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Fucoxanthin is a carotenoid found in brown seaweed that is being investigated for its fat burning abilities. It reduces fat mass, but has a time delay due to build up in fat tissue and does not stimulate the brain. Also appears healthy, but needs more corroborating evidence.
Our evidence-based analysis on fucoxanthin features 84 unique references to scientific papers.
Research Breakdown on Fucoxanthin
1.3Properties
1.4Biological Significance
2.5Metabolites
3.1AMPK
4.1Neuroinflammation
5.2Triglycerides
5.3Cholesterol
5.4Blood Pressure
5.5Athersclerosis
6.1Blood Glucose
6.2Diabetes
7Obesity and Fat Mass
7.1Adipokines
7.2Weight
7.4Other Mechanisms
7.5Intervention Research
7.6Inflammation
8.1Glucose Metabolism
9Skeleton and Bone Metabolism
10Interactions with Oxidation
10.1In vitro
10.2Radiation and DNA Damage
10.3Antioxidant Enzymes
11Inflammation and Immunology
11.1Macrophages
11.2T Cells
12Interactions with Organ Systems
12.1Liver
13Interactions with Cancer Metabolism
13.1Hepatoma
13.2Cervical Cancer
14.1Fatty acids
14.2Xanthigen and Punicic Acid
Fucoxanthin is a carotenoid structure that is found in seaweed and microalgae, and perhaps the second most famous sea-based carotenoid (of the 750 known carotenoids, over 250 of them are exclusively marine-sourced[1]) behind astaxanthin only. It is hypothesized to comprise up to 10% of all carotenoids in nature[2] and it has a role in gathering light for energy production via forming something known as a chlorophyll a/c-fucoxanthin complex;[3][4] it is a primary carotenoid that transfers light energy to photosynthetic machinery for energy production in plants (unlike secondary carotenoids such as β-carotene and astaxanthin which prevent excess light from being transferred).[5][6] It is a component of many dietary seaweeds and is thought to confer health promoting benefits associated with seaweed and the Japanese diet.
Fucoxanthin is a pigment (specifically, a brown pigment and a type of carotenoid) found in seaweed and microalgae that is used to fix light and aid the process of photosynthesis
Fucoxanthin can be found in the following species of seaweed and algae:
Fucus vesiculosus (Bladderwrack)[7] and other species including evanescens[8]
Myagropsis myagroides at 9.01mg/g[9]
Dictyota coriacea at 6.42mg/g[9]
Himanthalia elongata[10]
Petalonia binghamiae (Vinogradova) at 3.57+/-0.028 mg/g[11]
Undaria Pinnatifida (Wakame)[12][13]
Hijikia fusiformis (Hijiki)[13]
Turbinaria turbinate at 0.59+/-0.08mg/g[14]
Laminaria japonica (Ma-Kombu)[13]
Ecklonia cava[9]
The Sargassum family (fulvellum, coreanum, hemiphyllum, horneri, etc.)[13][9] with the species plagyophyllum having 0.71+/-0.01mg/g dry weight[14]
Sea urchin gonads at 2mcg/g,[15] also contains astaxanthin at 1mcg/g
Phaeodactylum tricornutum (Microalgae) at 15.42-16.51 mg/g[16]
Odontella aurita (Microalgae) at 6.34-20.63mg/g dry weight depending on nitrogen availability[6]
Isochrysis (species of microalgae) at 17mg/g (1.7% dry weight)[17]
Fucoxanthin is found in high levels in seaweed, although it is at even higher levels in microalgae; the level of fucoxanthin found in some particular species may be high enough to actually obtain the benefits of supplementation even when supplementing seaweed products
No fucoxanthin is found in the yolks of the eggs laid by hens fed fucoxanthin although metabolites such as fucoxanthinal are found.[18]
Fucoxanthin shares similar structural properties to the carotenoid class of nutrients like beta-carotene (the standard comparison) and more interesting derivatives like astaxanthin. However, fucoxanthin tends to be more interested in due to it's allenic bond and 5,6-monoepoxide aspects which are fairly unique.[19] It also contains a conjugated carbonyl group with anti-oxidant properties.[20]
There are some related molecules that are deemed metabolites of fucoxanthin but are not from human metabolism, but rather metabolism by the plant source of fucoxanthin (and thus they appear as co-existing nutrients), such as halocynthiaxanthin.[21]
Fucoxanthin is fat-soluble[22], thus it's absorption is enhanced in the presence of fatty acids (which has been demonstrated by mixing with medium chain triglycerides at 0.9% of the diet in rats[22]) and may be hindered in the presence of fat-blockers, although this latter part is conjecture.
