Abstract
Fucoxanthin (Fx) is a marine carotenoid found in edible brown seaweeds. We previously reported that dietary Fx metabolite into fucoxanthinol (FxOH), attenuates the weight gain of white adipose tissue of diabetic/obese KK-Ay mice. In this study, to evaluate anti-diabetic effects of Fx, we investigated improving the effect of insulin resistance on the diabetic model of KK-Ay mice. Furthermore, preventing the effect of FxOH on low-grade chronic inflammation related to oxidative stress was evaluated on 3T3-L1 adipocyte cells and a RAW264.7 macrophage cell co-culture system. A diet containing 0.1% Fx was fed to diabetic model KK-Ay mice for three weeks, then glucose tolerance was observed. Fx diet significantly improved glucose tolerance compared with the control diet group. In in vitro studies, FxOH showed suppressed tumor necrosis factor-α (TNF-α), and monocyte chemotactic protein-1 (MCP-1) mRNA expression and protein levels in a co-culture of adipocyte and macrophage cells. These findings suggest that Fx ameliorates glucose tolerance in the diabetic model mice. Furthermore, FxOH, a metabolite of Fx, suppresses low-grade chronic inflammation in adipocyte cells.
Highlights
IntroductionObesity is regarded as a major risk factor for type-2 diabetes, hypertension, and dyslipidemia [1]
Obesity is regarded as a major risk factor for type-2 diabetes, hypertension, and dyslipidemia [1].The cluster is called metabolic syndrome, of which the incidence is a worldwide problem [2].Obesity is characterized by low-grade chronic inflammation; it is the mechanism responsible for insulin resistance caused by obesity [3].Adipocytokines, such as tumor necrosis factor-α (TNF-α) and monocyte chemotactic protein-1 (MCP-1), are biologically-active mediators secreted from adipocytes cells
Brown adipose tissue (BAT) weight was increased in the Fx 0.1% group compared with the control group, not significantly
Summary
Obesity is regarded as a major risk factor for type-2 diabetes, hypertension, and dyslipidemia [1]. Obesity is characterized by low-grade chronic inflammation; it is the mechanism responsible for insulin resistance caused by obesity [3] Adipocytokines, such as TNF-α and MCP-1, are biologically-active mediators secreted from adipocytes cells. They are related to the development of insulin resistance and are associated with low-grade inflammation throughout the body [4,5]. The metabolites accumulate in the internal organs, such as liver and adipose tissue [24] It is, important to ascertain whether Fx metabolites, FxOH, act directly on WAT composed of adipocytes and/or macrophages. Preventing the effects of low-grade chronic inflammation of dietary Fx is important, rather than suppressing the accumulation of WAT. To assess whether FxOH can inhibit low-grade chronic inflammation in an adipocyte inflammation model efficiently, or not, a co-culture of adipocytes and macrophages system was used for experimentation
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