title: [Biochemical and pathological analysis of mice with type 2 diabetes mellitus induced by high-fat diet and low-dose streptozotocin injections].
abstract: OBJECTIVE
  To analyze the biochemical and pathological changes in mice with type 2 diabetes mellitus (T2DM) induced by high-fat diet combined with low-dose streptozotocin (STZ) injections.
  
  
  METHODS
  C57BL/6J mice were divided randomly into normal control group (NC group), high-fat diet group (HC group) and high-fat diet plus STZ group (HC+STZ group). The mice were fed on normal chow or a high-fat diet for 1 month before two introperitoneal injections of STZ (40 mg/kg) or citrate buffer with an interval of 24 h as appropriate. Fasting blood glucose (FBG) was detected every week for 4 weeks, and oral glucose tolerance test (OGTT) was performed one month after the injections, after which the biochemical profiles, islet and liver were evaluated by immunohistochemical and pathological analysis.
  
  
  RESULTS
  In HC+STZ group, FBG was above the cutoff value (13.89 mmol/L) in 75% of the mice at 1 week after STZ injections and in all the mice at two weeks except for the death of 1 mouse, with a success rate of modeling of 91.3%. FBG in HC group, though slightly higher than that in NC group, remained normal (6.8 mmol/L). The body weight in HC+STZ and HC groups was significantly higher than that in NC group after feeding but without obvious increases after the injections (P<0.01). Blood glucose in HC+STZ group at 0.5 to 2 h after OGTT and the area under curve (AUC) were higher than those in NC and HC groups (P<0.01); the AUC in HC group was a also higher than that in NC group (P<0.05). Plasma creatinine was significantly higher in HC+STZ group than in NC (P<0.01) and HC (P<0.05) groups. Insulin secretion by the islets decreased obviously in HC+STZ and HC group. The mice in HC+STZ group showed atrophy, fibrosis, and vacuolization in the islets with mild fatty liver but no visible renal pathologies.
  
  
  CONCLUSIONS
  High-fat diet and low-dose STZ injections can induce T2DM in mice with very similar biochemical and pathological changes to human T2DM and with such complications as fatty liver.
authors.affiliation: Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.E-mail: zengws@smu.edu.cn.
authors.forename: Weisen
authors.initials: W
authors.lastname: Zeng
authors.forename: Yuanjian
authors.initials: Y
authors.lastname: Huang
authors.forename: Congwen
authors.initials: C
authors.lastname: Shao
authors.forename: Baohuan
authors.initials: B
authors.lastname: Liang
authors.forename: Cheng
authors.initials: C
authors.lastname: Wei
authors.forename: Wanfu
authors.initials: W
authors.lastname: Xu
authors.forename: Yaru
authors.initials: Y
authors.lastname: Su
mesh_terms: D000818:Animals; D001786:Blood Glucose; D001835:Body Weight; D003924:Diabetes Mellitus, Type 2 / Q000503:physiopathology*; D059305:Diet, High-Fat; D005234:Fatty Liver / Q000503:physiopathology; D005951:Glucose Tolerance Test; D007328:Insulin; D007333:Insulin Resistance; D007515:Islets of Langerhans / Q000473:pathology; D007668:Kidney / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D013311:Streptozocin
chemical_list: D001786:Blood Glucose; D007328:Insulin; D013311:Streptozocin