研究者業績

淺田 陽平

アサダ ヨウヘイ  (asada yohei)

基本情報

所属
藤田医科大学 医学部 医学科 内分泌・代謝・糖尿病内科学 助教
学位
博士(医学)(2020年3月 藤田医科大学)

J-GLOBAL ID
201601002305478853
researchmap会員ID
7000015576

論文

 4
  • Takeshi Takayanagi, Hiroyuki Hirai, Yohei Asada, Takaaki Yamada, Seiji Hasegawa, Eisuke Tomatsu, Yoshiteru Maeda, Yasumasa Yoshino, Izumi Hiratsuka, Sahoko Sekiguchi-Ueda, Megumi Shibata, Yusuke Seino, Yoshihisa Sugimura, Hirohiko Akamatsu, Mitsuyasu Itoh, Atsushi Suzuki
    Molecular biology reports 49(7) 5875-5882 2022年7月  
    AIMS: Although skin manifestations are common in diabetic patients, its characteristics are poorly identified. This study explored the differentiation process of keratinocytes in type 2 diabetes mellitus (T2DM) in vivo. METHODS: Back skin of T2DM model KKAy/TaJcl mice (KKAy) and C57BL/6JJcl mice (control) aged 8 and 12 weeks was used. The mRNA expression of differentiation markers of keratinocytes was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The expression of each marker in situ was examined immunohistochemically. RESULTS: KKAy mice showed hyperglycemia versus control mice. The histological findings showed increased thickness and structural impairment of epidermal tissue in KKAy mice. The qRT-PCR revealed that the expression of integrin beta 1 and keratin 14 in KKAy and control mice was identical. However, the expression of involucrin at 8 weeks, keratin 10 at 12 weeks, and filaggrin and loricrin at 8 and 12 weeks was decreased in KKAy mice. Immunohistochemical findings showed that filaggrin was markedly decreased in KKAy mice, though Ki-67 remained unchanged. CONCLUSION: The terminal differentiation process was impaired in the diabetic skin, while keratinocyte proliferation was preserved. Damaged terminal differentiation of keratinocytes may contribute to impairment of the skin barrier function in diabetic dermatoses.
  • 植田 佐保子, 中島 優華, 松尾 悠志, 九鬼 伴樹, 淺田 陽平, 戸松 瑛介, 吉野 寧維, 平塚 いづみ, 藤沢 治樹, 垣田 彩子, 四馬田 恵, 清野 祐介, 高柳 武志, 牧野 真樹, 楯谷 一郎, 鈴木 敦詞
    日本内分泌学会雑誌 97(5) 1162-1162 2022年3月  
  • Mizuho Kondo-Ando, Yusuke Seino, Risa Morikawa, Kana Negi, Hidechika Todoroki, Tsukasa Kawakami, Yohei Asada, Ryo Yoshimoto, Chika Tanaka, Keiko Okamoto, Atsushi Masuda, Eisuke Tomatsu, Izumi Hiratsuka, Yasumasa Yoshino, Wakako Maki, Ayako Kakita, Megumi Shibata, Takeshi Takayanagi, Masaki Makino, Yoshihisa Sugimura, Shiho Asai, Akemi Ito, Shinji Ueno, Yuuka Fujiwara, Hitoshi Kuwata, Daisuke Yabe, Atsushi Suzuki
    Journal of diabetes and its complications 33(11) 107415-107415 2019年11月  
    AIMS: The aim of this study is to investigate the effects of a low-carbohydrate staple food (i.e., low-carbohydrate bread) on glucose and lipid metabolism and pancreatic and enteroendocrine hormone secretion in comparison with meals containing normal-carbohydrate bread, without consideration of the carbohydrate content of the side dishes. METHODS: T2DM patients (n = 41) were provided meals containing low-carbohydrate bread (LB) together with side dishes or normal-carbohydrate bread (NB) together with side dishes every other day as a breakfast. Blood glucose levels were evaluated by using a continuous glucose monitoring system; blood samples were collected before and 1 and 2 h after the breakfast. RESULTS: Postprandial blood glucose levels, plasma insulin, plasma glucose-dependent insulinotropic polypeptide (GIP) and plasma triglyceride were significantly lower and plasma glucagon levels were significantly higher in LB compared with those in NB. Plasma glucagon-like peptide-1 (GLP-1) levels did not differ in the LB and NB groups. CONCLUSIONS: These results indicate that changing only the carbohydrate content of the staple food has benefits on glucose and lipid metabolism in T2DM patients concomitant with the decrease of insulin and GIP secretion, which ameliorate body weight gain and insulin resistance.
  • Yohei Asada, Takeshi Takayanagi, Tsukasa Kawakami, Eisuke Tomatsu, Atsushi Masuda, Yasumasa Yoshino, Sahoko Sekiguchi-Ueda, Megumi Shibata, Tomihiko Ide, Hajime Niimi, Eishin Yaoita, Yusuke Seino, Yoshihisa Sugimura, Atsushi Suzuki
    International journal of endocrinology 2019 4194853-4194853 2019年  
    Osteoporosis patients with chronic kidney disease (CKD) are becoming common in our superaging society. Renal dysfunction causes phosphorus accumulation in the circulating plasma and leads to the development of CKD-mineral bone disorder (MBD). We have previously reported that type III Pi transporter-overexpressing transgenic (Pit-1 TG) rats manifest phosphate (Pi)-dependent podocyte injury. In the present study, we explored the effect of risedronate on Pi-induced podocyte injury in vivo. Pit-1 TG rats and wild-type rats at 5 weeks old were divided into a risedronate-treated group and an untreated group. We subcutaneously administered 5 μg/kg body weight of risedronate or saline twice a week during the experimental period. Risedronate did not alter serum creatinine levels at 5, 8, and 12 weeks of age. However, electron microscopy images showed that thickening of the glomerular basement membrane was improved in the risedronate treatment group. Furthermore, immunostaining for podocyte injury markers revealed that both desmin- and connexin43-positive areas were smaller in the risedronate-treated group than in the untreated group, suggesting that bisphosphonates could rescue Pi-induced podocyte injury. In conclusion, our findings suggest that risedronate could maintain glomerular barrier function by rescuing Pi-induced podocyte injury.

MISC

 11