Unlike beta-carotene, which can be converted into vitamin A, fucoxanthin is similar to astaxanthin in the sense that it is not a pro-vitamin and does not influence vitamin A status.[23]
Fucoxanthin is a non-vitamin carotenoid (ie. a carotenoid that does not form Vitamin A in the body) similar to astaxanthin.
Fucoxanthin has been noted to reduce the oxidative stress that is induced by a vitamin A deficiency in the rat,[24] and antioxidant enzyme activities in rats|published=2008 Dec|authors=Ravi Kumar S, Narayan B, Vallikannan B|journal=Eur J Nutr] suggesting that it may circumvent some aspects of vitamin A deficiency.
It appears fucoxanthin has a lesser bioavailability than other carotenoid-class nutrients,[25] while having a greater bioavailability in humans than it does in rats. In comparing two studies on pharmacokinetics in humans[25] and rats[26] the Tmax and AUC followed similar curves in relation to time, but the human Cmax and AUC were 33% and 46% despite being 15% the oral dose.[25]
Fucoxanthin is deacetylated in the intestines to fucoxanthinal, which is distributed through lymphatic tissue after absorption in the same manner as fat-soluble nutrients and fatty acids.[26][27][28] and no fucoxanthin nor metabolites around found in the liver prior to first pass metabolism.[28] Fucoxanthinol is the main circulating form of dietary fucoxanthin, insofar that circulating fucoxanthin cannot be determined in some studies due to complete deacetylation.[29][30]
Paradoxically, fucoxanthin is a molecule which is fat soluble and requires fatty acids in order to be absorbed yet also possesses the ability to inhibit pancreatic lipase and inhibit some degree of fat absorption.[28] The AUC of lymph absorption seems to be comparable between fucoxanthin (2mg/mL in the lumen) and without, suggesting a delayed absorption of triglycerides rather than hindering absorption. No fecal fat test was done in this study.[28] As fucoxanthin is metabolized into fucoxanthinol by a few enzymes, one of which is lipase (the others being cholesterol esterase and carboxylesterase), it is possible that this could be indirect inhibition from competitive antagonism.[29]
Fucoxanthin, via its metabolite fucoxanthinol, is readily taken up in the gut alongside fatty acids
Fucoxanthin is metabolized into predominately fucoxanthinol (deacetylation in the intestines) and Amarouciaxanthin A via the liver(with some other metabolization into Cis-Amarouciaxanthin A and two other unknown compounds)[26]. Fucoxanthinol appears to be the compounds responsible for most cardiac and hepatic implications and Amarouciaxanthin A the metabolite responsible for adipocytes (fat cells).[26] Conversion of fucoxanthin into these metabolites has been noted in liver (HepG2) cells and requires NAD(P)+ as a cofactor.[31]
Amarouciaxanthin A has been detected in rats via hepatic conversion[30] after ingestion of Fucoxanthin after 24 hours,[26] but has not been detected in humans in two studies lasting up to 24 hours.[25][32] It is not know whether or not Amarouciaxanthin A exists in humans or whether it takes longer than 24 hours to be converted.
No fucoxanthin circulates in the blood, as it all gets metabolized to fucoxanthinol; Amarouciaxanthin A has not yet been shown to exist in humans, but it is not known whether this is due to the research conducted being too short or due to inter-species differences
Levels of fucoxanthinol seem to peak in tissues 4 hours after ingestion whereas concentrations of Amarouciaxanthin A peak 24 hours after ingestion.[33] Another study looking at ingestion of 31mg fucoxathin (via Kombu extract dissolved in MCTs), it was found that increases in serum fucoxanthinol were seen until the 4 hour mark, where the next measurement at 8 hours noted a decline[25] and this Tmax was similar in rats at doses of 3.5mg/kg bodyweight.[26] In rats, a serum half-life of 0.92-1.23 days yet an adipose half-life of 2.76-4.81 days.[34]
Fucoxanthinol's serum parameters in humans after 31mg ingestion dissolved in MCTs was a Cmax of 44.2nmol/L, a Tmax of 4 hours or so, a half-life of 7 hours, and an AUC to infinity of 663.7 nmol/l/h.[25]
One other study measured the serum one week after daily ingestion of Wakame at 6.1mg fucoxanthin, and circulating levels of fucoxanthinol were found to be 0.8nmol/L.[32] This study did not actively dissolve the fucoxanthin in fatty acids, and thus this low circulating level may be due to poor absorption.
