Kashiwado Hospital

Chiba, Japan

Kashiwado Hospital

Chiba, Japan

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Horie A.,Diabetes Center | Tokuyama Y.,Kashiwado Hospital | Ishizuka T.,Sato Clinic | Suzuki Y.,Asahi General Hospital | And 5 more authors.
Hormone and Metabolic Research | Year: 2014

The aim of the present study was to determine whether the dipeptidyl peptidase (DPP)-4 inhibitor could repair pancreatic β-cell dysfunction and insulin resistance. Ten subjects with type 2 diabetes who had never received DPP-4 inhibitor treatment were enrolled in the study. Just before and 3 months after twice-daily administration of vildagliptin (50mg tablets), insulin secretion and insulin sensitivity were estimated using 2-compartment model analysis of C-peptide kinetics and insulin-modified minimal model parameters, respectively. The first-phase insulin secretion (CS1) was determined as the sum of the C-peptide secretion rate (CSR) from 0 to 5min (normal range 6.8-18.5ng/ml/min). The whole-body insulin sensitivity index (SI) was calculated using a minimal model software program (normal range 2.6-7.6×10-4/min/μU/ml). After vildagliptin treatment, reductions in mean (±SE) HbA1c were noted (43.28±1.53 vs. 40.98±1.77mmol/mol; p=0.019). Vildagliptin treatment increased the area under the curve for the C peptide reactivity (CPR) (AUCCPR; 26.66±5.15 vs. 33.02±6.12ng/ml·20min; p=0.003) and CS1 (0.80±0.20 vs. 1.35±0.38ng/ml/min; p=0.037) in response to an intravenous glucose load. Vildagliptin treatment significantly increased SI (0.46±0.27 vs. 1.21±0.48×10-4/min/μU/ml; p=0.037). The long-term administration of vildagliptin improved CS1 and Si suggesting that this drug has the capacity to repair impairments in pancreatic β-cell function and insulin resistance in type 2 diabetes. © Georg Thieme Verlag KG Stuttgart New York.


PubMed | Asahi General Hospital, The Diabetes Center, Sato Clinic and Kashiwado Hospital
Type: Journal Article | Journal: Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme | Year: 2014

The aim of the present study was to determine whether the dipeptidyl peptidase (DPP)-4 inhibitor could repair pancreatic -cell dysfunction and insulin resistance. Ten subjects with type 2 diabetes who had never received DPP-4 inhibitor treatment were enrolled in the study. Just before and 3 months after twice-daily administration of vildagliptin (50mg tablets), insulin secretion and insulin sensitivity were estimated using 2-compartment model analysis of C-peptide kinetics and insulin-modified minimal model parameters, respectively. The first-phase insulin secretion (CS1) was determined as the sum of the C-peptide secretion rate (CSR) from 0 to 5min (normal range 6.8-18.5ng/ml/min). The whole-body insulin sensitivity index (SI) was calculated using a minimal model software program (normal range 2.6-7.610(-4)/min/U/ml). After vildagliptin treatment, reductions in mean (SE) HbA1c were noted (43.281.53 vs. 40.981.77mmol/mol; p=0.019). Vildagliptin treatment increased the area under the curve for the C peptide reactivity (CPR) (AUCCPR; 26.665.15 vs. 33.026.12ng/ml20min; p=0.003) and CS1 (0.800.20 vs. 1.350.38ng/ml/min; p=0.037) in response to an intravenous glucose load. -Vildagliptin treatment significantly increased SI (0.460.27 vs. 1.210.4810(-4)/min/U/ml; p=0.037). The long-term administration of vildagliptin improved CS1 and Si suggesting that this drug has the capacity to repair impairments in pancreatic -cell function and insulin resistance in type 2 diabetes.


Ishizuka T.,Credo Sato Clinic | Tokuyama Y.,Kashiwado Hospital | Kanatsuka A.,Diabetes Center
Internal Medicine | Year: 2013

We herein report the case of a patient with slowly progressive type 1 diabetes and insulin independence lasting for >10 years despite the detection of continuously elevated glutamic acid decarboxylase autoantibody titers. We monitored the patient's clinical course and analyzed his endogenous insulin secretion and sensitivity using an intravenous glucose tolerance test (IVGTT) and oral glucose tolerance test (OGTT). His body mass index remained at approximately 22, while his serum C-peptide immunoreactivity level gradually decreased. The level of insulin secretion was significantly higher on the OGTT than the IVGTT. The patient's insulin sensitivity was within the normal limits. These results suggest that maintaining a lifestyle sufficient to preserve insulin secretion and/or normal insulin sensitivity is important and that β-cell responsiveness to incretins may, in part, contribute to insulin independence. © 2013 The Japanese Society of Internal Medicine.


Tokuyama Y.,Kashiwado Hospital | Yanagisawa Y.,Kashiwado Hospital | Ishizuka T.,Kashiwado Hospital
Journal of the Japan Diabetes Society | Year: 2013

A 59-year-old male with type 2 diabetes had been in good glycemie control with intensive insulin therapy. The therapy was switched from insulin to exenatide under continuous glucose monitoring. Hypoglycemia and consecutive hyperglycemia occurred several times soon after the initiation of exenatide and disappeared five days later. Exenatide monotherapy does not generally cause hypoglycemia. However, clinicians should pay attention to the occurrence of abrupt hypoglycemia after the initiation of exenatide, especially in patients with good glycemie control.


Tokuyama Y.,Kashiwado Hospital | Yanagisawa Y.,Kashiwado Hospital
Journal of the Japan Diabetes Society | Year: 2014

In order to validate the usefulness of 1,5-anhydroglucitol (AG) as an index of glycemic variability, we examined the correlation between the 1,5-AG value and the amplitude of glycemic fluctuation obtained from a continuous blood glucose monitoring system (CGM) in diabetic patients, the difference in the distribution of HbAlc and 1,5-AG among the different therapies, and the changes in the HbAlc and 1,5-AG levels before and after the administration of DPP-4 inhibitor. As a result a significant negative relationship was observed between 1,5-AG and the standard deviation (SD) of blood glucose and between 1,5-AG and the mean amplitude of glycemic excursions (MAGE). Among the diabetic patients with 1,5-AG< 10 μg/ml, the percentage of patients treated with sulfonylurea or insulin was higher than with other therapies, regardless of the HbAlc value, thus suggesting that sulfonylurea or insulin therapy could not sufficiently reduce glycemic variability. The administration of DPP-4 inhibitor decreased the HbAlc values and increased the 1.5AG values, thus suggesting that this medicine could effectively reduce glycemic variability. In conclusion, 1,5-AG is a useful and valuable index of glycemic variability and in order to suppress glycemic variability, it is desirable to adopt a treatment strategy aimed at 1,5-AG≥ 10 μg/ml.

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