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19 results on '"Tsuruta, Munehisa"'

3. Additional file 1 of Thyroid-related ophthalmopathy development in concurrence with growth hormone administration

Author

Iwata, Shimpei, Tsumura, Kenji, Ashida, Kenji, Tokubuchi, Ichiro, Demiya, Mutsuyuki, Kitamura, Miyuki, Ohshima, Hiroyuki, Yano, Mamiko, Nagayama, Ayako, Yasuda, Junichi, Tsuruta, Munehisa, Motomura, Seiichi, Yoshida, Shigeo, and Nomura, Masatoshi

Abstract

Additional file 1: Supplemental Table S1. Pituitary gland hormone responses to pituitary stimulation tests.

Published
2021
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4. Additional file 2 of Thyroid-related ophthalmopathy development in concurrence with growth hormone administration

Author

Iwata, Shimpei, Tsumura, Kenji, Ashida, Kenji, Tokubuchi, Ichiro, Demiya, Mutsuyuki, Kitamura, Miyuki, Ohshima, Hiroyuki, Yano, Mamiko, Nagayama, Ayako, Yasuda, Junichi, Tsuruta, Munehisa, Motomura, Seiichi, Yoshida, Shigeo, and Nomura, Masatoshi

Abstract

Additional file 2: Supplemental Figure S1. Hypothesis of pathological mechanisms in this case.

Published
2021
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5. Pasireotide‐induced hyperglycemia in a patient with Cushing's disease: Potential use of sodium‐glucose cotransporter 2 inhibitor and glucagon‐like peptide‐1 receptor agonist for treatment

Author

Shikata, Masato, primary, Ashida, Kenji, additional, Goto, Yuka, additional, Nagayama, Ayako, additional, Iwata, Shimpei, additional, Yano, Mamiko, additional, Hasuzawa, Nao, additional, Hara, Kento, additional, Mawatari, Kazutoshi, additional, Sakata, Kiyohiko, additional, Tsuruta, Munehisa, additional, Wada, Nobuhiko, additional, and Nomura, Masatoshi, additional

Published
2020
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7. Human Leukocyte Antigen (HLA) Subtype-Dependent Development of Myasthenia Gravis, Type-1 Diabetes Mellitus, and Hashimoto Disease: A Case Report of Autoimmune Polyendocrine Syndrome Type 3

Author

Gobaru, Mizuki, primary, Ashida, Kenji, additional, Yoshinobu, Satoko, additional, Nagayama, Ayako, additional, Kabashima, Masaharu, additional, Iwata, Shimpei, additional, Hasuzawa, Nao, additional, Tsuruta, Munehisa, additional, Wada, Nobuhiko, additional, Nakayama, Hitomi, additional, Motomura, Seiichi, additional, Tajiri, Yuji, additional, and Nomura, Masatoshi, additional

Published
2019
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8. Bromocriptine as a Potential Glucose-lowering Agent for the Treatment of Prolactinoma with Type 2 Diabetes

Author

Oshige, Tamami, primary, Nakamura, Yui, additional, Sasaki, Yuko, additional, Kawano, Seiko, additional, Ohki, Tsuyoshi, additional, Tsuruta, Munehisa, additional, Tokubuchi, Ichiro, additional, Nakayama, Hitomi, additional, Yamada, Kentaro, additional, Ashida, Kenji, additional, Tajiri, Yuji, additional, and Nomura, Masatoshi, additional

Published
2019
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9. Metreleptin Supplementation for Improving Lipid and Glycemic Profiles in Acquired Diabetes Lipodystrophy: A Case Report

Author

Nagayama, Ayako, primary, Ashida, Kenji, additional, Moritaka, Kanoko, additional, Hidaka, Mami, additional, Gobaru, Mizuki, additional, Tanaka, Seiji, additional, Hasuzawa, Nao, additional, Akasu, Shoko, additional, Goto, Yuka, additional, Motomura, Seiichi, additional, Hara, Kento, additional, Tsuruta, Munehisa, additional, Wada, Nobuhiko, additional, Nakayama, Hitomi, additional, Tajiri, Yuji, additional, and Nomura, Masatoshi, additional

Published
2019
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11. Changes in body composition during SGLT2 inhibitor treatment and their relevance to the improvement of insulin sensitivity

