This was a cross-sectional study in type2 diabetes patients in which their beta cell function was assessed by testing their response to a standardized meal.
Low fasting C peptide levels was common in the patients occurring in over half of them, suggesting low beta cell reserve. This was seen despite the relatively short duration of diabetes in the patients (mean duration 6.7
yrs). This has been reported in similar studies demonstrating low beta cell reserve in African patients with type2 diabetes [8
There was a progressive decrease in both fasting and postprandial beta cell responsiveness with increasing duration of diabetes in the patients though unlike in other studies [7
], this did not reach statistical significance. It is likely that this observation may be due to the different rates of beta cell deterioration in the patients. In addition, in our environment, a lot of patients with diabetes present to the clinic very late in their illness due to several factors such as ignorance, poor access to health facilities and patronage of alternative medical practitioners. Hence, a long period of hyperglycaemia and exposure of the beta cells to excessive glucose and the resultant glucotoxicity may result in earlier loss of beta cell function even in those with an apparently shorter duration of diabetes. Similarly in the study by Bakari, fasting plasma insulin did not correlate with duration of diabetes [9
Generally there was poor glycaemic control in majority of the patients. In addition, M0 and M1 showed significant correlations with HbA1c and indeed were significant predictors of HbA1c in the regression model. Indeed further statistical analyses showed that among the three tertiles of both M0 and M1, HbA1c was lowest in those in the highest tertiles of both M0 and M1 though even in the patients in the highest tertile of M1, mean HbA1c was still high (7.8
%). Similarly patients who had poor fasting and postprandial beta cell responsiveness and fell into the lower tertiles of M0 and M1 also had worse glycaemic control in all parameters i.e FPG, PPG and HbA1c than those in the higher tertiles. This was also observed in the study by Shim et al [13
] who reported that patients within the lowest tertile of postprandial C peptide levels had higher FPG, PPG and HbA1c levels. This suggests that the response of the beta cell is a significant determinant of glycaemic control in patients as also seen in studies by Shim et al [13
] and Albarrak [7
], in which both M1 and M0 were predictors of HbA1c.
However, when the patients were divided into two groups according to their glycaemic control those with poor glycaemic control had lower FCP, M0 and M1 than those with good glycaemic control though these differences were more significant for M1. Hence these differences were more marked with postprandial beta cell responsiveness which has been shown in other studies to be more predictive of glycaemic control than the fasting beta cell responsiveness [13
Most of the patients who were on insulin were seen in the lowest tertiles of M1 and M0, and none of the patients in the highest tertiles was on insulin treatment. This is as expected as those on insulin are likely those patients who had been poorly controlled on oral agents, suggesting poor beta cell function. Similarly, Oli et al [11
] reported that lower glucagon stimulated C peptide levels predicted sulphonyl urea failure and need for insulin treatment in Nigerian patients with type2 diabetes.
It was observed that a lot of the patients with poor beta cell function (lowest tertiles of M0 and M1) were managed with oral agents alone. Majority of them were on sulphonylureas which act by stimulating endogenous insulin release from the beta cells. Despite this, they still had poor beta cell stimulation from the meal and their drugs. It is possible that insulin treatment in this group would have resulted in better indices of glycaemic control in them.. The use of oral drugs in the patients with relatively poor beta cell responsiveness may have contributed to the high degree of poor glycaemic control.
One of the limitations of this study was the inability to collect multiple blood samples for the analysis of C peptide within the two hour sampling period, hence the need to use a simplified method for estimation of beta cell responsiveness. Though this equation has been used in a previous study [13
], it is not known if more detailed sampling and C peptide modeling would yield similar results. In addition, antibody testing was not done to clearly differentiate between type1 and type2 diabetic patients and this may have affected the C peptide measurements as a few patients may have been improperly classified as having type2 diabetes.