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Differences in susceptibility to develop parameters of diabetic nephropathy in four mouse strains with type 1 diabetes

Franzen, Stephanie (författare)
Linköpings universitet,Avdelningen för läkemedelsforskning,Hälsouniversitetet
Friederich-Persson, Malou (författare)
Uppsala universitet,Institutionen för medicinsk cellbiologi,Uppsala University, Sweden
Fasching, Angelica (författare)
Uppsala universitet,Institutionen för medicinsk cellbiologi,Uppsala University, Sweden
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Hansell, Peter (författare)
Uppsala universitet,Institutionen för medicinsk cellbiologi,Uppsala University, Sweden
Nangaku, Masaomi (författare)
University of Tokyo, Japan
Palm, Fredrik (författare)
Linköpings universitet,Uppsala universitet,Institutionen för medicinsk cellbiologi,Avdelningen för läkemedelsforskning,Hälsouniversitetet
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 (creator_code:org_t)
American Physiological Society, 2014
2014
Engelska.
Ingår i: American Journal of Physiology-Renal Physiology. - : American Physiological Society. - 1931-857X .- 1522-1466. ; 306:10, s. F1171-F1178
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • One-third of diabetes mellitus patients develop diabetic nephropathy, and with underlying mechanisms unknown it is imperative that diabetic animal models resemble human disease. The present study investigated the susceptibility to develop diabetic nephropathy in four commonly used and commercially available mouse strains with type 1 diabetes to determine the suitability of each strain. Type 1 diabetes was induced in C57Bl/6, NMRI, BALB/c, and 129Sv mice by alloxan, and conscious glomerular filtration rate, proteinuria, and oxidative stress levels were measured in control and diabetic animals at baseline and after 5 and 10 wk. Histological alterations were analyzed using periodic acid-Schiff staining. Diabetic C57Bl/6 displayed increased glomerular filtration rate, i.e., hyperfiltration, whereas all other parameters remained unchanged. Diabetic NMRI developed the most pronounced hyperfiltration as well as increased oxidative stress and proteinuria but without glomerular damage. Diabetic BALB/c did not develop hyperfiltration but presented with pronounced proteinuria, increased oxidative stress, and glomerular damage. Diabetic 129Sv displayed proteinuria and increased oxidative stress without glomerular hyperfiltration or damage. However, all strains displayed intras-train correlation between oxidative stress and proteinuria. In conclusion, diabetic C57Bl/6 and NMRI both developed glomerular hyperfiltration but neither presented with histological damage, although NMRI developed low-degree proteinuria. Thus these strains may be suitable when investigating the mechanism causing hyperfiltration. Neither BALB/c nor 129Sv developed hyperfiltration although both developed pronounced proteinuria. However, only BALB/c developed detectable histological damage. Thus BALB/c may be suitable when studying the roles of proteinuria and histological alterations for the progression of diabetic nephropathy.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Physiology (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Urologi och njurmedicin (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Urology and Nephrology (hsv//eng)

Nyckelord

C57Bl/6
NMRI
BALB/c
129Sv
diabetic nephropathy
kidney function
MEDICINE

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