• 2018-07
  • 2018-10
  • 2018-11
  • Lai et al investigated the inhibitory effects of xanthigen f


    Lai et al. [52] investigated the inhibitory effects of xanthigen, fucoxanthin, and punicic MLN9708 (70% in pomegranate seed oil) on the differentiation of 3T3-L1 preadipocytes. Xanthigen potently and dose-dependently suppressed accumulation of lipid droplets in adipocytes compared to its individual components, fucoxanthin and pomegranate seed oil. Xanthigen down-regulated the protein levels of key adipogenesis transcription factors and up-regulated various enzymes signaling in differentiated 3T3-L1 adipocytes. These findings indicate that xanthigen suppresses adipocyte differentiation and lipid accumulation through multiple mechanisms and may have therapeutical benefits in obesity [52]. Administration of alginic acids from the brown macroalgae Sargassum wightii was shown to prevent the inflammatory cell infiltration in arthritic rats by reducing the expression of C-reactive protein kinase and the corresponding increase in enzymes linked to inflammation (e.g. cyclooxygenase, lipooxygenase and myeloperoxidase) [53]. This mechanism could be useful in the treatment of obesity which appears to be associated with chronic low-grade inflammation [54]. In order to investigate a beneficial role of fucoidan, extracted from the sporophyll of U. pinnatifida, in adipogenesis by inhibiting inflammatory-related cytokines, Kim and Lee [55] assessed the obesity-specific therapeutic action of fucoidan adipocytes. The authors found that mRNA gene expression of key adipogenic markers (adipocyte protein 2, etc.) was down-regulated by fucoidan, and the expression of inflammation-related genes in adipocytes during adipogenesis was reduced. In addition, fucoidan also decreased the accumulation of lipids and reactive oxygen species in adipocytes. These findings show that fucoidan suppresses adipogenesis by inhibiting major markers and inflammation-related cytokines in adipocytes, suggesting that fucoidan may have anti-obesity effects [55]. In a study by Park et al. [56], the inhibitory effect of fucoidan on the lipid accumulation in differentiated adipocytes was examined. Fucoidan showed high lipid inhibition activity at 200μg/mL concentration. Lipolytic activity in adipocytes is highly dependent on hormone sensitive lipase, which is one of the most important targets of lipolytic regulation. Fucoidan increased hormone-sensitive lipase expression indicating stimulation of lipolysis [56]. These findings suggest that fucoidan reduces lipid accumulation by stimulating lipolysis and may be useful in the management of obesity. Kim et al. [57] investigated the antiobesity effects of fucoidan in an animal model of diet-induced obesity. Mice were fed a standard diet or high-fat diet for five weeks. The animals were then divided into four groups, i.e. a standard diet group, a high-fat diet group, and two high-fat diet groups containing 1% or 2% fucoidan. The fucoidan supplementation group showed a decrease in body-weight gain, food efficiency ratio and relative liver and epididymal fat mass compared with the high-fat diet group. The mice supplemented with fucoidan showed reduced plasma levels of triglyceride, total cholesterol and low-density lipoprotein levels. In addition, fucoidan affected the down-regulation expression patterns of epididymal adipose tissue genes [57]. These results suggest that fucoidan may inhibit adipogenesis and have a role in the control or prevention of obesity. Stearoyl-coenzyme A desaturase-1 is a rate-limiting enzyme which catalyzes the biosynthesis of monounsaturated fatty acids from saturated fatty acids. The down-regulation of stearoyl-coenzyme A desaturase-1 has been implicated in the prevention of obesity and also in the improvement of insulin and leptin sensitivity. Beppu et al. [58] investigated the effect of the marine caretenoid, fucoxanthin, on hepatic stearoyl-coenzyme A desaturase-1 in obese mouse models of hyperleptinemia KK-A(y) and leptin-deficiency ob/ob. In KK-A(y) mice, a two-week diet containing 0.2% fucoxanthin for 2 weeks significantly suppressed stearoyl-coenzyme A desaturase-1 mRNA and protein expression in the liver. The fatty acid composition of liver lipids was also affected, i.e. the ratio of oleic acid to stearic acid was reduced. Furthermore, serum leptin levels were significantly decreased in hyperleptinemia KK-A(y) mice after 2 weeks of fucoxanthin administration. The suppressive effects of fucoxanthin on hepatic stearoyl-coenzyme A desaturase-1 and body weight gain were not observed in ob/ob mice [58]. These findings indicate that fucoxanthin down-regulates the expression of stearoyl-coenzyme A desaturase-1 and changes the fatty acid composition of the liver via regulation of leptin signaling in hyperleptinemia KK-A(y) mice but not in leptin-deficient ob/ob mice. Since a large proportion of obesity in humans is characterized by leptin resistance and not leptin deficiency, fucoxanthin may be useful in the therapy of obese individuals by maintaining adequate homeostatic mechanisms [58].