fucoxanthin has been researched along with Weight-Gain* in 7 studies
1 review(s) available for fucoxanthin and Weight-Gain
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Fucoxanthin and lipid metabolism: A minireview.
Accumulating data suggest that food supplementation with seaweeds which traditionally are an important part of food culture in South-East Asian countries might lead to essential health benefits. In this short review, we summarize findings from experimental studies on the effects of fucoxanthin (a carotenoid derived from brown seaweeds) on lipid metabolism, adiposity, and related conditions and discuss the possible underlying mechanisms.. Supplementation of fucoxanthin or its derivatives consistently attenuated body and visceral fat weight gain, lipid accumulation in the liver, decreases insulin resistance, and improves the plasma lipid profile in rodents fed a high-fat diet. It should however be noted that in diabetic/obese KK-Ay mice with genetically compromised insulin signaling, fucoxanthin might increase the plasma levels of cholesterol and low-density lipoproteins. The anti-obesity effects of fucoxanthin are apparently mediated by the hormones leptin and adiponectin through their common target AMK-activated protein kinase, resulting in downregulation of lipogenic enzymes and upregulation of lipolytic enzymes. Fucoxanthin also suppresses adipocyte differentiation and induces the expression of uncoupling proteins in visceral adipose tissue.. The results of experimental studies suggest that consumption of fucoxanthin and its derivatives as nutritional supplements is a promising option for prevention and treatment of obesity and a wide variety of related pathologies, including metabolic syndrome, type 2 diabetes, and heart disease. Yet, clinical trials are warranted to assess a therapeutic value of fucoxanthin. Topics: Adipocytes; Adiponectin; Animals; Anti-Obesity Agents; Cell Differentiation; Diet, High-Fat; Humans; Ion Channels; Leptin; Lipid Metabolism; Lipids; Lipogenesis; Lipolysis; Liver; Mice; Mitochondrial Proteins; Rats; Uncoupling Protein 1; Weight Gain; Xanthophylls | 2015 |
6 other study(ies) available for fucoxanthin and Weight-Gain
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Fucoxanthinol, Metabolite of Fucoxanthin, Improves Obesity-Induced Inflammation in Adipocyte Cells.
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. Topics: 3T3-L1 Cells; Adipocytes; Adipose Tissue, White; Animals; beta Carotene; Blood Glucose; Cell Line; Chemokine CCL2; Diabetes Mellitus, Experimental; Diet; Disease Models, Animal; Inflammation; Insulin Resistance; Macrophages; Mice; Obesity; RNA, Messenger; Tumor Necrosis Factor-alpha; Weight Gain; Xanthophylls | 2015 |
Down-regulation of hepatic stearoyl-CoA desaturase-1 expression by fucoxanthin via leptin signaling in diabetic/obese KK-A(y) mice.
Stearoyl-coenzyme A desaturase-1 (SCD1) is a rate-limiting enzyme that catalyzes the biosynthesis of monounsaturated fatty acids from saturated fatty acids. Recently, SCD1 down-regulation has been implicated in the prevention of obesity, and the improvement of insulin and leptin sensitivity. In this study, we examined the effect of fucoxanthin, a marine carotenoid, on hepatic SCD1 in obese mouse models of hyperleptinemia KK-A(y) and leptin-deficiency ob/ob. In KK-A(y) mice, providing a diet containing 0.2 % fucoxanthin for 2 weeks markedly suppressed SCD1 mRNA and protein expressions in the liver. The fatty acid composition of liver lipids was also affected by an observed decrease in the ratio of oleic acid to stearic acid. Furthermore, serum leptin levels were significantly decreased in hyperleptinemia KK-A(y) mice after 2 weeks of fucoxanthin feeding. However, the suppressive effects of fucoxanthin on hepatic SCD1 and body weight gain were not observed in ob/ob mice. These results show that fucoxanthin down-regulates SCD1 expression and alters 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. Topics: Animals; Blood Glucose; Down-Regulation; Fatty Acids; Female; Leptin; Liver; Mice; Mice, Obese; Obesity; RNA, Messenger; Seaweed; Signal Transduction; Stearoyl-CoA Desaturase; Weight Gain; Xanthophylls | 2013 |
Fucoxanthin supplementation improves plasma and hepatic lipid metabolism and blood glucose concentration in high-fat fed C57BL/6N mice.
