Introduction
Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycaemia. There is always Beta-cell malfunction in diabetes mellitus, regardless of the kind. The hallmark of type 1 diabetes mellitus (T1DM) is the autoimmune-driven destruction of beta cells, which typically results in absolute insulin deficiency1 and eventually decreases insulin secretion and a corresponding decline in C-peptide levels, a marker of endogenous insulin secretion and beta cell function. Initially having normal or high C-peptide levels, type 2 diabetes mellitus is linked to insulin resistance and can become less severe as the condition progresses.2 Diabetes mellitus patients have hypertension two to three times more frequently than people without the condition, which increases the risk of cardiovascular disease and renal damage.3 According to studies, kidney failure is mostly caused by diabetes, which accounts for 44% of all new cases. According to recent studies, controlling high blood pressure is a crucial element in reducing this condition. Blood sugar levels must be tightly controlled, and protein consumption must be decreased. Before kidney damage occurs, treatment for preventing diabetic renal disease should start.
Along with insulin, the pancreas also produces a molecule called c-peptide. The hormone insulin regulates the body's glucose (blood sugar) levels. The body uses glucose as its primary energy source. If the body isn't producing enough insulin, diabetes may be present. There are studies that support the biological activity of C-peptide,4 which contrasts with the clinical significance of C-peptide as a measure of endogenous insulin production. Importantly, certain investigations have revealed that C-peptide possesses renoprotective qualities. Higher C-peptide levels have been linked in observational studies of people with diabetes mellitus type 1 or type 2 to lower prevalence of microvascular sequelae, including diabetic nephropathy,5, 6, 7, 8 summarized in.9 Additionally, after receiving a pancreas transplant, which replenishes both C-peptide and insulin from transplanted beta cells,10, 11 individuals with type 1 diabetes have demonstrated better renal function. Finally, limited studies in which type 1 diabetic experimental individuals received C-peptide have demonstrated that C-peptide may enhance renal function in these patients regardless of any potential impact on glucose management.12, 13 However, further research is needed to fully understand C- peptide therapeutic potential for people with diabetic kidney disease. Whether the potential advantage of C-peptide is exclusive to people with diabetes or is applicable to a larger population of patients is unknown at this time. The purpose of the study is to ascertain how T2DM affects nephropathy, circulating levels of C-peptide, HbA1C, and microalbuminuria.
Materials and Methods
This is a small case-control investigation. We assessed the baseline clinical and laboratory profiles of patients with type 2 diabetes mellitus, including newly diagnosed cases. Patients who had undergone screening for type 2 diabetes clinical studies provided the data. Each patient who was screened provided their informed consent, and the Institutional Ethics Committee had already authorised each trial. Males and females over the age of 18 were both included in the study. A thorough history was gathered, including information on the disease's duration. Each patient had a careful physical check-up. We also gathered information on concurrent illnesses and anti-diabetic medication. All patients had their body weight and body mass index (BMI) assessed. Biochemical blood tests included serum C peptide was measured using on DiaSorin, Italy and HbA1C, urea, creatinine, blood urea nitrogen, urine albumin were measured using dedicated reagent on Cobas c501 (Roche diagnostic, Germany). Using the MDRD algorithm, creatinine clearance was determined from serum creatinine value.
Inclusion criteria
T2DM with nephropathy patients (Age 30–70) will diagnose and selected for this study by the clinician and either the patient or his relatives who had given informed consent for the study.
Results
Table 1
Clinical characteristics of progression diabetic nephropathy and non-progression diabetic nephropathy (n=300)
Age, Body mass index (BMI), Systolic Blood Pressure (SBP), Diastolic Blood Pressure (DBP), mm Hg, Fating Blood Sugar (mg/dl), Postprandial Blood Sugar (mg/dl), Glycated Hemoglobin A1c (HbA1c⁒), Urea (mg/dl), Creatinine (mg/dl), Uric Acid (mg/dl), Hemoglobin (g/dl), Microalbuminuria (mg/dl) and C-peptide (ng/ml) Values are expressed as Mean + SD.
Table 2
Clinical correlation between fasting C-peptide, HbA1C, and microalbuminuria in progression diabetic nephropathy and non-progression diabetic nephropathy
Discussions
Numerous early investigations looked into the potential physiological impacts of C-peptide following the identification of the mode of insulin manufacturing. For glucose loading, it was sought after but not discovered to have any insulin-like effects on blood glucose levels and glucose disposal.14, 15 Recent research has shown that the C-peptide binds to cell surfaces specifically, indicating the presence of G protein-coupled membrane receptors. In those with type 1 diabetes who lack C-peptide, this may promote particular intracellular mechanisms that affect renal and nervous system function.15 A recent study discovered a weak correlation between serum C peptide, renal indices, and diabetes duration. The levels of serum C peptide, urine albumin excretion, and urine albumin creatinine ratio all had negative correlations with each other. Early on in the course of type 1 diabetes, glomerular hyperfiltration is a common complication.16 This condition is not resolved by adequate insulin therapy.17 However, type 2 diabetics who have insulin and C-peptide levels that are within or above the normal range do not exhibit glomerular hyperfiltration or hypertrophy.18, 19 C-peptide has a positive impact on renal function in diabetics, although the exact mechanism by which it does so is unknown. However, as demonstrated by investigations of renal function in animals with experimental diabetes, it is likely that C-peptide may have had a direct impact on the glomerular processing of albumin. In streptozotocin-diabetic rats, the effect of C-peptide on glomerular hyper filtration and protein leakage from the kidneys has been studied.20 Comparatively to diabetic control rats, the administration of C-peptide for 90 minutes was associated by decreased glomerular hyper filtration and a notable reduction in protein leakage. Both renal Na1-K1-ATPase and eNOS (endothelial nitric oxide synthase) can be stimulated by C-peptide. Particularly in renal and nerve tissue, both of these enzyme systems have been shown to exhibit reduced activity in type 1 diabetes.21, 22 Regional blood flow in the kidney as well as glomerular membrane permeability and transport can be affected by C-peptide. There is now proof that replacing C-peptide in type 1 diabetes leads to improved renal function, as shown by correction of glomerular hyper filtration and decreased urine albumin excretion, as well as amelioration of nerve dysfunction.23
According to the results of the current investigation, there is a bad link between disease duration and serum C peptide levels, which may signal growing beta cell failure. Additionally, there was a negative connection between HbA1C and serum C peptide level, which suggests that patients with low serum C peptide levels had poor glycaemic control and require insulin therapy. Even in mature-onset diabetes mellitus, C peptide is a more reliable indicator of insulin secretion than insulin, and measuring it is crucial for determining if a person is dependent on insulin. While not statistically significant, our study also found a negative connection between urine albumin levels and C peptide values. Protein leakage is reduced by C peptide's diminution of glomerular hyper filtration. There may not have been a significant link between C peptide level and urine albumin excretion rate since there were not many individuals in our study with below normal C peptide levels. Our study's limitations warrant discussion. A valid conclusion on the relationship between serum C peptide level and renal parameters cannot be drawn from the small number of patients with low serum C peptide levels.
Conclusion
There is no connection between serum C peptide levels, microalbuminuria, and HbA1c was discovered by the study. Low serum C peptide levels are possible in patients at risk for microalbuminuria. Combining insulin delivery and C-peptide replacement may be beneficial for T2DM patients. Longer-term C-peptide administration trials will be required to determine whether C-peptide may help in the prevention and treatment of diabetic nephropathy.
