title: Short-term intensive therapy in newly diagnosed type 2 diabetes partially restores both insulin sensitivity and β-cell function in subjects with long-term remission.
abstract: OBJECTIVE
  To examine the effect of intensive glycemic control therapy (IT) on insulin sensitivity and β-cell function in newly diagnosed type 2 diabetic patients compared with subjects with normal glucose tolerance (NGT) and those with impaired glucose tolerance (IGT).
  
  
  METHODS
  Forty-eight newly diagnosed type 2 diabetic patients were randomly assigned to IT for 2 weeks and followed up for 1 year. Intravenous glucose tolerance tests were conducted in NGT, IGT, and diabetic subjects. Blood glucose and insulin were measured before and after IT and at the 1-year follow-up.
  
  
  RESULTS
  IT lowered the homeostasis model assessment (HOMA) for insulin resistance (IR) significantly, from 3.12 ± 1.4 (mean ± SD) to 1.72 ± 0.8, a level comparable to the IGT (1.96 ± 1.1) and NGT (1.37 ± 0.6) subjects in the remission group; however, no HOMA-IR improvement was observed in nonremission subjects. HOMA-β in the remission group was improved (mean, interquartile range) from 18.4 (8.3-28.5) to 44.6 (32.1-69.1) and acute insulin response of insulin (AIRins) from 1.50 ± 0.22 to 1.83 ± 0.19 μIU/mL after IT, but was still significantly lower than those in NGT individuals (HOMA-β: 86.4 [56.7-185.2], P < 0.01; AIRins: 2.54 ± 0.39 μIU/mL, P < 0.01). After IT and at 1 year, the hyperbolic relationship between HOMA-β and HOMA sensitivity of remission subjects shifted close to that of IGT subjects.
  
  
  CONCLUSIONS
  IT in newly diagnosed type 2 diabetes not only partially restored β-cell function but also greatly restored insulin sensitivity. Compared with IGT and NGT subjects, β-cell function was less restored than insulin sensitivity after IT in the remission subjects.
authors.affiliation: Division of Endocrinology, Affiliated Drum Tower Hospital, Nanjing University, Nanjing, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Hu
authors.forename: Lirong
authors.initials: L
authors.lastname: Li
authors.forename: Yu
authors.initials: Y
authors.lastname: Xu
authors.forename: Tingting
authors.initials: T
authors.lastname: Yu
authors.forename: Guoyu
authors.initials: G
authors.lastname: Tong
authors.forename: Hong
authors.initials: H
authors.lastname: Huang
authors.forename: Yan
authors.initials: Y
authors.lastname: Bi
authors.forename: Jianping
authors.initials: J
authors.lastname: Weng
authors.forename: Dalong
authors.initials: D
authors.lastname: Zhu
mesh_terms: D000328:Adult; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D018149:Glucose Intolerance / Q000188:drug therapy; D005951:Glucose Tolerance Test; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D007333:Insulin Resistance / Q000502:physiology*; D007336:Insulin, Isophane / Q000627:therapeutic use; D061386:Insulin, Regular, Human / Q000627:therapeutic use; D050417:Insulin-Secreting Cells / Q000187:drug effects*; D000068880:Isophane Insulin, Human; D008297:Male; D008875:Middle Aged
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D061386:Insulin, Regular, Human; D000068880:Isophane Insulin, Human; D007336:Insulin, Isophane