ABSTRACT
OBJECTIVE Tostudytheeffectofmetforminonglucolipidmetabolicdisorderscaused byolanzapineorquetiapineinrats.METHODS Olanzapine1mg·kg-1·d-1wasgivenigorquetiapine 20 mg·kg -1·d -1 was given ig for 4 d,and the dose increased to 40 mg·kg -1·d -1 from the 5th day.Met-formin 100 mg·kg -1·d -1 was given ig from the 15th day.The treatment lasted 8 weeks.Body mass, fasting blood sugar (FBS)and postprandial 2 hours blood glucose (2hPBG)were measured at base-line,3 d,1 week,2 week,4 week,6 week and 8 week.At the end of the 8th week,serum cholesterol (TC),triglyceride (TG),low density lipoprotein (LDL-C),high density lipoprotein (HDL-C),fruc-tosamine(FA)andinsulin(IRS)weremeasured.RESULTS Therewasnosignificantstatisticaldiffer-ence between normal control group and metformin 1 00 mg·kg -1·d -1 group.At the end of the 6th week, compared with normal control group,the body mass and 2hPBG were significantly increased in olanzap-ine 1 mg·kg -1·d -1 group and quetiapine 40 mg·kg -1·d -1 group (P<0.05),respectively.At the end of the 8th week,body mass,2hPBG,INS,FA,TC,TG,LDL-C were significantly increased (P<0.05), and HDL-C decreased in olanzapine group and quetiapine group(P<0.05),respectively.FBS was increased only in olanzapine group(P<0.05).Compared with olanzapine group or quetiapine group, body mass,FBS,2hPBG,INS,FA,TC,TG,LDL-C were significantly decreased by metformin admin-istration(P<0.05).CONCLUSION Metformincaneffectivelypreventandtreatweightgainand glucolipid metabolic disorder caused by olanzapine or quetiapine.
ABSTRACT
[ABSTRACT]AIM:Toestablishatransgenicheterozygousmousemodelofprecancerouslesionsofcolorectal cancer with p110δmutation in the C57BL/6J background for serving the studies on colorectal cancer research mediated by p110δ.METHODS:The transgenic heterozygous mice were generated by crossing in p110δD910A/D910A mouse and ApcMin/+mouse, and the genotype was detected by PCR .Compared with ApcMin/+mice, transgenic heterozygous mice ( ApcMin/+;p110δD910A/D910A)were counted, and the number and size of intestine polyps were analyzed after methylene blue staining . The intestinal tissue structure was assessed by HE staining .RESULTS:The transgenic heterozygous mouse model of pre-cancerous lesions of colorectal cancer with p 110δmutation was established .The number and size of polyps in the transgenic heterozygous mice were declined .CONCLUSION: A transgenic heterozygous mouse model of precancerous lesions of colorectal cancer with p 110δmutation was successfully established .The initial phenotype of intestinal tumors in transgenic mice was observed .This model will greatly contribute to the related research of colorectal cancer in mice .