title: Glycemic variability correlates strongly with postprandial beta-cell dysfunction in a segment of type 2 diabetic patients using oral hypoglycemic agents.
abstract: OBJECTIVE
  Glucose fluctuations trigger activation of oxidative stress, a main mechanism leading to secondary diabetes complications. We evaluated the relationship between glycemic variability and beta-cell dysfunction.
  
  
  METHODS
  We conducted a cross-sectional study in 59 patients with type 2 diabetes (aged 64.2 +/- 8.6 years, A1C 6.5 +/- 1.0%, and BMI 29.8 +/- 3.8 kg/m(2)[mean +/- SD]) using either oral hypoglycemic agents (OHAs) (n = 34) or diet alone (nonusers). As a measure of glycemic variability, the mean amplitude of glycemic excursions (MAGE) was computed from continuous glucose monitoring data recorded over 3 consecutive days. The relationships between MAGE, beta-cell function, and clinical parameters were assessed by including postprandial beta-cell function (PBCF) and basal beta-cell function (BBCF) obtained by a model-based method from plasma C-peptide and plasma glucose during a mixed-meal test as well as homeostasis model assessment of insulin sensitivity, clinical factors, carbohydrate intake, and type of OHA.
  
  
  RESULTS
  MAGE was nonlinearly correlated with PBCF (r = 0.54, P < 0.001) and with BBCF (r = 0.31, P = 0.025) in OHA users but failed to correlate with these parameters in nonusers (PBCF P = 0.21 and BBCF P = 0.07). The stepwise multiple regression analysis demonstrated that PBCF and OHA combination treatment were independent contributors to MAGE (R(2) = 0.50, P < 0.010), whereas insulin sensitivity, carbohydrate intake, and nonglycemic parameters failed to contribute.
  
  
  CONCLUSIONS
  PBCF appears to be an important target to reduce glucose fluctuations in OHA-treated type 2 diabetes.
authors.affiliation: Institute of Diabetes Gerhardt Katsch, Karlsburg, Germany. kohnert@diabetes-karlsburg.de
authors.forename: Klaus-Dieter
authors.initials: KD
authors.lastname: Kohnert
authors.forename: Petra
authors.initials: P
authors.lastname: Augstein
authors.forename: Eckhard
authors.initials: E
authors.lastname: Zander
authors.forename: Peter
authors.initials: P
authors.lastname: Heinke
authors.forename: Karolina
authors.initials: K
authors.lastname: Peterson
authors.forename: Ernst-Joachim
authors.initials: EJ
authors.lastname: Freyse
authors.forename: Roman
authors.initials: R
authors.lastname: Hovorka
authors.forename: Eckhard
authors.initials: E
authors.lastname: Salzsieder
mesh_terms: D000284:Administration, Oral; D000328:Adult; D000368:Aged; D019540:Area Under Curve; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology*; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D007328:Insulin / Q000097:blood; D050417:Insulin-Secreting Cells / Q000502:physiology*; D008687:Metformin / Q000627:therapeutic use; D008875:Middle Aged; D008954:Models, Biological; D018384:Oxidative Stress; D019518:Postprandial Period / Q000502:physiology*; D013453:Sulfonylurea Compounds / Q000627:therapeutic use
chemical_list: D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; D008687:Metformin; D013453:Sulfonylurea Compounds