title: Early insulin secretion failure leads to diabetes in Chinese subjects with impaired glucose regulation.
abstract: BACKGROUND
  Both beta-cell dysfunction and decreased insulin sensitivity are involved in the pathogenesis of impaired glucose tolerance (IGT) and impaired fasting glucose (IFG), while their relative contribution in the progression to type 2 diabetes still remains controversial. The aim of the present study is to clarify this process in Chinese subjects by using cross-sectional method.
  
  
  METHODS
  2,975 Chinese subjects were classified into: normal glucose tolerance (NGT), impaired glucose regulations (IGR), and diabetes mellitus (DM) based on oral glucose tolerance test (OGTT). The IGR group was sub-classified as isolated IFG, isolated IGT and combined glucose intolerance (CGI). The DM group was sub-classified as normal fasting plasma glucose and 2-hour hyperglycemia (N0D2), fasting hyperglycemia and normal 2-hour plasma glucose (D0N2), and both fasting and 2-hour hyperglycemia (D0D2).
  
  
  RESULTS
  As far as insulinogenic index (IGI) was concerned, there was no difference between IFG and IGT in either gender, however, HOMA2-B% (homeostasis model assessment for beta-cell function) of IGT was higher than that of IFG and CGI in both male and female (P < 0.05). In the diabetic sub-groups, IGI of N0D2 was higher than that of D0N2, and both deteriorated compared with those of IGT and IFG, respectively. HOMA2-B% of N0D2 was still higher than that of D0N2 and D0D2. No significant difference was detected in OGIS and HOMA2-S% (homeostasis model assessment for insulin sensitivity) between IFG and IGT, and this was the case between N0D2 and D0N2. OGIS and HOMA-IR of IGR sub-groups were not different from those of their diabetic counterparts.
  
  
  CONCLUSIONS
  Failure of beta-cell function might be the main reason for both IGT and IFG developing into diabetes instead of aggravated insulin resistance.
authors.affiliation: Department of Endocrine and Metabolic Disease, Shanghai First People's Hospital affiliated to Shanghai Jiaotong University, Shanghai, PR China.
authors.forename: Lei
authors.initials: L
authors.lastname: Qian
authors.forename: Lihong
authors.initials: L
authors.lastname: Xu
authors.forename: Xiao
authors.initials: X
authors.lastname: Wang
authors.forename: Xuelian
authors.initials: X
authors.lastname: Fu
authors.forename: Yanyun
authors.initials: Y
authors.lastname: Gu
authors.forename: Fan
authors.initials: F
authors.lastname: Lin
authors.forename: Yongde
authors.initials: Y
authors.lastname: Peng
authors.forename: Guo
authors.initials: G
authors.lastname: Li
authors.forename: Min
authors.initials: M
authors.lastname: Luo
mesh_terms: D000328:Adult; D000368:Aged; D044466:Asian People; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D002681:China; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology*; D005215:Fasting; D005260:Female; D018149:Glucose Intolerance / Q000209:etiology*; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D018579:Patient Selection
chemical_list: D001786:Blood Glucose; D007328:Insulin