Higher circulating levels of fucoxanthinol appear to need mixture with fatty acids like Medium Chain Triglycerides (MCTs) for absorption
A study in rats noted that the metabolites of fucoxanthin, fucoxanthinol and Amarouciaxanthin A, appeared to both have affinity for adipose tissue rather than other tissues with 3.13–3.64 μmol/kg partitioned into adipose whereas 1.29–1.80 μmol/kg was recorded for kidneys and liver.[34] In rats, where Amarouciaxanthin A has been recorded, this metabolite appears to be more selective for adipose whereas fucoxanthinol is slightly more evenly distributed.[34]
Beyond the basic metabolites (fucoxanthinol and Amarouciaxanthin A), fucoxanthin can react with nitrate in a sacrifical manner (in protecting receptors from nitrosylation) to form nitrofucoxanthin,[35] which it appears may be anti-cancer in mechanisms.[35]
Additionally, a cis-isomer of fucoxanthinol may exist after ingestion of fucoxanthin.[25]
After metabolism in the liver, Amarouciaxanthin A appears to be deposited and stored for a rather long time in fat cells; this accumulation of Amarouciaxanthin A may be a reason behind it's influences on fat mass being chronic rather than acute.[28]
It has been found that bioaccumulation of fucoxanthin has not occurred in humans at a dose of 0.31mg fucoxanthin over 28 days,[25] which is the average fucoxanthin intake from food sources in Japan.
Bioaccumulation at the level of 100mg/kg bodyweight fucoxanthin in rats is associated with giving the tissue an orange tone, as fucoxanthin and their metabolites do possess pigmentation activity.[25]
A build-up effect occurs over time with sufficiently high (supplemental) dosages of oral fucoxanthin, with no significant toxicity being seen at the lower range of chronic oral intake and a non-toxic coloration of tissue at obscenely high doses
Fucoxanthin, at 1-10uM, has been shown to reduce the changes in CYP3A4 and MRP1 mRNA (-55%) (and CYP3A4 protein content) by rifampin in HepG2 cells; rifampin increases activity of these two proteins, and this attenuation of an increase may play a beneficial role in multidrug resistance associated with cancer treatment.[36] This effect appears to be mechanistically related to the CYP3A4 promoter and MRP1, as it also inhibits hCAR induction of CYP3A4 (88% attenuation) and does not influence PXR nor hCAR activity.[36]
Even without the PXR inducer, fucoxanthin was able to suppress CYP3A4 activity by 21% at 10uM in a concentration dependent manner and reduce protein content by 33% over 24 hours, by decreasing mRNA transcription rates.[36]
May reduce activity of CYP3A4, which is an enzyme that metabolizes more than 50% of pharmaceuticals in existence.[37] Would be prudent to ask a medical doctor about possible interactions.
In fat tissue of rats fed the seaweed Petalonia binghamiae (150mg/kg containing 3.57mg/g fucoxanthin) for 70 days, it appears that supplementation is associated with an increase in AMPK phosphorylation relative to high fat control.[11]
In 3T3-L1 adipocytes, 5-10μM fucoxanthin is able to increase AMPK activity secondary to increasing LKB1 phosphorylation in a concentration dependent manner (1μM not significantly active); this concentration was also sufficient to increase CPT-1a activity.[11]
Fucoxanthin appears to stimulate AMPK activity
Microglia are glial cells (support cells for neurons) that serve as a brain sensor for inflammation and possess an inflammatory response when 'activated' by cytokines[38] that, if prolonged and excessive, contributes to neurotoxicity;[39][40] supplements and drugs which suppress this inflammatory response, such as Spirulina, are thought to be neuroprotective.
