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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

Mean blood glucose level in mmol/L in each of the four groups over time.
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fig1: Mean blood glucose level in mmol/L in each of the four groups over time.

Mentions: At baseline, the knockout mice on average weighed 20.0 g, which was slightly less than the wild type mice, 20.8 g (P = 0.04). No difference was found between the two diabetic groups or between the two nondiabetic groups (Table 1). After 18 weeks an expected difference in body weight was observed between the diabetic and the nondiabetic mice independently of knockout status (P < 0.001). The nondiabetic mice weighed 3.2 g (CI: 2.0 g–4.3 g) more than the diabetic mice. Furthermore the diabetic knockout mice were significantly smaller than the diabetic wild type (P < 0.05). As presented in Table 1, blood glucose, estimated as area under the curve (AUC), did not differ between the two diabetic groups (P = 0.69) or between the two nondiabetic groups (P = 0.13). The overall fluctuations in blood glucose in each group are depicted in Figure 1.


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)

Mean blood glucose level in mmol/L in each of the four groups over time.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: Mean blood glucose level in mmol/L in each of the four groups over time.
Mentions: At baseline, the knockout mice on average weighed 20.0 g, which was slightly less than the wild type mice, 20.8 g (P = 0.04). No difference was found between the two diabetic groups or between the two nondiabetic groups (Table 1). After 18 weeks an expected difference in body weight was observed between the diabetic and the nondiabetic mice independently of knockout status (P < 0.001). The nondiabetic mice weighed 3.2 g (CI: 2.0 g–4.3 g) more than the diabetic mice. Furthermore the diabetic knockout mice were significantly smaller than the diabetic wild type (P < 0.05). As presented in Table 1, blood glucose, estimated as area under the curve (AUC), did not differ between the two diabetic groups (P = 0.69) or between the two nondiabetic groups (P = 0.13). The overall fluctuations in blood glucose in each group are depicted in Figure 1.

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