After the discovery of the mode of insulin biosynthesis, several early studies addressed the question of possible physiological effects of C-peptide. Insulin-like effects on blood glucose levels and glucose disposal after glucose loading were looked for but not found.[7
] Recently, new data have been presented demonstrating specific binding of C-peptide to cell surfaces in a manner that suggests the presence of G protein-coupled membrane receptors. C-peptide may thereby stimulate specific intracellular processes, influencing renal and nerve function in C-peptide-deficient type 1 diabetes patients.[3
In this study we found weak association of serum C peptide with renal parameters and duration of diabetes. Serum C peptide level was negatively correlated with creatinine clearance, urine albumin excretion and urine albumin creatinine ratio. Patients with type 1 diabetes frequently develop glomerular hyperfiltration early in the course of their disorder.[9
] Adequate insulin therapy does not correct this phenomenon.[10
] In contrast, patients with type 2 diabetes, in whom insulin and C-peptide levels are within or above the normal range, do not show glomerular hyperfiltration or hypertrophy.[11
] The mechanism underlying the beneficial effect of C-peptide on renal function in diabetes is not known. However, it is possible that C-peptide may have exerted a direct effect on the glomerular handling of albumin, as suggested by the studies of renal function in animals with experimental diabetes. The influence of C-peptide on glomerular hyperfiltration and renal protein leakage has been examined in streptozotocin diabetic rats.[5
] Administration of C-peptide for 90 minute was accompanied by diminished glomerular hyperfiltration and a marked reduction in protein leakage compared with diabetic control animals. C-peptide has the capacity to stimulate both renal Na+
-ATPase and eNOS (endothelial nitric oxide synthase). Both of these enzyme systems are known to show attenuated activities in type 1 diabetes, particularly in renal and nerve tissue.[13
] C-peptide can influence glomerular membrane permeability and transport, as well as regional blood flow of the kidney. There is now evidence to indicate that replacement of C-peptide in type 1 diabetes is accompanied by improved renal function, as evidenced by correction of glomerular hyperfiltration and diminished urinary albumin excretion, and amelioration of nerve dysfunction.[15
The present study has shown the negative correlation of serum C peptide level with duration of disease, which may be indicating progressive beta cell failure. HbA1C also showed negative correlation with serum C peptide level suggesting poor glycaemic control in patients with low serum C peptide level and indicating the need for insulin therapy. C peptide is the more stable indicator of insulin secretion than insulin and its measurement is important in the evaluation of insulin dependency even in maturity onset diabetes mellitus.
Our study also has shown negative correlation of C peptide value with urine albumin level, though statistically not significant. C peptide diminishes glomerular hyperfiltration and causes reduction in protein leakage.[5
] The number of patients with below normal C peptide was small in our study, which may be the reason for absence of significant correlation between C peptide level and urine albumin excretion rate.
Limitations of our study deserve comment. Number of patients with low serum C peptide level was very small to give any valid conclusion regarding the association of serum C peptide level with renal parameters. Furthermore, a cross-sectional study design tends to leave uncertainty regarding the temporal sequence of exposure-outcome relations. Thus, confirming the relation with prospective longitudinal data would be valuable.