5-50μM fucoxanthin in microglial cells that are treated with the Alzheimer's pigment Aβ42 appears to concentration dependently reduce the secretion of inflammatory signalling molecules (PGE2 and nitric oxide) suggesting an antiinflammatory effect.[41] This appears to be associated with an upregulation of antioxidant enzymes (SOD and glutathione) and a suppression of MAPK activation from Aβ42.[41]
The addition of 0.2% fucoxanthin to the high fat diet of rats is able to increase fecal total lipids (23.6%), fecal cholesterol (28.9%), and fecal triglycerides (135%) relative to high fat control.[42]
Appears to hinder cholesterol and triglyceride absorption, which may be a mechanism underlying both a reduction in cholesterol as well as weight loss effects
Mechanistically, the increase in liver mRNA levels of SREBP-1c, ACC, FAS, and G6PDH (all lipogenic proteins) and suppression of CPT-1 (lipolytic protein) seen with a high fat diet are normalized when the diet includes 0.2% fucoxanthin over four weeks.[42] These changes may occur in rats who are obese prior to fucoxanthin supplementation (and has been noted with 52 days supplementation of 0.083-0.167mg/kg bodyweight fucoxanthin).[43]
At least one study has noted that the suppression of SREBP-1c may be acute following the addition of 200μg/mL Petalonia binghamiae (0.36% fucoxanthin) to 3T3-LI adipocytes.[11]
A few genes and their proteins are increased in the liver in response to an obesogenic diet, and the increase seen appears to be reduced by fucoxanthin in either a rehabilitative (taken after obesity) manner or when taken alongside a high fat diet
In rats fed a high fat diet with 0.2% fucoxanthin for four weeks, there was a trend to decrease triglycerides[42] which has been noted to be statistically significant with 0.083-0.167mg/kg bodyweight fucoxanthin in obese rats (52 days of supplementation)[43] and with 70 days supplementation of Petalonia binghamiae (150mg/kg containing 3.57mg/g fucoxanthin).[11]
associated with fucoxanthin supplementation. The only human study conducted noted a decrease in triglycerides from 177mg/dl to 155mg/dl (non-fatty liver group) and 195mg/dl to 158mg/dl (fatty liver group) after 16 weeks of supplementation.[44]
Preliminary evidence suggest that fucoxanthin reduces triglycerides, reliability of this decrease not fully established
Mechanistically, the increase in HMG-CoA, CYP7A1, and ACAT (cholesterol producing proteins in the liver) seen with a high fat diet appears to be attenuated when the diet has a 0.2% fucoxanthin content.[42]
May prevent increases of cholesterol production in the liver in response to the diet
In rats fed a high fat diet with 0.2% fucoxanthin for four weeks, there is a significant increase in HDL-C relative to high fat control (58%) which was comparable to normal diets.[42]
Possibly due to HDL-C, total plasma cholesterol nonsignificantly increased.[42]
One animal study noted higher total cholesterol levels after consumption of Wakame (168+/-5mg/dl in obese control, 185+/-7 and 192+/-10 in wakame fed groups with no dose-dependence) yet lower LDL levels (9 and 7mg/dl relative to 13 in control) and non-significantly higher HDL levels (66 and 71, relative to 65mg/dl).[45]
When administered to humans at varying dosages, fucoxanthin was able to reduce blood pressure from 138/91mmHG (systolic/diastolic) to 119/79mmHG in persons with fatty liver.[44] In persons without fatty liver, blood pressure dropped from 128/93mmHG to 112/77mmHG.