This study investigated the effects of fucoxanthin isolated from marine plant extracts on lipid metabolism and blood glucose concentration in high-fat diet fed C57BL/6N mice. The mice were divided into high-fat control (HFC; 20% fat, w/w), low-fucoxanthin (low-Fxn; HFC+0.05% Fxn, w/w) and high-fucoxanthin (high-Fxn; HFC+0.2% Fxn, w/w) groups. Fxn supplementation significantly lowered the concentration of plasma triglyceride with a concomitant increase of fecal lipids in comparison to the HFC group. Also, the hepatic lipid contents were significantly lowered in the Fxn supplemented groups which seemed to be due to the reduced activity of the hepatic lipogenic enzymes, glucose-6-phosphate dehydrogenase, malic enzyme, fatty acid synthase and phosphatidate phosphohydrolase and the enhanced activity of beta-oxidation. Plasma high-density lipoprotein cholesterol concentrations and its percentage were markedly elevated by Fxn supplementation. Activities of two key cholesterol regulating enzymes: 3-hydroxy-3-methylglutaryl coenzyme A reductase and acyl coenzyme A: cholesterol acyltransferase, were significantly suppressed by Fxn regardless of the dosage. Relative mRNA expressions of acyl-coA oxidase 1, palmitoyl (ACOX1) and peroxisome proliferators activated receptor alpha (PPARalpha) and gamma (PPARgamma) were significantly altered by Fxn supplementation in the liver. Fxn also lowered blood glucose and HbA(1c) levels along with plasma resistin and insulin concentrations. These results suggest that Fxn supplementation plays a beneficial role in not only regulating the plasma and hepatic lipids metabolism but also for blood glucose-lowering action in high-fat fed mice. Topics: Animals; Blood Glucose; Dietary Fats; Dietary Supplements; Eating; Glucagon; Hemoglobin A; Insulin; Lipid Metabolism; Liver; Male; Mice; Mice, Inbred C57BL; Obesity; Phaeophyceae; Plant Extracts; RNA, Messenger; Weight Gain; Xanthophylls | 2010 |
Fucoxanthin-rich seaweed extract suppresses body weight gain and improves lipid metabolism in high-fat-fed C57BL/6J mice.
An ethanol extract of fucoxanthin-rich seaweed was examined for its effectiveness as a nutraceutical for body fat-lowering agent and for an antiobese effect based on mode of actions in C57BL/6J mice. Animals were randomized to receive a semi-purified high-fat diet (20% dietary fat, 10% corn oil and 10% lard) supplemented with 0.2% conjugated linoleic acid (CLA) as the positive control, 1.43% or 5.72% fucoxanthin-rich seaweed ethanol extract (Fx-SEE), equivalent to 0.05% or 0.2% dietary fucoxanthin for six weeks. Results showed that supplementation with both doses of Fx-SEE significantly reduced body and abdominal white adipose tissue (WAT) weights, plasma and hepatic triglyceride (TG), and/or cholesterol concentrations compared to the high-fat control group. Activities of adipocytic fatty acid (FA) synthesis, hepatic FA and TG synthesis, and cholesterol-regulating enzyme were also lowered by Fx-SEE supplement. Concentrations of plasma high-density lipoprotein-cholesterol, fecal TG and cholesterol, as well as FA oxidation enzyme activity and UCP1 mRNA expression in epididymal WAT were significantly higher in the Fx-SEE groups than in the high-fat control group. CLA treatment reduced the body weight gain and plasma TG concentration. Overall, these results indicate that Fx-SEE affects the plasma and hepatic lipid profile, fecal lipids and body fat mass, and alters hepatic cholesterol metabolism, FA synthesis and lipid absorption. Topics: Animals; Anti-Obesity Agents; Body Weight; Cholesterol; Dietary Fats; Dietary Supplements; Lipid Metabolism; Lipids; Male; Mice; Mice, Inbred C57BL; Obesity; Plant Extracts; Seaweed; Weight Gain; Xanthophylls | 2010 |
Anti-obese property of fucoxanthin is partly mediated by altering lipid-regulating enzymes and uncoupling proteins of visceral adipose tissue in mice.
