Insulin resistance and dysfunction of islet β cell in Chinese with impaired glucose regulation

( views:114, downloads:0 )
Author:
FU Fang-ming()
()
()
()
DONG Yan-hu()
LI li-ping()
()
()
()
()
()
()
Journal Title:
CHINESE JOURNAL OF DIABETES
Issue:
Volume 13, Issue 02, 2005
DOI:
Key Word:

Abstract: Objective To investigate insulin resistance (IR)and dysfunction of islet β cell in 277 Chinese with impaired glucose regulation(IGR). Methods 724 participants (256 males)in Qingdao were classified into four groups: normal glucose tolerance (NGT, n=447), impaired fasting glucose (IFG, n=142), impaired glucose tolerance (IGT, n=93), combined IFG and IGT (IFG+IGT, n=42). The levels of plasma glucose, lipids (TC, HDL-C, TG)and insulin were measured. HOMA-IR, HOMA-β and △I30/△G30 after OGTT were calculated. Multivariable logistic regression (MVLR)was used to analyze the factors related to IFG and IGT. Results The age, waist circumference, body mass index(BMI), and blood pressure were more elevated in the groups of IFG, IGT and IFG plus IGT than those in NGT. Age and TG were higher in IGT than in IFG. After adjusting age, sex, (systolic) blood pressure and BMI, IGR had significantly increased HOMA-IR. However, there was no difference in those among IFG, IGT, and IFG+IGT. HOMA-β decreased significantly in groups of IFG(4.53±0.06) and IFG+IGT (4.38±0.10)than that in groups of NGT(5.10±0.04)and IGT(5.11±0.07). Meanwhile, there was no difference in that between NGT and IGT. △I30/△G30 was lower in IGT(4.62±0.14) vs NGT, but was no difference among IFG(4.86±0.11), IFG+IGT(4.70±0.22) and NGT(4.99±0.11). Age, BMI, and IR were independent risk factors for IFG, and basic β cell function was protective factor for IFG. Age and BMI were independent risk factors, and early phase of insulin secretion was protective factor for IGT. Conclusion Both IR and insulin (secretion) deficiency (ISD)are present in IGR subjects. The IFG subjects have IR and ISD, but still maintain the early phase of insulin secretion. The IGT subjects have IR and defect of the early phase of insulin secretion, but still maintain basic β-cell function.

  • [1]Defronzo RA, Ferrannini E, Simensen DC. Fasting hyperglycemia in non-insulin-dependent diabetes mellitus, contributions of excessive hepatic glucose production and impaired tissue glucose uptake. Metabolism, 1989,38:387-395.
  • [2]Pimenta W, Korytkowski M, Mitrakou A, et al. Pancreatic β-cell dysfuction as the primary genetic lesion in NIDDM: evidence from studies in normal glucose-tolerant individuals with a first-degree NIDDM relative. JAMA, 1995, 273:1855-1861.
  • [3]Melchionda N, Forlani G, Marchesini G, et al. WHO and ADA criteria for the diagnosis of diabetes mellitus in relation to body mass index. Insulin sensitivity and secretion in resulting subcategories of glucose tolerance. Int J Obes Relat Metab Disord,2002,26: 90-96.
  • [4]Li CL, Tsai ST, Chou P. Comparison of metabolic risk profiles between subjects with fasting and 2-hour plasma glucose impairment: The Kinmen Study. J Clin Epidemiol,2002,55: 19-24.
  • [5]Gomez-Perez FJ, Aguilar-Salinas CA, Lopes-Alvarenga JC, et al. Lack of agreement between the World Health Organization category of impaired glucose tolerance and the American Diabetes Association category of impaired fasting glucose. Diabetes Care, 1998, 21:1886-1888.
  • [6]Davies MJ, Raymond NT, Day JL, et al. Impaired glucose tolerance and fasting hyperglycaemia have different characteristics. Diabet Med, 2000, 17:433-440.
  • [7]杜群,石福彦,田改生. 空腹血糖受损人群胰岛素分泌功能及胰岛素抵抗状态的探讨. 中国糖尿病杂志,2002,10:333-336.
WanfangData CO.,Ltd All Rights Reserved
About WanfangData | Contact US
Healthcare Department, Fuxing Road NO.15, Haidian District Beijing, 100038 P.R.China
Tel:+86-010-58882616 Fax:+86-010-58882615 Email:yiyao@wanfangdata.com.cn