Beta cell response to a mixed meal in nigerian patients with type 2 diabetes

Abstract

BackgroundThe pathophysiology of type2 diabetes involves both insulin resistance and poor beta cell function. Studies have been done in several populations to assess the relative importance of these mechanisms in individual patients. In our environment studies to assess beta cell function have been done with glucagon stimulation or an oral glucose tolerance test. This study was done to assess the response of the beta cell to a standardized mixed meal and its relationship with glycaemic control in patients with type2 diabetes.MethodsNinety 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.ResultsThe 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.ConclusionsMany 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.

Apparent Insulin Deficiency in an Adult African Population With New-Onset Type 2 Diabetes

“…The association between an increase in HbA1c concentrations and insulin deficiency as shown in our study has been replicated in most studies, further highlighting the key role of insulin in glucose homeostasis ( 8 , 9 , 19 , 21 ).…”

“…An increase in BMI reduced the odds of insulin deficiency by 11%. A similar direct relationship between fasting C-peptide, as a measure of pancreatic beta-cell secretory function, and BMI has been reported in similar studies investigating pancreatic beta-cell function in African and Caucasian patients with long-standing and recently diagnosed diabetes ( 7 – 9 , 18 , 19 ). In addition to its role in regulating glucose homeostasis, insulin is an anabolic hormone that promotes lipogenesis and protein synthesis through the tyrosine kinase receptor pathway ( 20 ).…”

“…Studies that have evaluated pancreatic beta-cell function using fasting or random C-peptide measurement in adult populations with newly diagnosed type 2 diabetes in SSA are limited. The few available studies have been conducted in adult patients with long-standing type 2 diabetes, reporting a wide variation in the documented prevalence of insulin deficiency ranging from 7% to 73% (7)(8)(9)(10)(11). Except for one study which used a lower cut-off of fasting C-peptide concentration of <0.2 nmol/l (0.6 ng/ml) to define low C-peptide levels (7), the rest of the above studies used a cut-off of <0.3 nmol/l (0.9 ng/ml).…”

Antipsychotic olanzapine-induced misfolding of proinsulin in the endoplasmic reticulum accounts for atypical development of diabetes

“…First, while it usually takes years to develop diabetes via insulin resistance, olanzapine-induced diabetes occurs within 6 months after commencing treatment ( Kinoshita et al, 2014 ; Nakamura et al, 2014 ; Nakamura and Nagamine, 2010 ). Second, discontinuing olanzapine treatment cures diabetes even after the level of HbA1c (a marker for blood glucose level) reaches >10%, a ratio which normally representing an irreversible level in patients with type I or type II diabetes ( Nakamura et al, 2014 ; Nakamura and Nagamine, 2010 ; Nathan et al, 2009 ; Young et al, 2012 ). Moreover, diabetic ketoacidosis, which is caused by insulin hyposecretion, often occurs in patients with type I diabetes, but also rapidly (within 6 months after treatment with olanzapine) affects patients with no diabetic symptoms before medication ( Kinoshita et al, 2014 ; Tsuchiyama et al, 2004 ).…”