title: Mitochondria are impaired in the adipocytes of type 2 diabetic mice.
abstract: OBJECTIVE
  The aim of this study was to confirm a link between mitochondrial dysfunction and type 2 diabetes.
  
  
  METHODS
  Cellular levels of mitochondrial proteins, cellular mitochondrial DNA content, and mitochondrial function and morphology were assessed by MitoTracker staining and electron microscopy, in white adipose tissue of 12-week-old male wild-type, obese (ob/ob), and diabetic (db/db) mice.
  
  
  RESULTS
  Levels of mitochondrial proteins were found to be very similar in the livers and muscles of all the mice studied. However, levels were greatly decreased in the adipocytes of db/db mice, but not in those of the wild-type and ob/ob mice. Levels of mitochondrial DNA were also found to be considerably reduced in the adipocytes of db/db mice. MitoTracker staining and under electron microscopy revealed that the number of mitochondria was reduced in adipocytes of db/db mice. Respiration and fatty acid oxidation studies indicated mitochondrial dysfunction in adipocytes of db/db mice. Interestingly, there was an increase in mitochondria and mitochondrial protein production in adipocytes of db/db mice treated with rosiglitazone, an agent that enhances insulin sensitivity.
  
  
  CONCLUSIONS
  Taken together, these data indicate that mitochondrial loss in adipose tissue is correlated with the development of type 2 diabetes.
authors.affiliation: Graduate School of Life Sciences and Biotechnology, Korea University, 1, 5-ka, Anam-dong, Sungbuk-gu, Seoul, 136-701, South Korea.
authors.forename: H-J
authors.initials: HJ
authors.lastname: Choo
authors.forename: J-H
authors.initials: JH
authors.lastname: Kim
authors.forename: O-B
authors.initials: OB
authors.lastname: Kwon
authors.forename: C S
authors.initials: CS
authors.lastname: Lee
authors.forename: J Y
authors.initials: JY
authors.lastname: Mun
authors.forename: S S
authors.initials: SS
authors.lastname: Han
authors.forename: Y-S
authors.initials: YS
authors.lastname: Yoon
authors.forename: G
authors.initials: G
authors.lastname: Yoon
authors.forename: K-M
authors.initials: KM
authors.lastname: Choi
authors.forename: Y-G
authors.initials: YG
authors.lastname: Ko
mesh_terms: D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D000818:Animals; D004272:DNA, Mitochondrial / Q000235:genetics; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D005260:Female; D008297:Male; D051379:Mice; D008854:Microscopy, Electron; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D024101:Mitochondrial Proteins / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D000077154:Rosiglitazone; D045162:Thiazolidinediones / Q000494:pharmacology
chemical_list: D004272:DNA, Mitochondrial; D024101:Mitochondrial Proteins; D045162:Thiazolidinediones; D000077154:Rosiglitazone