The diet-induced increase of MCP-1 (a atherogenic cytokine) appears to be prevented with daily ingestion of a wakame supplement containing fucoxanthin in rats.[45]
Mechanistically, in obese rats given a wakame lipid extract containing fucoxanthin was associated with an increase in GLUT4 mRNA concentration in skeletal muscle.[45]
In obese rats given 0.167mg/kg fucoxanthin in the diet for 52 days, a significant decrease in circulating blood glucose is seen relative to obese control.[43] This has also been noted with obese rats given a wakame lipid extract.[45]
Fucoxanthin, at 0.02% of the diet in rats, can significantly reduce blood glucose levels from 389.2+/-23.3mg/dl in diet-induced obese mice to 176.4+/-15.8mg/dl after 2 weeks of supplementation; via increasing GLUT4 translocation and skeletal muscle uptake of glucose.[46] This reduction of blood sugar is unique to diabetic mice, as it does not affect control mice with impaired glucose metabolism.[47]
Interestingly, fucoxanthin can increase the levels of DHA (a component of fish oil) in the liver tissue independent of fish oil supplementation; some anti-diabetic effects of fish oil pertaining to the liver (such as reduction of fatty liver build-up secondary to PPARs) may apply to fucoxanthin.[48] The combination of both these nutraceuticals has been shown to reduce the weight gain and blood glucose associated with diabetic mice as well.[49]
Fucoxanthin appears to have anti-diabetic effects by normalizing the function of skeletal muscle in diabetes; this effect of normalization does not affect non-diabetic animals
In obese rats (from a high fat diet) supplemented with fucoxanthin at 0.083-0.167mg/kg for 52 days, an increase in circulating adiponectin is seen alongside a decrease in leptin[43] and hyperleptinemia has been noted to be suppressed elsewhere.[45]
May increase adiponectin in obese rats
When 0.2% fucoxanthin is added to the rat diet over the course of 4 weeks, the weight gain seen is nonsignificantly attenuated.[42]
An increase in β3-adrenergic receptor content has been noted in white adipose tissue of rats fed fucoxanthin.[45]
Fucoxanthin primarily works via inducing (increasing) activity of Uncoupling Protein 1 (UCP1) in white adipose tissue[50] which uncouples a step in mitochondrial respiration and indirectly increases metabolic rate. Interestingly, higher rates of uncoupling are one of the bioenergetic reasons as to why 'brown' fat is different than white fat.[51] The induction of white adipose UCP1 is important due to low levels of brown adipose in adult humans.[52][53]
This mechanism is the main one attributed to increase metabolic rate and decrease body fat over time.[52][44]
Beta-oxidation is also increased with fucoxanthin, but the dose-dependent relationship is reliable only in epididymal tissue with less reliability in adipose.[54][55]
Fucoxanthin has been noted (in rats) to alter various lipid regulating enzymes. It decreases gene expression of the fat-regulating enzymes Malic Enzyme (ME), Glucose-6-Phosphate Dehydrogenase (G6PD), and Fatty acid Synthetase (FAS) in a relatively dose-dependent manner, although the rate of these enzymes is affected less significantly than the genetic signalling.[54] Glycerol-3-phosphate dehydrogenase, an enzyme associated with turing glycerol into triglycerides for storage, has also been shown to be decreased with fucoxanthin metabolites at 10uM.[56]
Increased expression of phosphorylated AMPK and phosphorylated forms of ACC have also been noted to be higher in fucoxanthin-treated animals on a high-fat diet relative to animals without fucoxanthin.[11] When incubated with adult adipocytes at 10uM, fucoxanthin activates AMPK in a dose dependent manner and can increase downstream transcription of CPT-1a, the rate limiting enzyme in fatty acid beta-oxidation.[11] Increasing activity of AMPK/ACC has been found by other researchers, and is more potent with punicic acid alongside the fucoxanthin.[57]
Fucoxanthin and its metabolites also decrease adipocyte differentiation via downregulation of PPAR-y, a protein that encourages adipocyte differentiation.[56][58] This has also been noted with Xanthigen, a blend of punicic acid (from pomegranate) and fucoxanthin.[57] These in vitro effects are also mirrored by the metabolite Amarouciaxanthin A, which is the one most prominent in adipose tissue after ingestion,[59] as well as the circulating metabolite, fucoxanthinol.[58] Amarouciaxanthin A, the metabolite most prominent in fat cells, appears to be the most potent metabolite in suppressing adipocyte differentiation.[56]
Protein content and mRNA levels of beta(3)adrenergic receptors in white adipose tissue have also been shown to be increased after fucoxanthin supplementation for 15 weeks in rats.[45]
One study done on 151 non-diabetic obese females found that Fucoxanthin (both via a blend called 'Xanthigen' with Pomegranate seed oil, as well as by itself) was able to induce fat loss and increase metabolic rate, although due to this being an exploratory study REE was only measured in 41 participants.[44] Metabolic rate was increased by up to 1915+/-246 kJ/day in the group given 8mg fucoxanthin daily (n=4), but interestingly this increase in metabolic rate only appeared after 16 weeks of supplementation with no acute effects on metabolic rate whatsoever when measured at 2 weeks.[44] The higher doses of fucoxanthin were able to be statistically different from placebo at 5 weeks, with lower doses requiring more time to exert significance.
