Open AccessAnalysis of factors influencing postprandial C‐peptide levels in Japanese patients with type 2 diabetes: Comparison with C‐peptide levels after glucagon load
Author(s) -
Funakoshi Shogo,
Fujimoto Shimpei,
Hamasaki Akihiro,
Fujiwara Hideya,
Fujita Yoshihito,
Ikeda Kaori,
Takahara Shiho,
Seino Yutaka,
Inagaki Nobuya
Publication year - 2011
Publication title -
journal of diabetes investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.089
H-Index - 50
eISSN - 2040-1124
pISSN - 2040-1116
DOI - 10.1111/j.2040-1124.2011.00126.x
Subject(s) - postprandial , medicine , glucagon like peptide 1 , diabetes mellitus , c peptide , type 2 diabetes , endocrinology , peptide , biochemistry , chemistry
Aims/Introduction: Postprandial serum C‐peptide levels are readily determined in clinical practice and have a good correlation with serum C‐peptide levels after glucagon load; the measurement is often used as an index of endogenous insulin secretion. However, the factors affecting postprandial serum C‐peptide levels remain to be evaluated. Materials and Methods: To investigate the clinical factors affecting postprandial serum C‐peptide, 2‐h postprandial C‐peptide levels after breakfast (PPCPR) were analyzed retrospectively for comparison with glucagon‐stimulated C‐peptide (CPR‐6min) levels measured during hospital admission in 273 Japanese patients with type 2 diabetes. Results: Multiple regression analysis showed that years from diagnosis, body mass index (BMI) and HbA 1c were the major independent variables predicting PPCPR ( R 2 = 0.315). HbA 1c was a major factor predicting PPCPR, but did not predict CPR‐6min. In addition, HbA 1c was negatively correlated with PPCPR ( r = −0.410, P < 0.0001) and PPCPR/CPR‐6min ( r = −0.313, P < 0.0001). Conclusions: PPCPR was correlated with common factors predicting CPR, including years from diagnosis and BMI, but also was negatively correlated with HbA 1c , a unique factor. These results show that chronic elevation of the glucose level might impair endogenous insulin secretion after meal load, but might have little effect on endogenous insulin secretion after glucagon load. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2011.00126.x, 2011)