The Journal of Clinical Endocrinology & Metabolism · 2003 · 125 citations · 33 references
Life SciencesEndocrinologyImmunologyImmunopathologyInflammationInnate ImmunityComplement RegulationComplement SystemComplement-mediated InjuryDiabetes MellitusImmune-mediated InjuryPlasma ProteinsComplement Activation PathwaysComplement System ActivationComplement System DysfunctionComplement-mediated DamageHepatic Portal SystemLectin-carbohydrate InteractionsLectinsMannose-binding Lectins
The hepatic protein mannan-binding lectin (MBL) activates the complement system on binding to carbohydrate patterns and is involved in first-line defense against invading microorganisms. Emerging evidence indicates that in some situations MBL may cause inexpedient complement activation and tissue injury through binding to endothelial glycosylations. MBL levels are suppressed by insulin treatment in critically ill patients, and, hypothetically, hepatic portal hypoinsulinemia could lead to increased levels of MBL in patients with type 1 diabetes. We measured MBL and C-reactive protein (CRP) levels in 132 normoalbuminuric type 1 diabetic patients and 66 healthy age- and sex-matched controls. The median MBL concentration was higher in diabetic patients than in healthy controls [1290 micro g/liter (interquartile range, IQR 354-2961 micro g/liter) vs. 970 micro g/liter (IQR 277-1607 micro g/liter), P = 0.025], whereas CRP concentrations were similar among patients and controls [1.42 mg/liter (IQR 0.95-2.21) vs. 1.21 mg/l (IQR 0.74-2.13), NS]. In diabetic subjects, CRP levels correlated with poor glycemic control as indicated by hemoglobin A(1c) and daily insulin dose, which was not the case with MBL. MBL concentrations were positively correlated with urinary albumin excretion (r = 0.22; P = 0.013) and increased with increasing urinary albumin excretion tertile (P = 0.036). In conclusion, our data demonstrate that circulating MBL concentrations are significantly elevated in patients with type 1 diabetes and suggest a possible role of MBL in the pathogenesis of renovascular complications in diabetes.
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Familial Clustering of Diabetic Kidney Disease
Elizabeth R. Seaquist, Frederick C. Goetz, Stephen S. Rich et al. · New England Journal of Medicine · 1989 · 1K citations
Medicine, Endocrinology, Nephrology +11
A second serine protease associated with mannan-binding lectin that activates complement
Steffen Thiel, Thomas Vorup‐Jensen, Cordula Stover et al. · Nature · 1997 · 811 citations