Related Experiment Videos
Elevation of complement components in diabetes mellitus
Insights
Complement system components are elevated in diabetes and glucose intolerance, correlating with blood glucose levels. This increase is not linked to diabetic complications, suggesting a metabolic origin.
Area of Science:
- Immunology
- Metabolic Disorders
- Clinical Chemistry
Background:
- The complement system is crucial for immune responses and implicated in immune-mediated diseases.
- Understanding complement system alterations in diabetes is vital for disease insight.
Purpose of the Study:
- To investigate the levels of specific complement components (C4, C3 activator, C3) in individuals with diabetes and glucose intolerance.
- To explore the relationship between complement component levels, glycemic control, age, and diabetic microvascular complications.
Main Methods:
- Measurement of serum levels for C4, C3 activator, and C3 in diabetic, glucose-intolerant, and control groups.
- Statistical analysis to correlate complement levels with fasting plasma glucose, age, albumin, and microvascular complications.
Main Results:
- Elevated levels of C4, C3 activator, and C3 were observed in both diabetics and individuals with glucose intolerance.
- Complement component levels positively correlated with fasting plasma glucose in the glucose-intolerant group.
- Complement elevation was independent of the presence or severity of diabetic microvascular complications.
Conclusions:
- The simultaneous increase in complement components and glucose intolerance suggests a metabolic basis for complement activation.
- The lack of association with microvascular complications argues against a significant role of complement in diabetic microangiopathy pathogenesis.
Abstract:
The serum proteins composing the complement system play a role in defense against infection and in the generation of immune-mediated disorders. To examine this system three components of the complement system in diabetes have been measured--an element in the classic (antibody-mediated) pathway, C4; an element in the properdin (non-antibody) pathway, C3 activator; and an element common to both pathways, C3. The levels of all three are increased both in diabetics and in individuals with glucose intolerance. In the glucose intolerant subjects elevation occurred either with or without fasting hyperglycemia. The levels of all three complement components were found to be positively correlated with fasting plasma glucose in the glucose intolerant group. An increase of complement components with age was found in the overall study population, and in two individual groups. For this reason a further comparison was made between nondiabetics and diabetics on the basis of age; the diabetic complement increase was still detectable. The levels of individual complement components were correlated with each other in both diabetic and nondiabetic groups. An inverse correlation was found between C3 activator and albumin level. The elevation of all complement components was found to be unrelated to the presence or severity of diabetic microvascular sequelae. The simultaneous development of complement elevation and glucose intolerance strongly suggests a metabolic basis for the increase in its components while the lack of association of complement elevation with diabetic sequelae argues against a role for complement in the pathogenesis of diabetic microangiopathy.