Aims/Introduction:  Type 2 diabetes is progressive in that therapy must be altered over time, which is partly as a result of the progressive loss of pancreatic β‐cell function. To elucidate the relationship between residual endogenous insulin secretion and the necessity of insulin therapy to achieve good glycemic control, indices using serum C‐peptide immunoreactivity (CPR) were analyzed in patients with type 2 diabetes.Materials and Methods:  The data of 201 Japanese patients with type 2 diabetes who achieved the target of glycemic control during admission were analyzed retrospectively. Indices using CPR including fasting CPR (FCPR), CPR 6 min after intravenous injection of glucagon (CPR‐6 min), increment of CPR (ΔCPR), secretory unit of islet in transplantation index (SUIT) and C‐peptide index (CPI) were compared between the group requiring insulin (insulin group) and the group not requiring insulin (non‐insulin group). A receiver–operator characteristic (ROC) curve was made, and optimal cut‐off point and likelihood ratio were determined for each index.Results:  All indices of CPR were lower in the insulin group compared with those in the non‐insulin group. Likelihood ratios at the optimal point of FCPR, CPR‐6 min, ΔCPR, SUIT, and CPI were 2.0, 2.1, 1.6, 2.3 and 2.8, respectively. Optimal cut‐off point of CPI was 1.1 ng/mg. Sensitivity and specificity at optimal point of CPI were 61 and 78%, respectively.Conclusions:  The advantage of CPI of the indices of CPR to select insulin therapy to achieve good glycemic control was shown, but limitations of the predictive abilities of the indices using CPR should be taken into account. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00096.x, 2011)

OBJECTIVEWe examined the relationship between intima-media thickness of common carotid artery (CCA-IMT) and silent cerebral infarction (SCI) with the magnetic resonance imaging (MRI) study in Japanese subjects with type 2 diabetes.RESEARCH DESIGN AND METHODSThe brain MRI study and the carotid ultrasonography were performed in a total of 217 consecutive Japanese subjects with type 2 diabetes. Various risk factors for SCI were examined using multiple logistic analyses.RESULTSThe SCI was found in 60.4% of the diabetic subjects. In the diabetic subjects, age, systolic blood pressure (SBP), pulse wave velocity, and CCA-IMT were significantly higher in the subjects with SCI than in those without it. Multiple logistic analyses indicated that age, SBP, and CCA-IMT were significant and independent risk factors of SCI in the diabetic subjects.CONCLUSIONSCCA-IMT, but not pulse wave velocity, was independently associated with SCI in Japanese subjects with type 2 diabetes.

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 HbA1c were the major independent variables predicting PPCPR (R2 = 0.315). HbA1c was a major factor predicting PPCPR, but did not predict CPR‐6min. In addition, HbA1c 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 HbA1c, 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)

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