Correlations of high molecular weight adiponectin, tumor necrosis factor-alpha and vascular endothelial growth factors with occurrence of colonic polyps in the prediabetic population.

We aimed to explore the correlations of high molecular weight adiponectin (HMW-ADP), tumor necrosis factor-alpha (TNF-α) and vascular endothelial growth factors (VEGFs) with the occurrence of colonic polyps in the prediabetic population. Two hundred patients with prediabetes were enrolled, and their clinical data were retrospectively analyzed. They were divided into group A (75 patients with colonic polyps) and group B (125 patients without colonic polyps). Eighty patients with normal glucose tolerance in the same period were divided into group C (32 patients with normal glucose tolerance and colonic polyps) and group D (48 patients with normal glucose tolerance but no colonic polyps). The correlations of serum HMW-ADP, TNF-α and VEGF levels with plasma glucose and insulin levels were explored by Pearson's analysis. The factors influencing the occurrence of colonic polyps were determined by logistic regression analysis. Serum HMW-ADP was negatively correlated with TNF-α, VEGFs, FPG, 2hPG, FI and HOMA-IR (r<0, P<0.05), whereas serum TNF-α and VEGFs were positively correlated with FPG, 2hPG, FI and HOMA-IR (r>0, P<0.05). Age, body mass index, waist-to-hip ratio, history of smoking, history of drinking, family history of colon cancer, TNF-α and VEGF were independent risk factors [odds ratio (OR)>1, P<0.05], and HMW-ADP was a protective factor (OR<1, P<0.05). The areas under the curves of serum HMW-ADP, TNF-α, VEGFs and their combination for predicting the occurrence of colonic polyps were 0.899, 0.787, 0.908 and 0.922, respectively. The combination of HMW-ADP, TNF-α and VEGFs can effectively predict the occurrence of colonic polyps in prediabetic patients.

Inhibition of Autophagy in Renal Cells With Human, Urine-derived, Stem-cell Exosomes to Improve Diabetic Nephropathy.

Context: Clinicians can use stem cells to repair kidney injury. The kidneys' exosome secretions hold the secret to this therapeutic impact. Exosomes from urine-derived stem cells can prevent and treat glomerular damage that diabetes can cause, but the underlying process has remained a mystery. Objective: The study aimed to investigate the protective impact of exosomes from urine-derived stem cells (USCs) against diabetic nephropathy (DN) and to determine the mechanisms involved. Design: The research team performed an animal study. Setting: The study took place at the Affiliated Hospital of Jiujiang University in Jiujiang, Jiangxi, China. Animals: The animals were rats, SD male rats, weighing 200-220g, 40 animals, purchased from Weitong Lihua Experimental Animal Technology Co., Ltd. (certificate number: SCXK (Beijing) 2021-0006). Intervention: Except for a control group, the rats in the groups had induced DN. The five groups, with 10 rats each, were: (1) the negative control group, which received 0.2 ml of PBS solution; (2) the DN group, a second negative control group, which received 0.2 ml of PBS solution, (3) the inhibitor group, an intervention group that received 20 mg/kg of autophagy inhibitor; (4) the exosomes group, an intervention group that received 100 ug/kg of exosomes; and (5) the exosomes + inhibitor group, an intervention group that received 100 ug/kg of exosomes + 20 mg/kg of autophagy inhibitor. From week 8, for four weeks the team injected the inhibitor, exosomes, and exosomes + inhibitor groups with the appropriate treatments using the rats' tail veins. Outcome Measures: The research team: (1) examined the USCs in the exosomes of stem cells; (2) assessed the rats' weights and fasting blood glucose (FBG), using a blood glucose meter; (3) used Coomassie brilliant blue (CBB) staining to determine the amount of protein in the rats' urine and assessed their biochemical indexes; and (4) used Western blot (WB) and a quantitative polymerase chain reaction (Q-PCR) to detect autophagy and the signal transduction pathway. Results: Human exosomes from USCs alleviated injury in the rats that DN caused by reducing urinary-protein levels, serum creatinine (SCR), blood urea nitrogen (BUN), glomerular cell accumulation, and kidney weights. In rats with induced DN, the exosomes + inhibitor significantly reduced the activation of the mTOR signaling pathway, reduced the autophagy of their kidney cells, increased the protein expression of Bcl-2 in the kidney tissues, and lessened the damage to glomerular cells. Conclusions: Human urine-derived stem cell exosomes can significantly reduce the activation of the mTOR signaling pathway, reduce the autophagy of rats' kidney cells, increase the protein expression of LC3B in kidney tissues, and reduce the damage to glomerular cells. By blocking the mTOR signaling pathway, human urogenic exosomes can alleviate the signs and symptoms of DN.