title: Metformin improves lipid metabolism disorders through reducing the expression of microsomal triglyceride transfer protein in OLETF rats.
abstract: OBJECTIVE
  This study aimed to investigate the role of MTP on lipid metabolism disorders in insulin-resistant rats and the potential mechanism through which metformin can improve lipid metabolism disorders.
  
  
  METHODS
  30 OLETF rats served as research subjects and 18 LETO rats of the same strain served as the control group (LETO group). After the first oral glucose tolerance test (at 8-week-old), 6 rats were randomly killed from each group. The remaining 24 OLETF rats were randomly divided into untreated group (OLETF group) and treated group (OLETF/M group, cured with metformin). By the end of the 10th and 20th week of treatment, MTP in the liver was measured for all rats in the study.
  
  
  RESULTS
  All OLETF rats exhibited diabetic phenotypes at 18-week-old, with their triglyceride level higher than in LETO rats at the same age. In OLETF rats, MTP level in the liver was higher than in LETO rats at 18-week-old, and the difference was significant at 28-week-old [(13.79±1.47) vs. (8.20±1.14), p<0.05]. Treatment with metformin for 20weeks decreased triglyceride [(1.06±0.23) vs. (2.20±0.62) mmol/L, p<0.05] and total cholesterol [(1.90±0.19) vs. (2.36±0.14) mmol/L, p<0.05] in OLETF rats. Metformin also decreased MTP level in the liver [(7.65±1.31) vs. (13.79±1.47), p<0.01].
  
  
  CONCLUSIONS
  MTP may be associated with the lipid metabolism disorder in OLETF rats and metformin could improve lipid metabolism through reducing the expression of MTP.
authors.affiliation: Department of Medicine, Tsinghua University Hospital, Beijing 100084, China.
authors.forename: Nianhong
authors.initials: N
authors.lastname: Wang
authors.affiliation: Department of Endocrinology, Peking University First Hospital, Beijing 100034, China. Electronic address: junqingzhang126@126.com.
authors.forename: Junqing
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Endocrinology, Peking University First Hospital, Beijing 100034, China.
authors.forename: Yiming
authors.initials: Y
authors.lastname: Wu
authors.affiliation: Department of Endocrinology, Peking University First Hospital, Beijing 100034, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Endocrinology, Peking University First Hospital, Beijing 100034, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Liu
authors.affiliation: Department of Endocrinology, Peking University First Hospital, Beijing 100034, China.
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Guo
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002352:Carrier Proteins / Q000096:biosynthesis* / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D050356:Lipid Metabolism / Q000187:drug effects*; D052439:Lipid Metabolism Disorders / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D008297:Male; D008687:Metformin / Q000627:therapeutic use*; D051381:Rats; D020334:Rats, Inbred OLETF
chemical_list: D002352:Carrier Proteins; D007004:Hypoglycemic Agents; C106092:microsomal triglyceride transfer protein; D008687:Metformin
keywords: Hypertriglyceridemia; Insulin-resistant; Microsomal triglyceride transfer protein; Otsuka Long Evans Tokushima Fatty (OLETF) rats; Type 2 diabetes mellitus