title: Effects of intravenous glucose load on insulin secretion in patients with ketosis-prone diabetes during near-normoglycemia remission.
abstract: OBJECTIVE
  Most patients with ketosis-prone type 2 diabetes (KPD) discontinue insulin therapy and remain in near-normoglycemic remission. The aim of this study was to determine the effect of glucotoxicity on beta-cell function during remission in obese patients with KPD.
  
  
  METHODS
  Age- and BMI-matched obese African Americans with a history of KPD (n = 8), severe hyperglycemia but without ketosis (ketosis-resistant type 2 diabetes, n = 7), and obese control subjects (n = 13) underwent intravenous infusion of 10% dextrose at a rate of 200 mg per m(2)/min for 20 h. beta-Cell function was assessed by changes in insulin and C-peptide concentrations during dextrose infusion and by changes in acute insulin response (AIR) and first-phase insulin release (FPIR) to arginine stimulation before and after dextrose infusion.
  
  
  RESULTS
  The mean +/- SD time to discontinue insulin therapy was 7.1 +/- 1.7 weeks in KPD and 9.6 +/- 2.3 weeks in ketosis-resistant type 2 diabetes (NS). During a 20-h dextrose infusion, changes in insulin, C-peptide, and the C-peptide-to-glucose ratio were similar among diabetic and control groups. During dextrose infusion, subjects with ketosis-resistant type 2 diabetes had greater areas under the curve for blood glucose than subjects with KPD and control subjects (P < 0.05). The AIR and FPIR to arginine stimulation as well as glucose potentiation to arginine assessed before and after dextrose infusion were not different among the study groups.
  
  
  CONCLUSIONS
  Near-normoglycemia remission in obese African American patients with KPD and ketosis-resistant type 2 diabetes is associated with a remarkable recovery in basal and stimulated insulin secretion. At near-normoglycemia remission, patients with KPD displayed a pattern of insulin secretion similar to that of patients with ketosis-resistant type 2 diabetes and obese nondiabetic subjects.
authors.affiliation: Department of Medicine, Emory University, Atlanta, Georgia, USA.
authors.forename: Aidar R
authors.initials: AR
authors.lastname: Gosmanov
authors.forename: Dawn
authors.initials: D
authors.lastname: Smiley
authors.forename: Gonzalo
authors.initials: G
authors.lastname: Robalino
authors.forename: Joselita M
authors.initials: JM
authors.lastname: Siqueira
authors.forename: Limin
authors.initials: L
authors.lastname: Peng
authors.forename: Abbas E
authors.initials: AE
authors.lastname: Kitabchi
authors.forename: Guillermo E
authors.initials: GE
authors.lastname: Umpierrez
mesh_terms: D000328:Adult; D001741:Black or African American; D001786:Blood Glucose / Q000032:analysis; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000008:administration & dosage / Q000378:metabolism*; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000378:metabolism* / Q000627:therapeutic use; D000078790:Insulin Secretion; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D007328:Insulin; D005947:Glucose