title: β- and α-cell dysfunctions in africans with ketosis-prone atypical diabetes during near-normoglycemic remission.
abstract: OBJECTIVE
  Ketosis-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.
  
  
  METHODS
  We 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.
  
  
  RESULTS
  Early 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.
  
  
  CONCLUSIONS
  Patients 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.
authors.affiliation: Department of Diabetes and Endocrinology, Saint-Louis University Hospital, Assistance Publique–Hôpitaux de Paris, University Paris-Diderot Paris-7, Paris, France.
authors.forename: Siméon-Pierre
authors.initials: SP
authors.lastname: Choukem
authors.forename: Eugene
authors.initials: E
authors.lastname: Sobngwi
authors.forename: Philippe
authors.initials: P
authors.lastname: Boudou
authors.forename: Lila-Sabrina
authors.initials: LS
authors.lastname: Fetita
authors.forename: Raphael
authors.initials: R
authors.lastname: Porcher
authors.forename: Fidaa
authors.initials: F
authors.lastname: Ibrahim
authors.forename: Bertrand
authors.initials: B
authors.lastname: Blondeau
authors.forename: Patrick
authors.initials: P
authors.lastname: Vexiau
authors.forename: Franck
authors.initials: F
authors.lastname: Mauvais-Jarvis
authors.forename: Fabien
authors.initials: F
authors.lastname: Calvo
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Gautier
mesh_terms: D000328:Adult; D044383:Black People; D002096:C-Peptide / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000503:physiopathology*; D016883:Diabetic Ketoacidosis / Q000097:blood* / Q000503:physiopathology*; D005260:Female; D005934:Glucagon / Q000097:blood; D050416:Glucagon-Secreting Cells / Q000502:physiology*; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood; D050417:Insulin-Secreting Cells / Q000502:physiology*; D008297:Male; D008875:Middle Aged
chemical_list: D002096:C-Peptide; D007328:Insulin; D005934:Glucagon