Introduction:We aimed to elucidate the relationship between CXC chemokine ligand 10 (CXCL10) and miR-16-5p, and their functions on the biological behaviour of type 1 diabetes mellitus (T1DM). Material and methods: The GSE72492 dataset from the GEO database was used to analyse gene expression. We discovered that CXCL10 was highly expressed in T1DM patients. The up-stream miRNA was predicted by Targetscan website. Low glucose (2.8 mmol/L) and high glucose (HG, 16.7 mmol/L) were utilised to treat b-TC-tet (pancreatic b cell) cells to form the model. The direct interaction between miR-16-5p and CXCL10 was verified by a dual-luciferase reporter assay. Real-time quantitative PCR (qRT-PCR) and western blotting analyses were used to detect RNA and protein expression. CCK8 and flow cytometry were used to detect cell proliferation and apoptosis. Results: We discovered that CXCL10 was highly expressed in T1DM patients. MiR-16-5p, which was lowly expressed in T1DM patients, was verified the upstream regulatory miRNA of CXCL10. The facilitating influence of miR-16-5p up-regulation on the proliferation of HG-induced b-TC-tet cells was reversed by CXCL10 over-expression, while the knockdown results were opposite. More importantly, the restraining impact of miR-16-5p high expression on the apoptosis of HG-induced b-TC-tet cells was accelerated by CXCL10 over-expression. Correspondingly, the level of Bcl-2 was enhanced while the levels of Bax and Cleaved Caspase-3 were lowered by miR-16-5p mimic, which were reversed by CXCL10 over-expression in HG-treated b-TC-tet cells. Conclusions: Our data offered evidence that miR-16-5p implicated in T1DM cell proliferation and apoptosis through targeting CXCL10, which might provide novel therapeutic information for T1DM. (Endokrynol Pol 2020; 71 (5): 404-410

BackgroundThe aim of this study was to evaluate the differently expressed genes (DEGs) relevant to type 2 diabetes mellitus (T2DM) and pathway by performing integrated bioinformatics analysis.Material/MethodsThe gene expression datasets GSE7014 and GSE29221 were downloaded in GEO database, and DEGs from type 2 diabetes mellitus and normal skeletal muscle tissues were identified. Biological function analysis of the DEGs was enriched by GO and KEEG pathway. A PPI network for the identified DEGs was built using the STRING database.ResultsThirty top DEGs were identified from 2 datasets: GSE7014 and GSE29221. Of the 30 top DEGs, 20 were up-regulated and 10 were down-regulated. The 20 up-regulated genes were enriched in regulation of mRNA, protein biding, and phospholipase D signaling pathway. The 10 down-regulated genes were enriched in telomere maintenance via semi-conservative replication, AGE-RAGE signaling pathway in diabetic complications, and insulin resistance pathway. In the PPI network of 20 up-regulated DEGs, there were 40 nodes and 84 edges, with an average node degree of 4.2. For the 10 down-regulated DEGs, we found a total of 30 nodes and 105 edges, with an average node degree of 7.0 and local clustering coefficient of 0.812. Among the 30 DEGs, 10 hub genes (CNOT6L, CNOT6, CNOT1, CNOT7, RQCD1, RFC2, PRIM1, RFC4, RFC5, and RFC1) were also identified through Cytoscape.ConclusionsDEGs of T2DM may play an essential role in disease development and may be potential pathogeneses of T2DM.

Background: Diabetic peripheral neuropathy (DPN) is one of the most common chronic complications of diabetes. As apelin is an adipocytokine closely associated with diabetes, this study explored the clinical significance of serum apelin levels in patients with type 2 DPN before and after treatment. Methods: In total, 44 patients with T2DM without DPN (non-DPN group), 41 patients with DPN who received antihyperglycemic treatment (DPN-A group), 44 patients with DPN who received antihyperglycemic treatment combined with nutritional neurotherapy (DPN-B group), and 40 healthy control individuals (NC group) were selected continuously enrolled in the present study. Enzyme-linked immunosorbent assays (ELISA) were performed to determine serum levels of apelin and tumor necrosis factor-α (TNF-α). Related apelin, fasting blood glucose (FBG), glycosylated hemoglobin A1c, TNF-α, body mass index, fasting C peptide, and nerve conduction velocity (NCV) were recorded in each group before and after treatment. Results: Serum levels of apelin and TNF-α were higher in patients with diabetes than those in the NC group, as well as in the DPN group as compared to the non-DPN group; furthermore, some NCV values were significantly reduced in the DPN group. After treatment, the serum levels of apelin, TNF-α, and FBG reduced in patients with diabetes; moreover, apelin levels were found significantly lower in the DPN-B group as compared to the DPN-A group, while some NCV values significantly increased in the DPN-B group. Apelin was negatively correlated with part of NCV values and positively correlated with TNF-α and FBG (P < .01). Conclusion: Our results show that the increase in serum apelin levels is an important clinical reference index for DPN, while a decrease indicates that the DPN treatment is effective.