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Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes.

Holt CB, Østergaard JA, Axelgaard E, Nielsen GK, Endo Y, Thiel S, Hansen TK - Mediators Inflamm. (2015)

Bottom Line: The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes.Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidney changes.In conclusion, the diabetes-induced effects on kidney weight and ACR were not modified by the presence or absence of ficolin B.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology and Internal Medicine, Aarhus University Hospital, 8000 Aarhus, Denmark ; Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark.

ABSTRACT

Background: The innate immune system may have adverse effects in diabetes and cardiovascular disease. The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes. Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidney changes. We hypothesize that mouse ficolin B exerts detrimental effects in the diabetic kidney as seen for MBL.

Methods: We induced diabetes with streptozotocin in female wild-type mice and ficolin B knockout mice and included two similar nondiabetic groups. Renal hypertrophy and excretion of urinary albumin and creatinine were quantified to assess diabetic kidney damage.

Results: In the wild-type groups, the kidney weighed 24% more in the diabetic mice compared to the controls. The diabetes-induced increase in kidney weight was 29% in the ficolin B knockout mice, that is, equal to wild-type animals (two-way ANOVA, P = 0.60). In the wild-type mice the albumin-to-creatinine ratio (ACR) was 32.5 mg/g higher in the diabetic mice compared to the controls. The difference was 62.5 mg/g in the ficolin B knockout mice, but this was not significantly different from the wild-type animals (two-way ANOVA, P = 0.21).

Conclusions: In conclusion, the diabetes-induced effects on kidney weight and ACR were not modified by the presence or absence of ficolin B.

No MeSH data available.


Related in: MedlinePlus

Albumin-to-creatinine ratio (mg/g) is illustrated for each of the four groups. The black error bars are illustrating mean ± standard deviation. WT: wild-type; KO: knockout.
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fig3: Albumin-to-creatinine ratio (mg/g) is illustrated for each of the four groups. The black error bars are illustrating mean ± standard deviation. WT: wild-type; KO: knockout.

Mentions: The albumin-to-creatinine ration (ACR) was higher among the diabetic wild-type mice, 76 mg/g (CI: 50–103 mg/g), compared to the nondiabetic wild-type mice, 44 mg/g (CI: 25–63 mg/g), P = 0.07. Similarly, the ACR of diabetic knockout mice was 96 mg/g (CI: 71–122 mg/g) compared to the nondiabetic knockout group, 34 mg/g (CI: 23–44 mg/g), P < 0.001. As depicted in Figure 3 no interaction was observed between diabetes and ficolin B knockout, P = 0.21.


Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes.

Holt CB, Østergaard JA, Axelgaard E, Nielsen GK, Endo Y, Thiel S, Hansen TK - Mediators Inflamm. (2015)

Albumin-to-creatinine ratio (mg/g) is illustrated for each of the four groups. The black error bars are illustrating mean ± standard deviation. WT: wild-type; KO: knockout.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4539181&req=5

fig3: Albumin-to-creatinine ratio (mg/g) is illustrated for each of the four groups. The black error bars are illustrating mean ± standard deviation. WT: wild-type; KO: knockout.
Mentions: The albumin-to-creatinine ration (ACR) was higher among the diabetic wild-type mice, 76 mg/g (CI: 50–103 mg/g), compared to the nondiabetic wild-type mice, 44 mg/g (CI: 25–63 mg/g), P = 0.07. Similarly, the ACR of diabetic knockout mice was 96 mg/g (CI: 71–122 mg/g) compared to the nondiabetic knockout group, 34 mg/g (CI: 23–44 mg/g), P < 0.001. As depicted in Figure 3 no interaction was observed between diabetes and ficolin B knockout, P = 0.21.

Bottom Line: The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes.Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidney changes.In conclusion, the diabetes-induced effects on kidney weight and ACR were not modified by the presence or absence of ficolin B.

View Article: PubMed Central - PubMed

Affiliation: Department of Endocrinology and Internal Medicine, Aarhus University Hospital, 8000 Aarhus, Denmark ; Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark.

ABSTRACT

Background: The innate immune system may have adverse effects in diabetes and cardiovascular disease. The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes. Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidney changes. We hypothesize that mouse ficolin B exerts detrimental effects in the diabetic kidney as seen for MBL.

Methods: We induced diabetes with streptozotocin in female wild-type mice and ficolin B knockout mice and included two similar nondiabetic groups. Renal hypertrophy and excretion of urinary albumin and creatinine were quantified to assess diabetic kidney damage.

Results: In the wild-type groups, the kidney weighed 24% more in the diabetic mice compared to the controls. The diabetes-induced increase in kidney weight was 29% in the ficolin B knockout mice, that is, equal to wild-type animals (two-way ANOVA, P = 0.60). In the wild-type mice the albumin-to-creatinine ratio (ACR) was 32.5 mg/g higher in the diabetic mice compared to the controls. The difference was 62.5 mg/g in the ficolin B knockout mice, but this was not significantly different from the wild-type animals (two-way ANOVA, P = 0.21).

Conclusions: In conclusion, the diabetes-induced effects on kidney weight and ACR were not modified by the presence or absence of ficolin B.

No MeSH data available.


Related in: MedlinePlus