新生Ｃｈｉｎｅｓｅ　ＨａｍｓｔｅｒにおけるＭｏｎｏｓｏｄｉｕｍ　Ｇｌｕｔａｍａｔｅ誘発糖尿病に対する合成Ｔｒｙｐｓｉｎ　Ｉｎｈｉｂｉｔｏｒの予防効果および治療効果

• 酒井 芳紀

  旭川医科大学第二内科

• 渡辺 清

  旭川医科大学第二内科

• 建部 高明

  旭川医科大学第二内科

• 石井 兼央

  旭川医科大学第二内科

書誌事項

タイトル別名

• The therapeutic effect of synthetic trypsin inhibitor on monosodiumglutamate-induced diabetes mellitus in newborn Chinese hamsters.

抄録

The mechanism of the therapeutic action of synthetic trypsin inhibitor (STI) on monosodiumglutamate (MSG)-induced diabetes mellitus in newborn Chinese hamsters was investigated from the aspects of the trophic effect on the pancreas, pancreatic endocrine function, activity of hepatic enzymes in the carbohydrate metabolism and plasma lipid levels. Futhermore, it was studied whether the difference of the starting period of the STI treatment would affect the incidence and severity of diabetes mellitus or not. N. N-dimethylcarbamoylmethyl 4-(4-guanidinobenzoyloxy)-phenylacetate) methansulfonate (FOY-305) was used as STI and was administered by the oral route. The results are as follows. 1. MSG-induced diabetic hamsters not treated with STI developed to insulin-deficient diabetes mellitus. 2. Diabetes mellitus was ameliorated with all three different initial periods of STI treatment, i. e., during the lactation period and at the 4th and 11th weeks after birth, respectively. Namely, it was clarified that STI had preventive and therapeutic effects on MSG-induced diabetes mellitus in Chinese hamsters. 3. The following data were obtaned from the results using sacrificed hamsters at the 29th week after birth in the group in which the STI treatment was begun during the lactation period. (a) A good amount of plasma and pancreatic insulin was preserved, and activities of hexokinase, pyruvate kinase, glucose-6-phosphatase and phosphoenolpyruvate carboxykinase were kept within normal range by STI treatment. (b) Elevation of pancreatic glucagon content was suppressed, and the plasma glucagon level and stomach glucagon content were significantly lowered as compared with the normal control group. These results were thought as secondary phenomena produced by insulin, but it was also indicated that STI acted directly on A cells of the pancreas and stomach thus suppressing secretion and biosynthesis of glucagon. (c) Plasma levels of free fatty acid, triglyceride, total cholesterol, HDL-cholesterol, and phospholipid were not improved by STI. But blood lipoperoxide was significantly improved by STI. (d) The pancreata of Chinese hamsters, whether diabetic or non-diabetic were hypertrophied by STI. It was surmised that the effect of released CCK-PZ from the duodenum by STI led to this phenomenon, but in this mechanism, the possibility that it suppresses degeneration and promotes regeneration of B-cell might be also included.

収録刊行物

• 糖尿病

  糖尿病 27 (10), 1083-1093, 1984

  一般社団法人 日本糖尿病学会

キーワード

• 新生Chinese hamster
• Monosodium glutamate誘発糖尿病
• 膵に対する栄養効果
• 糖尿病発症抑制

詳細情報

• CRID: 1390282679881779328
• NII論文ID: 130004337151
• DOI: 10.11213/tonyobyo1958.27.1083
• ISSN: 1881588X
• ISSN: 0021437X
• 本文言語コード: ja
• データソース種別:
  • JaLC
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可