4.4 Article

The protective role of Kangen-karyu against fructose-induced metabolic syndrome in a rat model

Journal

JOURNAL OF PHARMACY AND PHARMACOLOGY
Volume 59, Issue 9, Pages 1271-1278

Publisher

PHARMACEUTICAL PRESS-ROYAL PHARMACEUTICAL SOC GREAT BRITIAN
DOI: 10.1211/jpp.59.9.0012

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The protective effect of Kangen-karyu extract and its mechanisms against fructose-induced metabolic syndrome have been investigated using a rat model. Male Wistar rats were fed a high fructose (65%) diet or standard chow for one week, and for two subsequent weeks were treated with 50 or 100 mg kg(-1) body weight/day Kangen-karyu extract or vehicle. Serum glucose, glycosylated protein, triglyceride (TG), total cholesterol, and blood pressure levels of high-fructose-fed rats were increased compared with those of normal rats. However, Kangen-karyu extract ameliorated the high-fructose-induced metabolic syndrome including hyperglycaemia and hypertriglyceridaemia. In addition, the increase of hepatic TG content in rats given the high fructose diet was significantly inhibited with the regulation of sterol regulatory element-binding protein (SREBP)-1 expression by Kangen-karyu extract. On the other hand, peroxisome proliferator-activated receptor alpha and SREBP-2 protein levels were not affected by the feeding of the high fructose diet or Kangen-karyu extract. Moreover, Kangen-karyu extract administration to high-fructose-fed rats markedly reduced the thiobarbituric acid-reactive substance levels in serum, hepatic homogenate, and mitochondria. Furthermore, it inhibited the increase of cyclooxygenase (COX)-2 with the regulation of nuclear factor-kappa B (NF-kappa B) and bcl-2 proteins in the liver, suggesting that the protective potential of Kangen-karyu extract against metabolic syndrome would be attributed to the regulation of COX-2, NF-kappa B, and bcl-2 signalling pathways. This study indicated that Kangen-karyu extract significantly improved high-fructose-induced metabolic syndrome such as hyperglycaemia, hyperlipidaemia, and hypertension through the reductions of TG and cholesterol contents with the regulation of hepatic SREBP-1 protein and the NF-kappa B signalling pathway.

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