Abstract
Atherosclerosis is well known as an inflammatory disease that can lead to clinical complications such as heart attack or stroke. C-peptide as a cleavage product of proinsulin is in the last few decades known as an active peptide with a number of different effects on microvascular and macrovascular complications in type 2 diabetic patients. Patients with insulin resistance and early type 2 diabetes show elevated levels of C-peptide in blood. Several last findings demonstrated deposition of C-peptide in the vessel wall in ApoE-deficient mice and induction of local inflammation. Besides that, C-peptide has proliferative effects on human mesangial cells. This review discusses recently published proinflammatory effects of C-peptide in different tissues.
Highlights
C-peptide is a small peptide of 31 amino acids and short half-life of approximately 30 minutes
It has been identified by Steiner 1967 as a by-product of proinsulin and its main role was in assisting in the arrangement of the correct structure of insulin [1]
These effects were similar to those induced by monocyte chemokine MCP-1 or Tlymphocyte chemokine RANTES
Summary
C-peptide is a small peptide of 31 amino acids and short half-life of approximately 30 minutes It has been identified by Steiner 1967 as a by-product of proinsulin and its main role was in assisting in the arrangement of the correct structure of insulin [1]. C-peptide has a central glycine-rich region which allows a correct positioning of A and B chains for insulin to achieve its tertiary structure [1]. It is secreted into the bloodstream in equimolar amounts together with insulin in response to glucose stimulation. The metabolic syndrome, prediabetes, and type 2 diabetes mellitus accelerate vascular disease and increase development of the disease [14]
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