Overall, weight loss over 16 weeks was 5.5+/-1.4kg in the group with more than 11% fat content in the liver, and 4.9+/-1.2kg in the group with less (11% being the border defining 'Non-Alcoholic Fatty Liver Disease').[44]
In rats, fucoxanthin has been shown to reduce fat mass over 70 days (150mg/kg seaweed at around 0.5mg/kg bodyweight fucoxanthin[11]) 52 days at merely 0.083mg/kg daily[43]
Animal studies suggest that fucoxanthin increases fat loss reliably and at very low doses, easily attainable from daily consumption of brown seaweed. The lone human study appears to reflect results in animal research, and fucoxanthin appears to have a moderately potent but highly delayed effect on inducing fat loss; preliminary research, however
Fucoxanthin has been shown to reduce the release if inflammatory cytokines such as IL-6, MCP-1 and TNF-a from adipose tissue of diabetic rats with apparently no effect on non-diabetic rats; suggesting a conditional anti-inflammatory effect[47] which may precede its anti-diabetic effects as MCP-1 and TNF-a are known to be pro-diabetic.[60][61]
Fuxocanthin, at an oral intake of 0.02% of the diet in rats, has been demonstrated to increase GLUT4 translocation[45] and protein content of the insulin receptor in rat skeletal muscle, and increased Akt phosphorylation in diabetic rats by 1.7-1.8 fold.[46] Skeletal muscle mass appears to mediate many of fucoxanthin's anti-diabetic effects via taking up glucose.[46]
GLUT4 mRNA content in obesity-induced mice with fucoxanthin appears to reach the levels of non-obese controls[45] while blood glucose and insulin trend towards normal.[45]
Glucose uptake of skeletal muscle appears to be enhanced when diabetic mice are given fucoxanthin, but the biomarker of this (decreased blood glucose) has been shown to not occur in normal mice. It is possible that fucoxanthin alleviates abnormalities in skeletal muscle function associated with diabetes, but does not indiscriminately enhance glucose uptake (and thus limited usage in healthy individuals for glucose control). More studies would be needed to confirm
A fucoxanthin containing seaweed, Sargassum fusiforme, has been implicated in increasing osteoblast formation while decreasing osteoclast differentiation and theoretically exerting anti-osteoporotic effects.[62]
Fucoxanthin, via inhibiting NF-kB transactivation, has also been implicated in preventing conversion of macrophages to osteoclast-like cells, and also induced apoptosis of these cells.[63] At 2.5uM-5uM, fucoxanthin both reduced conversion to osteoclast-like cells and induced apoptosis in these cells while 10uM reduced cell viability or macrophages.[63]
In DPPH assays, fucoxanthin has been shown to be active with an EC50 value of 0.14mg/mL[6] and elsewhere 12.5-14.8µg/mL,[10] 164.60µM,[64] which are less than the reference of Vitamin C.[6] Many carotenoids do not show direct free radical scavenging properties in DPPH assay (β-carotene, β-cryptoxanthin, zeaxanthin, and lutein)[65][64] making fucoxanthin somewhat unique in this regard, and the metabolite known as fucoxanthinol appears to be more potent with an EC50 of 153.78µM.[64] Similar trends are seen in an ABTS assay where fucoxanthin appears to scavenge free radicals with an EC50 value of 30µg/mL[6] or 8.94µM;[64] a potency again less than Vitamin C.[6]
Against hydroxyl radicals, fucoxanthin appears to be 7.9-fold less potent than its metabolite fucoxanthinol and 13.5-fold less potent than the reference compound Vitamin E (assessed via chemiluminescence and ESR).[64] That being said, fucoxanthin is still capable of protecting cells from H2O2 induced cytotoxicity to a degree[66] and elsewhere it has been noted to have a potency slightly higher than Trolox yet still less than both astaxanthin, Vitamin E, and quercetin as reference compounds.[67] Fucoxanthin appears to also protect against lipid peroxidation via scavenging peroxyl radicals and can act as a chain breaking antioxidant similar to Vitamin E.[68]
Against singlet oxygen (of which carotenoids are known to sequester[69]) and reactive nitrogen species (ONOO-), fucoxanthin appears to be less antioxidative than β-carotene.[64][67] It has shown significantly protective properties against hypochlorous acid in vitro exceeding that of cysteine and other carotenoids (lutein and zeaxanthin), but still to a lesser degree than astaxanthin.[67]
