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Your search keyword '"Taro Yasuma"' showing total 3 results
Start Over Author "Taro Yasuma" Publisher american diabetes association
3 results on '"Taro Yasuma"'

1. Amelioration of Diabetes by Protein S

Author

Josephine A. Hinneh, Isaac Cann, John Morser, Iwasa Motoh, Esteban C. Gabazza, Paloma Gil-Bernabe, Ziaurahman Roeen, Taro Yasuma, Corina N. D’Alessandro-Gabazza, Kota Nishihama, Yutaka Yano, Masaaki Toda, Tetsu Kobayashi, Rumi Mifuji-Moroka, and Yoshiyuki Takei

Subjects
Blood Glucose, Male, 0301 basic medicine, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Apoptosis, Mice, Transgenic, Type 2 diabetes, 030204 cardiovascular system & hematology, Protein S, Cell Line, Diabetes Mellitus, Experimental, Diabetic nephropathy, Mice, 03 medical and health sciences, 0302 clinical medicine, Insulin resistance, Insulin-Secreting Cells, Internal medicine, Diabetes mellitus, Adipocytes, Internal Medicine, medicine, Animals, Humans, Diabetic Nephropathies, Muscle, Skeletal, Protein kinase B, Glucose tolerance test, biology, medicine.diagnostic_test, Liver cell, Glucose Tolerance Test, Middle Aged, medicine.disease, Diabetes Mellitus, Type 1, 030104 developmental biology, Endocrinology, Diabetes Mellitus, Type 2, Liver, biology.protein, Female, Insulin Resistance
Abstract

Protein S is an anticoagulant factor that also regulates inflammation and cell apoptosis. The effect of protein S on diabetes and its complications is unknown. This study compared the development of diabetes between wild-type and transgenic mice overexpressing human protein S and the development of diabetic glomerulosclerosis between mice treated with and without human protein S and between wild-type and protein S transgenic mice. Mice overexpressing protein S showed significant improvements in blood glucose level, glucose tolerance, insulin sensitivity, and insulin secretion compared with wild-type counterparts. Exogenous protein S improved insulin sensitivity in adipocytes, skeletal muscle, and liver cell lines in db/db mice compared with controls. Significant inhibition of apoptosis with increased expression of BIRC3 and Bcl-2 and enhanced activation of Akt/PKB was induced by protein S in islet β-cells compared with controls. Diabetic wild-type mice treated with protein S and diabetic protein S transgenic mice developed significantly less severe diabetic glomerulosclerosis than controls. Patients with type 2 diabetes had significantly lower circulating free protein S than healthy control subjects. This study shows that protein S attenuates diabetes by inhibiting apoptosis of β-cells and the development of diabetic nephropathy.

Published
2016
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2. Erratum. Amelioration of Diabetes by Protein S. Diabetes 2016;65:1940–1951

Author

Isaac Cann, Ziaurahman Roeen, John Morser, Yutaka Yano, Taro Yasuma, Paloma Gil-Bernabe, Corina N. D’Alessandro-Gabazza, Rumi Mifuji-Moroka, Kota Nishihama, Masaaki Toda, Yoshiyuki Takei, Josephine A. Hinneh, Iwasa Motoh, Esteban C. Gabazza, and Tetsu Kobayashi

Subjects
Text mining, biology, business.industry, Endocrinology, Diabetes and Metabolism, Diabetes mellitus, Internal Medicine, medicine, biology.protein, Bioinformatics, medicine.disease, business, Protein S
Published
2016
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3. Amelioration of Diabetes by Protein S.

Author

Taro Yasuma, Yutaka Yano, D'Alessandro-Gabazza, Corina N., Masaaki Toda, Gil-Bernabe, Paloma, Tetsu Kobayashi, Kota Nishihama, Hinneh, Josephine A., Rumi Mifuji-Moroka, Roeen, Ziaurahman, Morser, John, Cann, Isaac, Iwasa Motoh, Yoshiyuki Takei, Gabazza, Esteban C., Yasuma, Taro, Yano, Yutaka, Toda, Masaaki, Kobayashi, Tetsu, and Nishihama, Kota

Subjects
*PROTEIN S, *INFLAMMATION, *APOPTOSIS, *GENE expression, *DIABETIC nephropathies, *ANIMAL experimentation, *ANIMALS, *BLOOD proteins, *BLOOD sugar, *CELL lines, *DIABETES, *FAT cells, *GLUCOSE tolerance tests, *INSULIN resistance, *TYPE 1 diabetes, *ISLANDS of Langerhans, *LIVER, *MICE, *TYPE 2 diabetes, *SKELETAL muscle
Abstract

Protein S is an anticoagulant factor that also regulates inflammation and cell apoptosis. The effect of protein S on diabetes and its complications is unknown. This study compared the development of diabetes between wild-type and transgenic mice overexpressing human protein S and the development of diabetic glomerulosclerosis between mice treated with and without human protein S and between wild-type and protein S transgenic mice. Mice overexpressing protein S showed significant improvements in blood glucose level, glucose tolerance, insulin sensitivity, and insulin secretion compared with wild-type counterparts. Exogenous protein S improved insulin sensitivity in adipocytes, skeletal muscle, and liver cell lines in db/db mice compared with controls. Significant inhibition of apoptosis with increased expression of BIRC3 and Bcl-2 and enhanced activation of Akt/PKB was induced by protein S in islet β-cells compared with controls. Diabetic wild-type mice treated with protein S and diabetic protein S transgenic mice developed significantly less severe diabetic glomerulosclerosis than controls. Patients with type 2 diabetes had significantly lower circulating free protein S than healthy control subjects. This study shows that protein S attenuates diabetes by inhibiting apoptosis of β-cells and the development of diabetic nephropathy. [ABSTRACT FROM AUTHOR]

Published
2016
Full Text
View/download PDF

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