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Metabolism and Regulation of Food Intake

開催日 2014/9/13
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Orally GABA administration prevents ZFDM animal model from developing diabetes resulting from keeping the islet reactions

  • P3-202
  • 古川 和樹 / Kazuki Furukawa:1 阿部 巧 / Takumi Abe:1 野村 真悟 / Masato Nomura:1 永井 裕次郎 / Yujiro Nagai:2 岩谷 和輝 / Kazuki Iwaya:2 佐津川 満 / Mitsuru Satsukawa:2 河本 哲宏 / Tetsuhiro Kawamoto:2 吉田 祥子 / Sachiko Yoshida:1 
  • 1:豊橋技術科学大学・環境生命工学 / Dept Environ & Life Sci, Toyohashi Univ of Technology, Aichi, Japan 2:東海漬物・漬物機能研究所 / Tokai Pickling Co., Ltd., Aichi, Japan 

Pancreatic β cells contain high amount of GABA and release it with insulin for hyperglycemia. Aging or developing diabetes become GABA release slow down and insulin release was decreased. Previously we observed orally GABA administration to normal rat prevented aged degradation of the islet. To visualize GABA release from living islet cells, we have investigated sliced rat pancreas using the redoxenzyme-linked photo assay, as intrinsic GABA release could become index of dynamic insulin release from β cells to glucose application. Here, we showed orally GABA administration to diabetic animal model, ZFDM rat prevented diabetes onset. ZFDM rats that are kept in either hyperglycemic condition or not, normally show high blood glucose level after 20-week old and have an onset of diabetes. On the other hand, ZFDM rat administrated 1000 mg/kg GABA per day from 8-week old, kept their blood glucose level in both glycemic conditions. They did not show both glucose tolerance and insulin hypersecretion, whereas their other physical examinations, for example, the amount of cholesterol and Adiponectin, were not different from no GABA administrated ones. The islet of GABA administrated animals was less damaged than no administrated ones. We suggested administrated GABA would act in the islet like the paracrine, and inhibit hyperexcitation of the β cells under both glycemic conditions.

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