%0 Journal Article
%T Beta cell response to a mixed meal in nigerian patients with type 2 diabetes
%A Ekenechukwu E Young
%A Sonny Chinenye
%A Chioma N Unachukwu
%J BMC Endocrine Disorders
%D 2012
%I BioMed Central
%R 10.1186/1472-6823-12-11
%X Ninety patients with type 2 diabetes were recruited into the study. Weight, height, body mass index and waist circumference were measured. Blood samples were analysed for fasting plasma glucose (FPG) and fasting C peptide (FCP) and glycated haemoglobin (HbA1c). Patients were given their usual drugs for management of their diabetes and then served with a standard meal calculated to contain 50£¿g of carbohydrate, made up of 53£¿% carbohydrate, 17£¿% of protein and 30£¿% of lipids, providing 500£¿kcal. Blood samples 2 hours after the start of the meal were analysed for postprandial glucose (PPG) and postprandial C peptide (PCP). Fasting (M0) and postprandial beta cell responsiveness (M1) were calculated.The mean FPG and PPG were 7.51+/£¿ 3.39£¿mmol/l and 11.02+/£¿4.03£¿mmol/l respectively while the mean glycated haemoglobin (HbA1c) was 9.0+/£¿2.5£¿%. The mean fasting C peptide was 1.44+/£¿1.80ug/ml. Many of the patients (56.7£¿%) had low FCP levels. The mean postprandial C peptide was 4.0+/£¿2.8£¿ng/ml. There were significant correlations between M1, HbA1c and PPG (p£¿=£¿0.015, 0.024, 0.001 respectively) and also between M0, HbA1c, PPG and FPG (p£¿=£¿0.001, 0.002, 0.001). HbA1c decreased across increasing tertiles of M0 (p£¿<£¿0.001) and also M1 (p£¿=£¿0.002). In step-wise linear regression analysis, M0 and M1 significantly predicted HbA1c.Many of the patients had low C peptide levels with poor beta cell response to the meal. The patients had poor glycaemic control and poor beta cell function. Both fasting and postprandial beta cell responsiveness were significant determinants of blood glucose and glycated haemoglobin levels. It is likely that putting these patients on insulin may have led to better glycaemic control in them.
%K Beta cell
%K Type2 diabetes
%K Meal stimulation
%K Glycaemic control
%U http://www.biomedcentral.com/1472-6823/12/11/abstract