This study investigated the anti-obesity effects of fucoxanthin in diet-induced obesity mice fed a high-fat diet (20% fat, wt/wt). The mice were supplemented with two doses of fucoxanthin (0.05 and 0.2%, wt/wt) for 6 wk. Fucoxanthin significantly lowered body weight and visceral fat-pads weights compared with the control group without altering food intake. In epididymal adipose tissue of fucoxanthin-fed mice, adipocyte sizes and mRNA expression of lipogenic and fatty acid beta-oxidation enzymes were significantly altered in a dose-dependent manner. Plasma leptin level was significantly lower in the fucoxanthin groups than in the control group, while the adiponectin level was elevated. Fucoxanthin significantly down-regulated various lipogenic enzyme activities in epididymal adipose tissue with a simultaneous decrease in fatty acid beta-oxidation activity. The 0.2% fucoxanthin supplement led to increase mRNA expression of uncoupling protein-1 (UCP-1) and UCP-3 in brown adipose tissue and that of UCP-2 in the epididymal white adipose tissue. However, the 0.05% fucoxanthin only elevated UCP-1 mRNA expression in epididymal white adipose tissue. These results suggest that the anti-obesity effect of fucoxanthin could be mediated by altering lipid-regulating enzymes and UCPs in the visceral fat tissues and plasma adipokine levels. Topics: Adipokines; Adipose Tissue, Brown; Animals; Anti-Obesity Agents; Cell Size; Dietary Fats; Intra-Abdominal Fat; Ion Channels; Lipid Metabolism; Male; Mice; Mice, Inbred C57BL; Mitochondrial Proteins; Obesity; Random Allocation; Time Factors; Uncoupling Agents; Uncoupling Protein 1; Uncoupling Protein 2; Uncoupling Protein 3; Undaria; Weight Gain; Xanthophylls | 2009 |
Dietary combination of fucoxanthin and fish oil attenuates the weight gain of white adipose tissue and decreases blood glucose in obese/diabetic KK-Ay mice.
Fucoxanthin is a marine carotenoid found in edible brown seaweeds. We previously reported that dietary fucoxanthin attenuates the weight gain of white adipose tissue (WAT) of diabetic/obese KK- A(y) mice. In this study, to evaluate the antiobesity and antidiabetic effects of fucoxanthin and fish oil, we investigated the effect on the WAT weight, blood glucose, and insulin levels of KK- A(y) mice. Furthermore, the expression level of uncoupling protein 1 (UCP1) and adipokine mRNA in WAT were measured. After 4 weeks of feeding, 0.2% fucoxanthin in the diet markedly attenuated the gain of WAT weight in KK- A(y) mice with increasing UCP1 expression compared with the control mice. The WAT weight of the mice fed 0.1% fucoxanthin and 6.9% fish oil was also significantly lower than that of the mice fed fucoxanthin alone. In addition, 0.2% fucoxanthin markedly decreased the blood glucose and plasma insulin concentrations in KK- A(y) mice. The mice fed with the combination diet of 0.1% fucoxanthin and fish oil also showed improvements similar to that of 0.2% fucoxanthin. Leptin and tumor necrosis factor (TNFalpha) mRNA expression in WAT were significantly down-regulated by 0.2% fucoxanthin. These results suggest that dietary fucoxanthin decreases the blood glucose and plasma insulin concentration of KK- A(y) along with down-regulating TNFalpha mRNA. In addition, the combination of fucoxanthin and fish oil is more effective for attenuating the weight gain of WAT than feeding with fucoxanthin alone. Topics: Adipose Tissue; Animals; Blood Glucose; Diabetes Mellitus; Diet; Female; Fish Oils; Mice; Mice, Obese; Obesity; Weight Gain; Xanthophylls | 2007 |