Relationship between the level of fasting plasma glucose and beta cell functions in Chinese with or without diabetes.
- Author:
Can PANG
1
;
Yu-qian BAO
;
Chen WANG
;
Jun-xi LU
;
Wei-ping JIA
;
Kun-san XIANG
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Aged; Aged, 80 and over; Blood Glucose; analysis; Diabetes Mellitus; blood; physiopathology; Fasting; blood; Female; Humans; Insulin; secretion; Insulin Resistance; Insulin-Secreting Cells; physiology; Male; Middle Aged
- From: Chinese Medical Journal 2008;121(21):2119-2123
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDType 2 diabetes is a chronic disease characterized by a progressive loss of beta cell functions. However, the evaluation of beta cell functions is either expensive or inconvenient for clinical practice. We aimed to elucidate the association between the changes of insulin responsiveness and the fasting plasma glucose (FPG) during the development of diabetes.
METHODSA total of 1192 Chinese individuals with normal blood glucose or hyperglycemia were enrolled for the analysis. The early insulinogenic index (DeltaI30/DeltaG30), the area under the curve of insulin (AUC-I), and homeostasis model assessment were applied to evaluate the early phase secretion, total insulin secretion, and insulin resistance respectively. Polynomial regression analysis was performed to estimate the fluctuation of beta cell functions.
RESULTSThe DeltaI30/DeltaG30 decreased much more rapidly than the AUC-I accompanying with the elevation of FPG. At the FPG of 110 mg/dl (a pre-diabetic stage), the DeltaI30/DeltaG30 lost 50% of its maximum while the AUC-I was still at a compensated normal level. The AUC-I exhibited abnormal and decreased gradually at the FPG of from 130 mg/dl to higher (overt diabetes), while the DeltaI30/DeltaG30 almost remained at 25% of its maximum value. When hyperglycemia continuously existed at > 180 mg/dl, both the DeltaI30/DeltaG30 and AUC-I were totally lost.
CONCLUSIONThe increased fasting plasma glucose reflects progressive decompensation of beta cell functions, and could be used to guide the strategy of clinical treatments.