Tetsuya Nakazawa
Tohoku University
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Publication
Featured researches published by Tetsuya Nakazawa.
Journal of Clinical Investigation | 1998
Fumiko Ikehata; Jo Satoh; Koji Nata; Akira Tohgo; Tetsuya Nakazawa; Ichiro Kato; Seiichi Kobayashi; Takako Akiyama; Shin Takasawa; Takayoshi Toyota; Hiroshi Okamoto
Cyclic ADP-ribose (cADPR) has been shown to be a mediator for intracellular Ca2+ mobilization for insulin secretion by glucose in pancreatic beta cells, and CD38 shows both ADP-ribosyl cyclase to synthesize cADPR from NAD+ and cADPR hydrolase to hydrolyze cADPR to ADP-ribose. We show here that 13.8% of Japanese non-insulin-dependent diabetes (NIDDM) patients examined have autoantibodies against CD38 and that the sera containing anti-CD38 autoantibodies inhibit the ADP-ribosyl cyclase activity of CD38 (P </= 0.05). Insulin secretion from pancreatic islets by glucose is significantly inhibited by the addition of the NIDDM sera with anti-CD38 antibodies (P </= 0.04-0.0001), and the inhibition of insulin secretion is abolished by the addition of recombinant CD38 (P </= 0.02). The increase of cADPR levels in pancreatic islets by glucose was also inhibited by the addition of the sera (P </= 0.05). These results strongly suggest that the presence of anti-CD38 autoantibodies in NIDDM patients can be one of the major causes of impaired glucose-induced insulin secretion in NIDDM.
Immunopharmacology | 1997
Masamitsu Fukuzawa; Jo Satoh; Mikio Sagara; Gen Muto; Yoshiko Muto; Sachiko Nishimura; Shuichi Miyaguchi; Xiao Ling Qiang; Yoshiyuki Sakata; Tetsuya Nakazawa; Fumiko Ikehata; Setsu Ohta; Takayoshi Toyota
It has been reported that angiotensin converting enzyme (ACE) inhibitors have beneficial effects on insulin resistance and congestive heart failure, in which elevations of serum tumor necrosis factor-α (TNF-α) level have been indicated. Therefore, in this study, we examined effect of ACE inhibitors on TNF-α production both in vitro and in vivo by using human blood mononuclear cells and mice, respectively. LPS (20 μg/ml)-induced in vitro TNF-α production, measured by bioassay and enzyme-linked immunosorbent assay, was significantly inhibited with captopril, delapril and cilazapril in a concentration of 10−3 mol/l. A single, oral administration of captopril, delapril and cilazapril at more than 10-fold doses of common clinical use in man significantly inhibited LPS (2 mg/kg)-induced serum TNF-α activity in Balb/c mice. These results indicate that ACE inhibitors such as captopril, delapril and cilazapril have an inhibitory effect on TNF-α production not only in vitro as previously reported, but also in vivo, although relatively high concentrations and large doses were required in this study.
Diabetes Research and Clinical Practice | 1999
Masamitsu Fukuzawa; Jo Satoh; X. Qiang; Shuichi Miyaguchi; Yoshiyuki Sakata; Tetsuya Nakazawa; Fumiko Ikehata; Setsu Ohta; Takayoshi Toyota
It has recently been indicated that tumor necrosis factor-alpha (TNF-alpha) production is increased under chronic hyperglycemia and TNF-alpha has harmful effects on insulin sensitivity and possibly on chronic diabetic complications. Therefore it will be favorable for diabetes treatment if anti-diabetic agents also have anti-TNF-alpha activities. In this study, we have investigated effects of hypoglycemic sulfonylureas (gliclazide and glibenclamide) and a thiazolidinedione (troglitazone) on lipopolysaccharide-induced TNF-alpha production, which was evaluated by immunoassay and bioassay, in vivo using mice and partly in vitro using human peripheral blood mononuclear cells. Gliclazide significantly inhibited TNF-alpha production in vivo and also in vitro at a concentration of 10(-3) mol/l. However, glibenclamide had neither effect on TNF-alpha production nor action. On the other hand, troglitazone inhibited action rather than production of TNF-alpha in vivo. In vitro troglitazone (10(-4) mol/l) significantly reduced cytolytic activity of TNF-alpha against LM cells. These results indicate that gliclazide and troglitazone have inhibitory effect on TNF-alpha.
