Aims/Introduction Asprosin is a novel secreted adipokine that is induced by fasting and promotes hepatic glucose release. In healthy humans, circulating asprosin shows circadian oscillation with an acute drop coinciding with the onset of eating. The present study investigated whether this circadian oscillation still exists in patients with type 2 diabetes mellitus. Materials and Methods We recruited 60 patients with type 2 diabetes mellitus and 60 individuals with normal glucose tolerance (NGT). All participants completed a 75‐g oral glucose tolerance test. Fasting and 2‐h postprandial serum asprosin concentrations were measured by the enzyme‐linked immunosorbent assay method. Partial correlation coefficients were calculated to analyze the relationships between serum asprosin level and parameters of glucose metabolism. Multiple logistic regression analysis was used to determine the association of serum asprosin level with diabetes. Results Both fasting and postprandial asprosin levels were significantly higher in patients with type 2 diabetes mellitus. The postprandial asprosin level was apparently lower than fasting asprosin level in individuals with NGT. The fasting asprosin level closely correlated with type 2 diabetes mellitus after multiple adjustment (odds ratio 2.329, P = 0.023). Asprosin correlated negatively with change in blood glucose (r = −0.502, P < 0.001) and change in C‐peptide (r = −0.467, P < 0.001) in individuals with NGT, but not in type 2 diabetes mellitus patients. Conclusions Serum asprosin level decreased coinciding with the onset of the oral glucose tolerance test in individuals with NGT, whereas this circadian oscillation was disturbed in type 2 diabetes mellitus patients. The impaired response of asprosin to glucose fluctuation in type 2 diabetes mellitus patients might be one of the reasons for the onset of type 2 diabetes mellitus.

BackgroundPneumatosis cystoides intestinalis (PCI) is characterized by gas-filled cysts in the intestinal submucosa and subserosa. There are few reports of PCI occurring in duodenum and rectum. Here we demonstrated four different endoscopic manifestations of PCI and three cases with intestinal stricture all were successfully managed by medical conservative treatment.Case presentationThere are 6 cases of PCI with varied causes encountered, in which the etiology, endoscopic features, treatment methods and prognosis of patients were studied. One case was idiopathic, while the other one case was caused by exposing to trichloroethylene (TCE), and the remaining four cases were secondary to diabetes, emphysema, therioma and diseases of immune system. Of the six patients, all complained of abdominal distention or diarrhea, three (50%) reported muco-bloody stools, two (33.3%) complained of abdominal pain. In four other patients, PCI occurred in the colon, especially the sigmoid colon, while in the other two patients, it occurred in duodenum and rectum. Endoscopic findings were divided into bubble-like pattern, grape or beaded circular forms, linear or cobblestone gas formation and irregular forms. After combination of medicine and endoscopic treatment, the symptoms of five patients were relieved, while one patient died of malignant tumors.ConclusionPCI endoscopic manifestations were varied, and radiology combined with endoscopy can avoid misdiagnosis. The primary bubble-like pattern can be cured by endoscopic resection, while removal of etiology combined with drug therapy can resolve majority of secondary cases, thereby avoiding the adverse risks of surgery.

Signaling by viral nucleic acids and subsequently by type I IFN is central to antiviral innate immunity. These signaling events are also likely to engage metabolic changes in immune and nonimmune cells to support antiviral defense. In this study, we show that cytosolic viral recognition, by way of secondary IFN signaling, leads to upregulation of glycolysis preferentially in macrophages. This metabolic switch involves induction of glycolytic activator 6-phosphofructose-2-kinase and fructose-2,6-bisphosphatase (PFKFB3). Using a genetic inactivation approach together with pharmacological perturbations in mouse cells, we show that PFKFB3-driven glycolysis selectively promotes the extrinsic antiviral capacity of macrophages, via metabolically supporting the engulfment and removal of virus-infected cells. Furthermore, the antiviral function of PFKFB3, as well as some contribution of its action from the hematopoietic compartment, was confirmed in a mouse model of respiratory syncytial virus infection. Therefore, different from the long-standing perception of glycolysis as a proviral pathway, our findings establish an antiviral, immunometabolic aspect of glycolysis that may have therapeutic implications.