著者
葛谷 健 中川 昌一 佐藤 譲 金澤 康徳 岩本 安彦 小林 正 南條 輝志男 佐々木 陽 清野 裕 伊藤 千賀子 島 健二 野中 共平 門脇 孝
出版者
一般社団法人 日本糖尿病学会
雑誌
糖尿病 (ISSN:0021437X)
巻号頁・発行日
vol.42, no.5, pp.385-404, 1999-05-30 (Released:2011-03-02)
参考文献数
47
被引用文献数
86

糖尿病は, インスリン作用の不足による慢性高血糖を主徴とし, 種々の特徴的な代謝異常を伴う疾患群である. その発症には遺伝因子と環境因子がともに関与する. 代謝異常の長期間にわたる持続は特有の合併症を来たしやすく, 動脈硬化症をも促進する. 代謝異常の程度によって, 無症状からケトアシドーシスや昏睡に至る幅広い病態を示
著者
香野 修介 今村 洋一 小路 眞護 林 秀樹 山田 研太郎 野中 共平
出版者
一般社団法人 日本糖尿病学会
雑誌
糖尿病 (ISSN:0021437X)
巻号頁・発行日
vol.41, no.12, pp.1089-1094, 1998-12-30 (Released:2011-03-02)
参考文献数
15
被引用文献数
2

[目的] さまざまな血糖コントロールの糖尿病患者およびインスリノーマ患者に対し低血糖誘発試験を行い, インスリン拮抗ホルモン分泌動態や低血糖症状を観察し, 低血糖閾値を検討した.[成績] 1回/月以上の低血糖の既往がある群は, ない群より明らかに閾値は低下していた.また閾値上昇群 (健常者閾値平均+2SD以上) のHbA1cは閾値低下群 (平均-2SD) に比べ著明に高く, HbA1cとエピネフリン分泌閾値とは平行していた.インスリノーマ患者の低血糖閾値は著明に低下していたが術後上昇し, 逆に血糖コントロール不良者の閾値は上昇していたが約1カ月間血糖コントロールすると低下傾向となった.[結論] 低血糖閾値は持続的な高血糖により上昇し, 低血糖の既往によりそれは低下する.そして低下した低血糖閾値は低血糖を回避することで, 逆に上昇した低血糖閾値は血糖コントロールにより改善傾向へ向かうと思われる.
著者
市原 紀久雄 島 健二 黒田 耕平 野中 共平 垂井 清一郎
出版者
一般社団法人 日本糖尿病学会
雑誌
糖尿病 (ISSN:0021437X)
巻号頁・発行日
vol.16, no.6, pp.498-504, 1973-11-30 (Released:2011-08-10)
参考文献数
21

Although diet regulation is a basal therapeutic means for diabetes, little is known about its primary effect on diabetic metabolism, including insulin secretion. The purpose of this investigation is to throw a light on this problem.Twenty-two non-ketotic diabetics were selected for study, who were newly-diagnosed or had interrupted the treatment of diabetes for long time, having no other diseases which might affect carbohydrate metabolism.In these patients, blood glucose, FFA and IRI response to oral loading of 100 g glucose were compared before and after 4 week diet regulation. The diet which was indicated to them was composed of 60% carbohydrate, 15-20% protein and 20-25% fat. The total calorie was restricted in relation to their weight and physical activity. The patients were asked to weigh their daily food. 24h intake of carbohydrate, protein and fat, and total calorie were calculated as accurately as possible. According to this calculation, dietetic intakes of seven of these twenty-two patients were found not to be significantly changed between before and after the instruction of diet regulation. Therefore, we divided all patients studied into two groups, namely control group (7 cases) and diet treatment group (15 cases).After the diet regulation in the latter group, fasting glucose was decreased from 164.1±14.6 mg% to 121.7±7.1 mg%(p<0.01), glucose tolerance was significantly improved and insulin response estimated by measuring the area under the curve was increased from 6, 807±958 μU·min/m/ to 10, 392±1, 657 μU·Eminim/(p<0.01) in spite of lowered level of blood glucose. However, the sluggishness in early insulin response to glucose was not markedly changed. Insulinogenic index was also significantly increased at 180 minutes after oral glucose loading. Plasma FFA response to oral glucose was ameliorated at 120 minutes.On the other hand, the control group did not show any significant changes in blood glucose and IRI and FFA response to glucose loading before and after 4 week observation periods.Therefore, the metabolic effects of the diet regulation should be at least in part ascribed to the increased secretion of insulin. These results support the classical concept, “Resting the Pancreas”, brought about by caloric restriction.