| Project/Area Number |
10670468
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
TSUKADA Hideaki Kyoto University, Departmemt of Metabol and Clinical Nutrition, Assistant., 医学研究科, 助手 (30207336)
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| Co-Investigator(Kenkyū-buntansha) |
FUJITA Jun Kyoto University, Departmemt of Metabol and Clinical Nutrition, Assistant., 医学研究科, 助手 (00303826)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Disaccharidase / Ginseng Radix / SGLT / Glucose transporter / GLUT2 / Ussing's method / Triglitazone / Okadaic acid / 糖輸送担体 / Triglitazone / グルコース輸送 / 内視鏡生検 |
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| Research Abstract |
In this study NaィイD1+ィエD1-dependent glucose transport in human small intestine could be examined using endoscopic biopsy. Comparative study of inhibitory effect on glucose and maltose absorption elucidated that chemicals inhibits disaccharidase such as acarbose or inhibits sodium dependent glucose transporter such as Ginseng Radix (ref,1). Ginseng radix (GR) has been reported to inhibit hyperglycemia. This agent has been mainly used to treat diabetes in clinical practice. It has been reported that the action mechanism of GR involves enhancement of insulin biosynthesis and increased glucose transporter (GLUT-2) expression in the liver. When short-circuit current (Isc) in the human duodenal mucosa was measured before GR administration, Isc was 5.7±3.7uA/cm2 with sugar free Ringer's solution on both the mucosal and serosal sides. Addition of 10mM glucose or maltose to the mucosal side chamber increased Isc 2-10minutes after administration. Subsequently, GR administration inhibited the increase in Isc within 2 minutes in both the glucose-treated group and the maltose-treated group. These results suggests that Ginseng Radix ameliorates hyperglycemia by inhibiting NaィイD1+ィエD1-glucose co-transporter directly. Triglitazone inhibits electrogenic bicarbonate secretion in human small intestine (ref.2). Okadaic acid evokes an increase in water and electrolyte permeability of intestinal epithelium by opening the paracellular pathway (ref.3). Human gastric mucosa obtained by endoscopic biopsy is also useful for electrophysiological study (ref.4).
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