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Author
Takatori, Shingo
Goda, Mitsuhiro
Iwatani, Yukiko
Jin, Xin
Takada-Doi, Shima
Abstract
Royal jelly (RJ) is known to contain excellent nutrition and a variety of biological activities. The present study was designed to investigate the effects of RJ on insulin resistance (hyperinsulinemia) in fructose-drinking rats (FDR; insulin resistance animal model). Male Wistar rats (6 weeks old) received 15% fructose solution in drinking water for 8 weeks. FDR showed significant increases in plasma levels of insulin and triglyceride, Homeostasis Model Assessment ratio (HOMA-R, an index of insulin resistance), and systolic blood pressure, but not blood glucose levels, when compared with control rats. RJ (100, 300mg/kg, p.o.) treatment for 8 weeks significantly decreased the plasma levels of insulin and triglyceride, HOMA-R, without affecting blood glucose or total cholesterol levels and tended to lower systolic blood pressure. In isolated and perfused mesenteric vascular beds of FDR, RJ treatment resulted in a significant reduction in sympathetic nerve-mediated vasoconstrictor response to periarterial nerve stimulation (PNS) and tended to increase the calcitonin gene-related peptide (CGRP) nervemediated vasodilator response to PNS, compared with those in untreated FDR. However, RJ treatment did not significantly affect norepinephrine-induced vasoconstriction or CGRP-induced vasodilation. These results suggest that RJ could be an effective functional food to prevent insulin resistance associated with the development of hypertension.
Keywords
royal jelly
fructose-drinking rat
insulin resistance
periarterial nerve function
Note
コンテンツの著作権は日本薬学会が有します。
Published Date
2008-11-01
Publication Title
Biological & Pharmaceutical Bulletin
Volume
volume31
Issue
issue11
Publisher
日本薬学会
Publisher Alternative
The Pharmaceutical Society of Japan
Start Page
2103
End Page
2107
ISSN
09186158
NCID
AA10885497
Content Type
Journal Article
language
英語
Copyright Holders
© The Pharmaceutical Society of Japan
File Version
publisher
Refereed
True
DOI
PubMed ID
Web of Science KeyUT