Home >> Redox Report, Volume 7, Number 5

Astaxanthin protects β-cells against glucose toxicity in diabetic db/db mice

Authors: Uchiyama, Kazuhiko1; Naito, Yuji1; Hasegawa, Goji1; Nakamura, Naoto1; Takahashi, Jiro2; Yoshikawa, Toshikazu1

Source: Redox Report, Volume 7, Number 5, October 2002 , pp. 290-293(4)

Publisher: Maney Publishing

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Abstract:

Oxidative stress induced by hyperglycemia possibly causes the dysfunction of pancreatic β-cells and various forms of tissue damage in patients with diabetes mellitus. Astaxanthin, a carotenoid of marine microalgae, is reported as a strong anti-oxidant inhibiting lipid peroxidation and scavenging reactive oxygen species. The aim of the present study was to examine whether astaxanthin can elicit beneficial effects on the progressive destruction of pancreatic β-cells in db/db mice - a well-known obese model of type 2 diabetes. We used diabetic C57BL/KsJ-db/db mice and db/m for the control. Astaxanthin treatment was started at 6 weeks of age and its effects were evaluated at 10, 14, and 18 weeks of age by non-fasting blood glucose levels, intraperitoneal glucose tolerance test including insulin secretion, and β-cell histology. The non-fasting blood glucose level in db/db mice was significantly higher than that of db/m mice, and the higher level of blood glucose in db/db mice was significantly decreased after treatment with astaxanthin. The ability of islet cells to secrete insulin, as determined by the intraperitoneal glucose tolerance test, was preserved in the astaxanthin-treated group. Histology of the pancreas revealed no significant differences in the β-cell mass between astaxanthin-treated and -untreated db/db mice. In conclusion, these results indicate that astaxanthin can exert beneficial effects in diabetes, with preservation of β-cell function. This finding suggests that anti-oxidants may be potentially useful for reducing glucose toxicity.

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Document Type: Regular Paper

DOI: http://dx.doi.org/10.1179/135100002125000811

Affiliations: 1: First Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan 2: Fuji Chemical Industry Co. Ltd, Toyama, Japan

Publication date: 2002-10-01

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