Studies have shown that there are differences between genders regarding to the occurrence and development of liver diseases, which may be associated with sex hormones. However, the mechanisms behind it are largely unknown. In this study, we first investigated the differences of liver injury between male and female mice, using the CCl4 induced liver injury mouse model. It showed that the liver damage of male mice was much more severe than that of female mice. Both the acute injury and fibrosis of the liver were reduced when androgens were depleted by castration of male mice. The vulnerability of male liver was associated with testis endocrine and excessive activation of inflammatory response in the liver. Castrated male mice with testosterone supplementation showed aggravated liver inflammatory response and fibrosis. The activity of NOD-like receptor protein 3 (NLRP3) inflammasome was increased when testosterone supplementation was provided. However, the enhanced inflammatory response and fibrosis due to testosterone supplementation were negated by inhibiting the activation of NLRP3 using the specific small molecule inhibitor MCC950. It suggests that testosterone is a key factor that influences liver injury by regulating NLRP3 inflammasome activation mediated inflammatory response.Irisin, a newly identified myokine, is critical to modulating metabolism and biological homeostasis. However, whether irisin protects the skeletal muscles against the metabolic stresses remains unknown. In this study, we determine the effect of irisin on high glucose and fatty acid induced damages using irisin overexpressed mouse C2C12 myoblast (Irisin-C2C12) and skeletal muscle from irisin-injected mice. As compared to empty vector transfected control, irisin overexpression resulted in a marked increase of cell viability and decrease of apoptosis under high glucose stress. Progression of cell cycle into G2/M phase under proliferative condition was observed by irisin overexpression. Furthermore, glucose uptake, glycogen accumulation and phosphorylation of AMPKα / insulin receptor β subunit (IRβ) / Erk1/2 in response to insulin stimulation were enhanced by irisin overexpression. In irisin-C2C12 myoblasts, these responses of phosphorylation were preserved under palmitate (PA) treatment which induced insulin resistance. These effects of irisin were reversed by inhibiting AMPK with compound C. Additionally, high glucose-induced suppression of mitochondrial membrane potential was also prevented by irisin. Moreover, suppression of IR in Irisin-C2C12 myoblasts by co-transfection of shRNA against IR also mitigated the effects of irisin while not affecting the AMPKα phosphorylation. Furthermore, soleus muscles from irisin injected mice showed elevated phosphorylation of AMPKα and Erk1/2 and glycogen contents. Our results indicate that irisin counteracts to the stresses generated by high glucose and fatty acid and serves as a novel approach to eliciting cellular protection. Furthermore, AMPK activation is a crucial factor which regulates insulin action as a downstream target.Enhanced meal-related enteroendocrine secretion, particularly of glucagon-like peptide-1 (GLP-1), contributes to weight-loss and improved glycemia after Roux-en-Y gastric bypass (RYGB). Dietary glucose drives GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) secretion postoperatively. Understanding how glucose triggers incretin secretion following RYGB could lead to new treatments of diabetes and obesity. In vitro, incretin release depends on glucose absorption via sodium-glucose cotransporter-1 (SGLT1). We investigated the importance of SGLT1/SGLT2 for enteropancreatic hormone concentrations and glucose metabolism after RYGB in a randomized, controlled, crossover study. Ten RYGB-operated patients ingested 50 g of oral glucose ± acute pretreatment with 600 mg of the SGLT1/SGLT2-inhibitor canagliflozin. Paracetamol and 3-O-methyl-D-glucopyranose (3-OMG) were added to the glucose drink to evaluate rates of intestinal entry and absorption of glucose, respectively. Blood samples were collected for 4 h. The primary outcome was 4-h plasma GLP-1 (incremental area-under-the-curve, iAUC). Secondary outcomes included glucose, GIP, insulin and glucagon. Canagliflozin delayed glucose absorption (time-to-peak 3-OMG 50 vs. 132 min, p less then 0.01) but did not reduce iAUC GLP-1 (6067 vs. 7273 min∙pmol/l, p=0.23), although peak GLP-1 concentrations were lowered (-28%, p=0.03). Canagliflozin reduced GIP (iAUC -28%, p=0.01; peak concentrations -57%, p less then 0.01), insulin and glucose excursions, whereas plasma glucagon (AUC 3216 vs. 4160 min∙pmol/l, p=0.02) and amino acids were increased. In conclusion, acute SGLT1/SGLT2-inhibition during glucose ingestion did not reduce 4-h plasma GLP-1 responses in RYGB-patients, but attenuated the early rise in GLP-1, GIP and insulin, whereas late glucagon concentrations were increased. The results suggest that SGLT1-mediated glucose absorption contributes to incretin hormone secretion after RYGB.Objectives To explore infant-feeding intentions and behavior of physician mothers as well as their breastfeeding enablers and obstacles. Study Design A cross-sectional online survey was conducted among female physicians with at least one biological child recruited through the Academy of Breastfeeding Medicine. The main outcomes were duration of exclusive breastfeeding (EBF) and duration of any breastfeeding (BFD). We determined predictors of EBF and BFD. Results The 570 participants reported intention to breastfeed at least 12 months in 78.1% of cases. Breastfeeding rates were 97.8%, 85.5%, and 55.4% at birth, 6, and 12 months. EBF rates were 88.5%, 76.3%, and 40.9% at birth, 3, and 6 months. Younger participant age, breastfeeding discontinuation not due to work-related demands, and heightened maternal satisfaction with BFD were associated with longer EBF and BFD. EBF at birth, less maternal stress, availability of time to express milk, and collegial support were associated with longer EBF. CDK activity Longer maternal BFD goal, longer maternity leave, existence of laws or regulations to support breastfeeding among working mothers, later child order, and lower level of maternal depression were associated with longer BFD. Conclusions Maternal infant-feeding intentions and work-related factors both play important roles in physician mothers’ infant-feeding behavior. Longer maternity leave, regulations to support breastfeeding among working mothers, and workplace support might significantly improve physician mothers’ BFD.