Yoshitaka Akiyama1, Tomoko Morita-Ohkubo1, Natsuko Oshitani1, Yuko Ohno2, Yoshimasa Aso3, Toshihiko Inukai4, Masafumi Kakei5, Masanobu Kawakami5, Takuya Awata6, Shigehiro Katayama6, Masafumi Matsuda1. 1. 1Department of Endocrinology and Diabetes, Saitama Medical Center, Saitama Medical University, 1981 Kamoda, Kawagoe-shi, Saitama Japan. 2. 2Central Laboratory, Saitama Medical Center, Saitama Medical University, 1981 Kamoda, Kawagoe-shi, Saitama Japan. 3. 3Department of Endocrinology and Metabolism, Dokkyo Medical University, 880 Kita-Kobayashi, Mibu, Shimotuga, Tochigi Japan. 4. 4Department of Diabetes, Endocrinology and Hematology, Dokkyo Medical University Koshigaya Hospital, 2-1-50 Minami-Koshigaya, Koshigaya, Saitama Japan. 5. 5Department of Internal Medicine, Omiya Medical Center, Jichi Medical School, Amanuma-Cho 1-847, Saitama, Japan. 6. 6Division of Endocrinology and Diabetes, Faculty of Medicine, Saitama Medical University, 38 Morohongo, Moroyama, Iruma-gun, Saitama Japan.
Abstract
AIMS: Both sitagliptin (SIT) and mitiglinide (MIT) can lower postprandial hyperglycemia. The purpose of this study was to examine differences in insulin and glucagon secretion after SIT or MIT administration when similar levels of plasma glucose (PG) were achieved for both agents following an oral glucose load. PATIENTS AND METHODS: We directly compared the effects of these two agents in 16 type-2 diabetic patients (M/F = 10/6, age 66 ± 3 years old, HbA1c 6.6 ± 0.5 %). Patients received SIT (50 mg qd for 1 week and 100 mg qd for an additional week) or MIT (10 mg tid for 2 weeks). After 2 weeks, patients crossed over to the other treatment. 75-g oral glucose tolerance tests were conducted before the study and after interventions. RESULTS: The area under the curve (AUC) up to 180 min for the PG response was similar for both agents. While basal insulin secretion rates (ISR) were similar, incremental AUC of ISR was significantly lower in the SIT treatment (522 ± 108 vs 702 ± 288 pmol/min min, p < 0.01), although the difference between the SIT and MIT treatments in the Matsuda index-which reflects insulin sensitivity-remained nonsignificant. Glucose-stimulated insulin secretion was similarly increased by the MIT and SIT treatments. Suppression of the AUC for glucagon was observed in the SIT treatment, while MIT treatment failed to suppress the glucagon concentration (-432 ± 2322 vs MIT 1116 ± 2520 pg/ml min, p < 0.05). The basal proinsulin/insulin ratio was lower in the SIT treatment (0.23 ± 0.04 vs MIT 0.26 ± 0.36, p < 0.05). CONCLUSIONS: Although either SIT or MIT can be employed to reduce postprandial hyperglycemia, SIT induces changes in hormonal profiles that are more favorable to islet functions than MIT does.
AIMS: Both sitagliptin (SIT) and mitiglinide (MIT) can lower postprandial hyperglycemia. The purpose of this study was to examine differences in insulin and glucagon secretion after SIT or MIT administration when similar levels of plasma glucose (PG) were achieved for both agents following an oral glucose load. PATIENTS AND METHODS: We directly compared the effects of these two agents in 16 type-2 diabetic patients (M/F = 10/6, age 66 ± 3 years old, HbA1c 6.6 ± 0.5 %). Patients received SIT (50 mg qd for 1 week and 100 mg qd for an additional week) or MIT (10 mg tid for 2 weeks). After 2 weeks, patients crossed over to the other treatment. 75-g oral glucose tolerance tests were conducted before the study and after interventions. RESULTS: The area under the curve (AUC) up to 180 min for the PG response was similar for both agents. While basal insulin secretion rates (ISR) were similar, incremental AUC of ISR was significantly lower in the SIT treatment (522 ± 108 vs 702 ± 288 pmol/min min, p < 0.01), although the difference between the SIT and MIT treatments in the Matsuda index-which reflects insulin sensitivity-remained nonsignificant. Glucose-stimulated insulin secretion was similarly increased by the MIT and SIT treatments. Suppression of the AUC for glucagon was observed in the SIT treatment, while MIT treatment failed to suppress the glucagon concentration (-432 ± 2322 vs MIT 1116 ± 2520 pg/ml min, p < 0.05). The basal proinsulin/insulin ratio was lower in the SIT treatment (0.23 ± 0.04 vs MIT 0.26 ± 0.36, p < 0.05). CONCLUSIONS: Although either SIT or MIT can be employed to reduce postprandial hyperglycemia, SIT induces changes in hormonal profiles that are more favorable to islet functions than MIT does.
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