Objective To establish a stable and reliable mouse model as an alternative to the traditional model of impaired glucose tolerance induced by calorie restriction and its effect on glucose homeostasis.Methods Forty 16-week-old SPF C57BL/6J mice (half male and half female) were randomly divided into four groups by sex and the way of feeding.The mice in the ad libitum (AL) group had free access to basic diet, while the mice in the intermittent fasting (IF) group had normal diet and fasting on alternate days, with free access to water on the fasting days.The changes of body weight and blood glucose concentration in each group were monitored, and intraperitoneal glucose tolerance test and insulin tolerance test in mice were performed before and after the 12-week IF treatment.Results At 12 weeks after IF treatment, the body weight and blood glucose concentration of mice did not show significant difference.After i.p.injection of glucose, the blood glucose concentration of IF mice was less increased than the AL group, and after the insulin injection, the blood glucose concentration was more decreased.Compared to the AL group, the areas under the curve of tolerance test in the IF group were significantly decreased (P < 0.05).Conclusions After IF treatment, the mice show an enhanced sensitivity to insulin and improved glucose tolerance.This establishment method of mouse model of intermittent fasting is easy and simple, therefore, can be used as an effective alternative to traditional calorie restriction model of impaired glucose tolerance.

Tumor dormancy refers to the status of disseminated cancer cells that remain in a viable yet not proliferating state for a prolonged period. Dormant cells will eventually "re-awake" resume their proliferation, and produce overt metastasis. The dormancy mechanism of cancer has attracted attention because of the close relationship between late recurrence and tumor dormancy. In this review, we illustrate the latest discoveries on the biological underpinnings of breast cancer dormancy and offer clinicians an overview of dormancy in breast cancer to guide them in the basic understanding of the complexity that underlies this process.

Objective To investigate the effect of knockdown of O-GlcNAc transferase (OGT) on hepatocyte fat synthesis.Methods Liver cell line L02 were used to established the model of hepatic steatosis.The levels of OGT and O-GlcNAc protein were detected by Western blot.The OGT knockdown cell line of L02 cells was established,and its lipid formation ability was detected after induction of oleic acid (OA).Real-time quantitative PCR (qRT-PCR) and Western blot were used to detect mRNA and protein expression of enzymes related to fat synthesis.An independent sample t test was used.Results Western blot showed that the expression of OGT and O-GlcNAc was increased in L02 cells after adipogenesis (P ＜ 0.05).After shOGT lentivirus infects L02 cells,OGT mRNA levels were down-regulated (P ＜ 0.01).Oil red O staining showed that the lipid in L02 shOGT cells decreased,qRT-PCR showed that the mRNA expressions of fat synthase (ACC1),(FASN) and (SCDl) were decreased,the difference was statistically significant (P ＜ 0.05),protein Expression is consistent with mRNA expression.Conclusion Knockdown of OGT can inhibit hepatocyte fat synthesis by reducing O-GlcNAc levels.

Animals ; Gastrointestinal Microbiome ; Gastrointestinal Tract ; microbiology ; Humans ; Obesity ; microbiology ; pathology ; therapy