A total of 74 patients were included.A significant association was observed between high levels of MBL and severe DR; 47% of patients with severe/proliferative DR had high levels of MBL, whereas 12% of the patients with diabetes but no DR had high levels of MBL (p = 0.008; odds ratio [OR]: 6.06; 95% confidence interval [CI]: 1.4-25.0).
In the present study, we induced diabetes in MBL knockout mice and in wild type C57BL/6J mice by low-dose streptozotocin injection and measured blood glucose and urine albumin-to-creatinine ratio to monitor development of diabetes.
We hypothesize that long-term exposure to uncontrolled high blood glucose in diabetes may mediate formation of neoepitopes in several tissues and that MBL is able to recognize these structures and thus activate the lectin pathway.
MBL improved the area under the receiver operating characteristic curve of the diabetes duration for DRfrom 0.82(95% confidence interval [CI], 0.77-0.86) to 0.88(95% CI, 0.82-0.96; P<0.01) and for VDTR from 0.85(95% CI, 0.77-0.92) to 0.90(95% CI, 0.83-0.96; P<0.01).
The present study characterizes mannose-binding lectin (MBL), an activator of the complement system and thereby important for inflammatory activation, in patients with diabetes and myocardial infarction.
To assess the role of MBL2 in diabetes susceptibility, this gene was analyzed in the Pima Indian population, which has a high prevalence of type 2 diabetes.
Polymorphisms in the MBL gene and serum MBL levels were determined in 199 type 1 diabetic patients with overt nephropathy and 192 type 1 diabetic patients with persistent normoalbuminuria matched for age, sex, and duration of diabetes, as well as in 100 healthy control subjects.