Aims/IntroductionStudies suggest that salivary proteins can be used as potential non‐invasive markers for clinical diagnosis and screening for diabetes. Previous reports showed that plasma alpha 2‐macroglobulin (A2MG) levels were higher in diabetic patients, especially with diabetic complications. We investigated the relationship between salivary A2MG values and clinical characteristics in patients with type 2 diabetes.Materials and MethodsA total of 91 adults were recruited from our outpatient clinics. The study the patients' collected general and biochemical data, and blood glucose (fasting glucose, glycated hemoglobin [HbA1c]) data. Plasma and salivary A2MG levels were examined by enzyme‐linked immunosorbent assay.ResultsThe salivary A2MG levels were significantly positively correlated with plasma A2MG levels, fasting glucose HbA1c and periodontitis status. After 3 months of follow up, the net change of salivary A2MG values positively correlated with the net change of fasting glucose, HbA1c and triglyceride levels, but negatively correlated with high‐density lipoprotein cholesterol changes. Furthermore, the correlations between salivary A2MG and fasting glucose HbA1c were better than plasma A2MG, respectively.ConclusionsOur data show that salivary A2MG levels have better correlation with fasting glucose HbA1c and periodontitis status than plasma A2MG in diabetic patients. Salivary A2MG concentration might serve as a non‐invasive marker for clinical diabetic control.

Adiponectin is a major adipokine that seems to have a crucial role in the protection from many metabolic abnormalities. There have been several reports that suggest a strong inverse relationship between plasma levels of adiponectin and the severity of obesity and its comorbidities, such as insulin resistance, type 2 diabetes and cardiovascular disease. Restoring adiponectin levels has salient benefits in many of the obesity-related diseases, which provides a strong rationale for adiponectin-based therapeutics for treating metabolic abnormalities. A Japanese team of researchers has screened and identified an orally active compound that binds to and activates the adiponectin receptor 1 (AdipoR1) and AdipoR2 receptors that are named AdipRon. This molecule ameliorates insulin resistance and glucose intolerance in obese animal models, and also extends the shortened lifespan of diabetic obese mice. If this work can be extended to humans, the improved safety and efficacy of these orally active adiponectin agonists could offer a promising new approach to treating obesity-related diseases.

Background Cigarette smoking is the most significant cause of oral cancer progression. Cigarette smoke condensate (CSC) has been shown to induce endoplasmic reticulum (ER) stress. Binding immunoglobulin protein (BiP) being as an ER stress regulator, has been reported to be implicated in malignant behaviors. Therefore, the aim of this study was to investigate the role of the ER stress-responsive protein, BiP, in CSC-induced oral squamous cell carcinoma (OSCC) malignancy. Methods The biological role of BiP in CSC-induced tumor progression was investigated in OSCC cells (YD38 and SCC25) and in a tumor xenograft mouse model. The expressions of related genes were investigated using quantitative RT-PCR and Western blot analysis. Cell migration and invasion were assessed using scratch wound healing and Transwell invasion assays. The effects of conditioned media from OSCC cells on the angiogenic activities of endothelial cells were analyzed using a tube formation assay. The interaction between miR-30a and BiP mRNA was detected using a luciferase reporter assay. Results Our results demonstrated that CSC increased the expression of BiP in time- and dose-dependent manners in YD38 and SCC25 cells, and that silencing BiP abrogated CSC-induced cell invasion and tumor-associated angiogenesis. Notably, the putative miR-30a binding site was observed in the 3′untranslated region (UTR) of BiP mRNA, and miR-30a suppressed BiP expression by targeting 3′UTR of BiP transcript. In addition, CSC increased the expression of BiP in OSCC cells by downregulating miR-30a. We also showed that BiP promoted invasion and tumor-associated angiogenesis by increasing the production and secretion of vascular endothelial growth factor in CSC-exposed OSCC cells. Moreover, BiP inhibition suppressed OSCC growth and reduced tumor vessel density in tumor-bearing mice administered with CSC. Conclusions These observations suggest that epigenetic regulation of BiP via miR-30a downregulation is involved in CSC-induced OSCC progression.