Immunopharmacology | 2000
Masamitsu Fukuzawa; Jo Satoh; Setsu Ohta; Kazuma Takahashi; Shuichi Miyaguchi; X. Qiang; Yoshiyuki Sakata; Tetsuya Nakazawa; Yumiko Takizawa; Takayoshi Toyota
Abstract It is well known that some anti-hypertensive drugs affect insulin sensitivity and that tumor necrosis factor-α (TNF-α) is a mediator of obesity-associated insulin resistance. In this study, we have investigated the effect of anti-hypertensive drugs, calcium (Ca) channel blockers (amlodipine, manidipine and nicardipine), an α1-blocker (doxazosin), a β1-blocker (metoprolol), and a thiazide diuretic (hydrochlorothiazide), on lipopolysaccharide (LPS)-induced TNF-α production. TNF-α production, measured with a bioassay and an immunoassay, was evaluated both in vivo and in vitro, by utilizing mice and a human peripheral blood mononuclear cell culture, respectively. Nicardipine, or amlodipine, manidipine and doxazosin significantly inhibited TNF-α production in mice at doses more than one or ten times higher than those used clinically, respectively. On the other hand, metoprolol increased TNF-α production at doses of more than 10 times those used clinically, whereas hydrochlorothiazide did not alter production of the cytokine. The in vivo effects of these drugs were not necessary parallel to the in vitro effects. Because high doses of these drugs in mice correspond to clinical doses and effects in human, these actions may be related to beneficial and/or harmful effects of these drugs on TNF-α mediated diseases, including insulin resistance.
Journal of Biological Chemistry | 1998
Toshinari Takamura; Ichiro Kato; Noriko Kimura; Tetsuya Nakazawa; Hideto Yonekura; Shin Takasawa; Hiroshi Okamoto
Journal of Autoimmunity | 2001
Tetsuya Nakazawa; Jo Satoh; Kazuma Takahashi; Yoshiyuki Sakata; Fumiko Ikehata; Yumiko Takizawa; Shin-ichiro Bando; Toshimune Housai; Yan Li; Chen Chen; Takayuki Masuda; Shigeo Kure; Ichiro Kato; Shin Takasawa; Tadatsugu Taniguchi; Hiroshi Okamoto; Takayoshi Toyota
European Journal of Endocrinology | 2002
Jun-ichi Tani; Kouki Mori; Saeko Hoshikawa; Tetsuya Nakazawa; Jo Satoh; Yoshinori Nakagawa; Sadayoshi Ito; Katsumi Yoshida
Gene | 2005
Tetsuya Nakazawa; Shin Takasawa; Naoya Noguchi; Koji Nata; Akira Tohgo; Mitsuko Mori; Kan-ichi Nakagawara; Takako Akiyama; Takayuki Ikeda; Akiyo Yamauchi; Iwao Takahashi; Takeo Yoshikawa; Hiroshi Okamoto
Clinical Immunology and Immunopathology | 1997
Yoshiko Muto; Jo Satoh; Gen Muto; Takayuki Masuda; Mikio Sagara; Masamitsu Fukuzawa; Shuichi Miyaguchi; X. Qiang; Yoshiyuki Sakata; Tetsuya Nakazawa; Fumiko Ikehata; Takayoshi Toyota
Clinical Immunology | 2000
Gen Muto; Jo Satoh; Yoshiko Muto; Kazuma Takahashi; Tetsuya Nakazawa; Mikio Sagara; Shuichi Miyaguchi; Masamitsu Fukuzawa; X. Qiang; Yoshiyuki Sakata; Yumiko Takizawa; Yan Li; Shin-ichiro Bando; Toshimune Housai; Akira Tamagawa; Takayoshi Toyota