title: Diabetes per se and metabolic state influence gene expression in tissue-dependent manner of BB/OK rats.
abstract: BACKGROUND
  Several epidemiologic studies have clearly established that long-term near normoglycaemia strongly protects against onset and progression of late complication of diabetes. Therefore, insulin treatment plays a crucial role in determining the quality of life of affected individuals. Here we studied the effects of exogenous insulin on gene expression levels in well- and poorly compensated diabetic subjects in comparison to non-diabetic BB/OK rats to find out whether diabetes per se and the quality of insulin treatment have an effect on gene expression and whether it is tissue specific.
  
  
  METHODS
  Six non-diabetic and 12 diabetic BB/OK rats were studied. Diabetic subjects were either treated with insulin implants (well compensated) or treated with 1U insulin daily (poorly compensated) to guarantee survival. Four weeks after onset of diabetes, the animals were killed and expression of Yy1, Ppargamma, Nfkappab, Pref-1, Tgfb1, Il-10, and Lepr was measured in thymus, spleen, liver, heart, and bone.
  
  
  RESULTS
  In general, between diabetic and non-diabetic subjects, significant expression changes were detected in spleen for Il-10, in heart for Il-10 and Ppargamma, in liver for Yy1, Nfkappab, and Lepr, as well as in bone for all genes studied except Tgfb1. Except Lepr, no expression changes were observed in thymus. Between well- and poorly compensated rats, significant differences on expression level were found for Yy1 (liver), Ppargamma (heart), Nfkappab (bone), Pref-1 (spleen), and Lepr (thymus, liver, heart).
  
  
  CONCLUSIONS
  The insulin treatment compensates not only metabolic disturbances but also changes gene expression profile in BB/OK rats in a tissue-dependent manner.
authors.affiliation: Department of Laboratory Animal Science, Medical Faculty, University of Greifswald, Germany.
authors.forename: Nora
authors.initials: N
authors.lastname: Klöting
authors.forename: Niels
authors.initials: N
authors.lastname: Follak
authors.forename: Ingrid
authors.initials: I
authors.lastname: Klöting
mesh_terms: D000818:Animals; D001842:Bone and Bones / Q000502:physiology; D004268:DNA-Binding Proteins / Q000235:genetics; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy / Q000235:genetics* / Q000378:metabolism*; D050981:Erythroid-Specific DNA-Binding Factors; D005786:Gene Expression Regulation; D006321:Heart / Q000502:physiology; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology; D016753:Interleukin-10 / Q000235:genetics; D047908:Intracellular Signaling Peptides and Proteins; D008099:Liver / Q000502:physiology; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D016328:NF-kappa B / Q000235:genetics; D047495:PPAR gamma / Q000235:genetics; D051381:Rats; D011913:Rats, Inbred BB; D011956:Receptors, Cell Surface / Q000235:genetics; D054411:Receptors, Leptin; D013154:Spleen / Q000502:physiology; D013950:Thymus Gland / Q000502:physiology; D014157:Transcription Factors / Q000235:genetics; D016212:Transforming Growth Factor beta / Q000235:genetics; D053773:Transforming Growth Factor beta1; D050986:YY1 Transcription Factor
chemical_list: D004268:DNA-Binding Proteins; D050981:Erythroid-Specific DNA-Binding Factors; D007004:Hypoglycemic Agents; D007328:Insulin; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D016328:NF-kappa B; D047495:PPAR gamma; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; C508962:Tgfb1 protein, rat; D014157:Transcription Factors; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D050986:YY1 Transcription Factor; C494700:Yy1 protein, rat; C064045:delta protein; D016753:Interleukin-10