Author

Nakayama, Hitomi, primary, Ohtsuka, Yoshie, additional, Kawahara, Mamiko, additional, Nakamura, Yui, additional, Iwata, Shinpei, additional, Yoshinobu, Satoko, additional, Soga, Rika, additional, Oshige, Tamami, additional, Kawano, Seiko, additional, Kakino, Satomi, additional, Tsuruta, Munehisa, additional, Tajiri, Yuji, additional, and Yamada, Kentaro, additional

Published
2016
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12. Cross-sectional and Longitudinal Analyses of Factors Contributing to the Progressive Loss of the β-cell Function in Type 2 Diabetes

Author

Nakayama, Hitomi, primary, Kato, Tomoko, additional, Nakayama, Satoshi, additional, Kaku, Hiroh, additional, Muraishi, Kazuhisa, additional, Tokubuchi, Ichiro, additional, Hara, Kento, additional, Kato, Tamotsu, additional, Wada, Nobuhiko, additional, Tsuruta, Munehisa, additional, Ohki, Tsuyoshi, additional, Tanaka, Kayo, additional, Mitsuzaki, Kenshi, additional, Tajiri, Yuji, additional, and Yamada, Kentaro, additional

Published
2015
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13. Age-related changes in the diurnal variation of ketogenesis in patients with type 2 diabetes and relevance to hypoglycemic medications

Author

Nakayama, Hitomi, primary, Tokubuchi, Ichiro, additional, Wada, Nobuhiko, additional, Tsuruta, Munehisa, additional, Ohki, Tsuyoshi, additional, Oshige, Tamami, additional, Sasaki, Yuko, additional, Iwata, Shinpei, additional, Kato, Naoka, additional, Ohtsuka, Yoshie, additional, Matsuo, Yuko, additional, Tajiri, Yuji, additional, and Yamada, Kentaro, additional

Published
2015
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19. Cross-sectional and Longitudinal Analyses of Factors Contributing to the Progressive Loss of the β-cell Function in Type 2 Diabetes.

Author

Nakayama H, Kato T, Nakayama S, Kaku H, Muraishi K, Tokubuchi I, Hara K, Kato T, Wada N, Tsuruta M, Ohki T, Tanaka K, Mitsuzaki K, Tajiri Y, and Yamada K

Subjects
Adult, Aged, Cross-Sectional Studies, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 physiopathology, Disease Progression, Female, Glucagon metabolism, Glycated Hemoglobin metabolism, Humans, Insulin metabolism, Insulin Resistance, Longitudinal Studies, Male, Middle Aged, Overweight complications, Regression Analysis, Thinness metabolism, Triglycerides blood, Body Mass Index, C-Peptide blood, Diabetes Mellitus, Type 2 metabolism, Insulin-Secreting Cells metabolism, Overweight metabolism
Abstract

Objective: Type 2 diabetes is a progressive disease characterized by insulin resistance and insulin secretory dysfunction. In this study, we assessed the factors contributing to an insulin secretory defect in type 2 diabetes patients., Methods: The subjects consisted of 382 patients with type 2 diabetes, aged 57±13 years. We estimated the β-cell function using 6-min post-glucagon increments in C-peptide (ΔCPR)., Results: A significant inverse correlation was observed between the time since the diagnosis of diabetes and ΔCPR. A simple liner regression analysis showed that ΔCPR decreases at a rate of 0.056 ng/mL/year. According to a multiple regression model, body mass index (BMI) and log (triglyceride) were positively correlated with ΔCPR. Time since the diagnosis of diabetes, diabetes in 1st degree relatives, the presence of diabetic retinopathy, and HbA1c were inversely correlated with ΔCPR. In 50 patients who underwent the glucagon stimulation test twice, the ΔCPR decreased from 2.27±1.47 to 1.72±1.08 ng/mL over a period of 6.5±0.9 years. A multiple regression analysis revealed the BMI and fasting plasma glucose level to be significant contributing factors to the decline in ΔCPR., Conclusion: The duration of diabetes, a low BMI, genetic factors, and the presence of microangiopathy may be associated with β-cell dysfunction in diabetic patients. The observations in this study suggest that obese subjects showed a rapid decline in the β-cell function despite an initial high CPR response. Environmental factors causing insulin resistance and glucotoxicity may therefore be involved in progressive β-cell failure.

Published
2015
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