed, EMBASE and The Cochrane Library databases (up to 31 March 2017). Pooled standard mean difference (SMD) with 95% CI was calculated by fixed-effect or random-effect model analysis. Heterogeneity test was performed by the Q-statistic and quantified using I2, and publication bias was evaluated using a funnel plot and Egger’s linear regression test. Results In total, 317 articles were obtained after searching databases, and 11 studies with 866 patients with T2DM and 629 controls were finally included. Meta-analysis revealed that, compared with the control group, the T2DM group had a significantly higher plasma/serum FGF-21 level (p < 0.001), with the SMD of 1.34% and 95% CI (0.70 to 1.98). Meta-regression analysis and subgroup analyses suggested that body mass index (BMI), triglycerides (TG) and total cholesterol (TC) were likely related to the observed FGF-21 differences between two groups. Conclusions Overall, our study suggests that patients with T2DM have significantly higher plasma/serum FGF-21 levels, and the FGF-21 levels were influenced by BMI, TC and TG.