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Mannan-binding lectin in diabetic kidney disease: the impact of mouse genetics in a type 1 diabetes model

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  1. Diabetes i familien – familien og diabetes

    Publikation: Bidrag til tidsskriftBidrag til avis - Kommentar/debatFormidling

  2. Diabetespatienter er afhængige af et løft af det nære sundhedsvæsen

    Publikation: AndetUdgivelser på nettet - Net-publikationFormidling

  3. Forord

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  4. Kun gode relationer kan nedbryde ’Sundhedsvæsnets Bermudatrekant’

    Publikation: Bidrag til tidsskriftBidrag til avis - Kommentar/debatFormidling

  • Jakob Appel Østergaard
  • Mette Bjerre
  • Satish Posettihalli RamachandraRao
  • Kumar Sharma
  • Jens Randel Nyengaard
  • Troels Krarup Hansen
  • Steffen Thiel
  • Allan Flyvbjerg
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UNLABELLED: BACKGROUND. Mannan-binding lectin (MBL) is involved in the development of diabetic nephropathy. MBL is a part of the innate immune system where it can activate the complement system. Serum MBL level predicts later renal impairment in diabetes patients. Direct involvement of MBL in the development of diabetic kidney disease is observed in one animal strain. However, this involvement may differ among the animal strains. We thus examined the impact of the genetic background on the role of MBL in diabetic nephropathy.

MATERIALS/METHODS: C57BL/6JBomTac and 129S6/SvEvTac mice were compared. In both strains, experimental type 1 diabetes was induced in wild-type (WT) and MBL-knockout (MBL-KO) mice by streptozotocin. Nondiabetic WT and MBL-KO mice were used as controls. We tested if MBL modified the diabetes-induced kidney changes by two-way ANOVA allowing for interaction.

RESULTS: MBL aggravated diabetes-induced kidney growth and glomerulus enlargement in C57BL/6JBomTac mice. MBL did not modify diabetes effects on glomerular basement membrane thickness or mesangial volume in any strain. Diabetes-induced changes in renal gene transcription of growth factors and matrix components were unaffected by MBL.

CONCLUSIONS: Strain-specific MBL effects were found on downstream diabetic kidney changes. This emphasizes the importance of genetic background in this model of diabetic complications.

OriginalsprogEngelsk
TidsskriftExperimental Diabesity Research
Vol/bind2012
Sider (fra-til)678381
ISSN1543-8600
DOI
StatusUdgivet - 2012
Eksternt udgivetJa

ID: 51724428