diabetes mellitus (dM) is a growing health concern in society. Type 1 and type 2 dM are the two main types of diabetes; both types are chronic diseases that affect glucose metabolism in the body and the impaired regulation of glucose and lipid metabolism promotes the development and progression of dM. during the physiological metabolism process, the liver serves a unique role in glucose and lipid metabolism. The present article aimed to review the association between dM and glucose metabolism in the liver and discuss the changes of the following hepatic glucose fluxes: Gluconeogenesis, glucose/glucose 6-phosphate cycling, glycogenolysis, glycogenesis and the pentose phosphate pathway. Moreover, the incidence of fatty liver in dM was also investigated. Contents 1. introduction 2. Metabolic processing of glucose in the liver under diabetic conditions 3. conclusion

K.W. and X.D. contributed equally to this study.

Diabetic vascular complications are closely associated with long‐term vascular dysfunction and poor neovascularization. Endothelial progenitor cells (EPCs) play pivotal roles in maintaining vascular homeostasis and triggering angiogenesis, and EPC dysfunction contributes to defective angiogenesis and resultant diabetic vascular complications. Fibroblast growth factor 21 (FGF21) has received substantial attention as a potential therapeutic agent for diabetes via regulating glucose and lipid metabolism. However, the effects of FGF21 on diabetic vascular complications remain unclear. In the present study, the in vivo results showed that FGF21 efficiently improved blood perfusion and ischaemic angiogenesis in both type 1 and type 2 diabetic mice, and these effects were accompanied by enhanced EPC mobilization and infiltration into ischaemic muscle tissues and increases in plasma stromal cell–derived factor‐1 concentration. The in vitro results revealed that FGF21 directly prevented EPC damage induced by high glucose, and the mechanistic studies demonstrated that nicotinamide adenine dinucleotide (NAD+) was dramatically decreased in EPCs challenged with high glucose, whereas FGF21 treatment significantly increased NAD+ content in an AMPK‐dependent manner, resulting in improved angiogenic capability of EPCs. These results indicate that FGF21 promotes ischaemic angiogenesis and the angiogenic ability of EPCs under diabetic conditions by activating the AMPK/NAD+ pathway.

Objective: To compare the safety and efficacy of warfarin plus aspirin versus aspirin alone for the treatment of children with giant coronary artery aneurysm (CAA) secondary to Kawasaki disease (KD). Methods: We searched the PubMed, EMBASE, Cochrane Library, CNKI, WANFAN and VIP databases. We selected case-controlled trials of warfarin plus aspirin versus aspirin alone for the treatment of children with giant CAA secondary to KD. Results: Six retrospective studies met our inclusion criteria. There was no significant difference between the warfarin plus aspirin and aspirin alone groups in the rate of CAA regression (OR 1.38, 95% CI 0.52-3.68, p = 0.52) or the incidence of persistent CAA (OR 2.34, 95% CI 0.16-33.50, p = 0.53), coronary artery stenosis (OR 0.55, 95% CI 0.18-1.72, p = 0.30) or thrombus formation (OR 0.50, 95% CI 0.15-1.69, p = 0.26). There was evidence that warfarin plus aspirin reduced the incidence of coronary artery occlusion (OR 0.08, 95% CI 0.02-0.29, p < 0.0001), cardiac infarction (OR 0.27, 95% CI 0.11-0.63, p = 0.003) and death (OR 0.18, 95% CI 0.04-0.88, p = 0.03). Conclusion: Warfarin plus aspirin therapy reduced the incidence of occlusion, cardiac infarction and death in children with giant CAA secondary to KD.