Morphological Changes and Increased Sucrase and Isomaltase Activity in Small Intestines of Insulin-Deficient and Type 2 Diabetic Rats

Accession number;03A0491624
Title;Morphological Changes and Increased Sucrase and Isomaltase Activity in Small Intestines of Insulin-Deficient and Type 2 Diabetic Rats
Author; ADACHI T (Osaka Prefecture Univ., Osaka, Jpn) MORI C (Chiba Univ., Chiba, Jpn) SAKURAI K (Chiba Univ., Chiba, Jpn) SHIHARA N (Kyoto Univ., Kyoto, Jpn) TSUDA K (Kyoto Univ., Kyoto, Jpn) YASUDA K (Kyoto Univ., Kyoto, Jpn)
Journal Title;Endocr J
Journal Code:F0625A
ISSN:0918-8959
VOL.50;NO.3;PAGE.271-279(2003)
Figure&Table&Reference;FIG.5, TBL.2, REF.38
Pub. Country;Japan
Language;English
Abstract;The small intestine plays an important role in the digestion and absorption of many nutrients. To investigate the contribution of carbohydrate digestion to diabetes mellitus, we examined the morphological changes of the small intestine, and the expression of sucrase-isomaltase, which is one of the intestinal disaccharidases, in diabetic model rat, that is the streptozotocin-induced (STZ) diabetic rat (insulin-deficient model), and the Otsuka Long-Evans Tokushima Fatty (OLETF) rats and the Goto-Kakizaki (GK) rats (type 2 diabetic models). Intestinal hyperplasia was observed in STZ, OLETF, and GK rats. Moreover, in the small intestine of each diabetic strain, the proliferating cell nuclear antigen (PCNA)-labeling index, which is a marker of proliferation, was higher than in the respective control. Cdx1 and Cdx2, known to be transcriptional factors related to intestinal proliferation and differentiation, were more highly expressed in STZ, OLETF and GK rats than in the respective controls. These findings indicate that small intestinal hyperplasia, and thereby the resultant increase of total activity of disaccharidases such as sucrase and isomaltase in the entire small intestine, might be one of the reasons for postprandial hyperglycemia in diabetes mellitus. (author abst.)
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