β- and α-Cell Dysfunctions in Africans With Ketosis-Prone Atypical Diabetes During Near-Normoglycemic Remission

Abstract

OBJECTIVEKetosis-prone atypical diabetes (KPD) is a subtype of diabetes in which the pathophysiology is yet to be unraveled. The aim of this study was to characterize β- and α-cell functions in Africans with KPD during remission.RESEARCH DESIGN AND METHODSWe characterized β- and α-cell functions in Africans with KPD during remission. The cohort comprised 15 sub-Saharan Africans who had been insulin-free for a median of 6 months. Patients in remission were in good glycemic control (near-normoglycemic) and compared with 15 nondiabetic control subjects matched for age, sex, ethnicity, and BMI. Plasma insulin, C-peptide, and glucagon concentrations were measured in response to oral and intravenous glucose and to combined intravenous arginine and glucose. Early insulin secretion was measured during a 75-g oral glucose tolerance test. Insulin secretion rate and glucagon were assessed in response to intravenous glucose ramping.RESULTSEarly insulin secretion and maximal insulin secretion rate were lower in patients compared with control participants. In response to combined arginine and glucose stimulation, maximal insulin response was reduced. Glucagon suppression was also decreased in response to oral and intravenous glucose but not in response to arginine and insulin.CONCLUSIONSPatients with KPD in protracted near-normoglycemic remission have impaired insulin response to oral and intravenous glucose and to arginine, as well as impaired glucagon suppression. Our results suggest that β- and α-cell dysfunctions both contribute to the pathophysiology of KPD.

Microalbuminuria in Diabetic Patients in the Bamenda Health District

“…Furthermore, no statistical correlation was recorded in the present study between microalbuminuria and systolic/diastolic blood pressure. This is contrary to the findings of Ghosh et al [13]. Similar results have been reported by studies [16].…”

“…Varied results have also been reported in diabetics in sub-Saharan Africa. Choukem et al reported a prevalence of 31% [13] [16]. This variation can be attributed to factors such as differences in the populations (difference in ethnicity), definitions of MA, method of urine collection/storage, methods of measurement of MA, and sample size [12,17].…”

Clinical and biological characteristics of diabetic patients under age 40 in Cameroon: Relation to autoantibody status and comparison with Belgian patients

“…Such biomarkers of beta cell function and antibody status in this patient group are in agreement with its described heterogeneity. There was no case of diabetic ketoacidosis as none of our patients showed the clinical pattern that characterizes ketosis prone diabetes from patients in the same unit [30,31]. Further steps towards improved diagnosis in this heterogeneous patient group may require both C-peptide and GADA determinations, while additional markers could be developed following the recently described alterations in amino acid metabolism [32], in combination with determination of PAX4 risk haplotypes [33].…”

Ketosis Onset Type 2 Diabetes Had Better Isletβ-Cell Function and More Serious Insulin Resistance

“…The group distribution was A + β − , A − β + , A − β − , and A + β + [22, 23]. Choukem et al showed that β - and α -cell dysfunctions both contribute to the pathophysiology of KPD; in addition, KPD displays a defect in β -cell sensitivity to glucose and has reduced β -cell mass [24]. Umpierrez et al demonstrated that hyperglycemia, but not lipotoxicity, played the crucial role in the pathogenesis of KPD in obese African patients [25].…”