Fucoxanthin appears to have direct antioxidative properties, and these antioxidative properties seem to be more general than other carotenoids. That being said, they are not overly potent and have failed to outperform the reference compounds (Vitamin C, Vitamin E, β-carotene) and astaxanthin is another carotenoid compound that seems to generally outperform fucoxanthin
In cells exposed to UV-B irradiation fucoxanthin is able to cause concentration dependent cytoprotection secondary to sequestering reactive oxygen species (ROS), with the increase in ROS seen in cells from radiation (169.31% of baseline) being reduced progressively to 138.65% (5μM), 101.36% (50μM), 85.43% (100μM), and 71.08% (250μM) with 5μM (a somewhat physiologically relevant concentration) sequestering 18.11% of ROS and increasing cell survival from 43.48 to 59.73%.[70]
Appears to be somewhat protective against UV(B) radiation damage secondary to the direct antioxidative properties
In mouse liver cells (BNL CL.2 cell line), fucoxanthin at 5μM appears to activate a gene known as Nrf2 secondary to causing pro-oxidative effects within a cell;[71] a process known as hormesis.[72] Activation of Nrf2 results in activation of the genome's antioxidant response element (ARE) and creation of two antioxidant enzymes known as Heme-oxygenase 1 (HO-1) and NQO1.[71]
In liver cells, fucoxanthin may be able to hormetically induce an antioxidant response from the genome (ARE activation secondary to activatin Nrf2, resulting in HO-1 induction)
Antiinflammatory properties of seaweeds against LPS appears to correlate highly with the fucoxanthin content[9] and be the main contributor of said antiinflammatory effects;[73] accordingly, in LPS-stimulated macrophages fucoxanthin (15-60uM) is able to suppress the inflammatory response as assessed by iNOS and COX-2 induction as well as cytokine and nitric oxide secretion.[9] While fucoxanthin require a high dose to be active, injections of fucoxanthin appear to be as potent as prednisone against LPS-induced inflammation when assessed by a gram per gram basis in rats.[74]
The above antiinflammatory mechanisms are hypothesized to occur secondary to inhibiting translocation of NF-kB[75] since elsewhere fucoxanthin has been noted to inhibit degradation of IκBα, a mechanism that ultimately prevents NF-kB translocation.[73][75]
These properties are likely to apply to fucoxanthinol[76] and other structurally similar metabolites found in seaweeds.[77]
Fucoxanthin is able to suppress macrophage activation from LPS, which is a standard antiinflammatory response. While it appears to be quite potent at maximal efficacy (similar to prednisone), maximal efficacy may require an impractically high concentration of fucoxanthin to reach the immune cells and thus not be relevant to oral supplementation
Fucoxanthin and fucoxanthinol have been shown to inhibit proliferation of CD4(+) T-cells in response of IL-17 stimulation,[78] which shows promise in treating disease states associated with TGF(b) and IF-17 related inflammation.[78] This effect on T-cells was not seen with related compounds lutein, lycopene, nor astaxanthin and was not as effective as the research standard of all-trans retinoic acid (ATRA) and these effects were hypothesized to be secondary to Treg cell development via the retinoic acid receptor.[78]
In the intervention on humans, it was found that Xanthigen-600 (contributing 2.4mg fucoxanthin daily) reduced ALT from 48+/-7 to 26+/-7 U/l, AST from 51+/-5 to 29+/-6 U/l, and GGT levels from 47+/-7 to 31+/-5 U/l. 2 weeks after the trial ended, these changes were maintained.[44]
Non-alcoholic Fatty Liver Disease, or NAFLD, is increased deposition of triglycerides and fatty acids in the liver which adversely influences a variety of health parameters. In the intervention on humans, it was found that Xanthigen-600 (contributing 2.4mg fucoxanthin daily) had no effect on liver fat for 8 weeks of supplementation, but then by week 16 reduced liver fat by 15.3+/-4.1% in the group with baseline liver fat over 11% (the study's definition of NAFLD), and by 9.4+/-3.1% in the group with less than 11% baseline liver fat.[44] These effects correlate well with fucoxanthin's effects on adipose tissue, and may be secondary to general fat burning.
Fucoxanthin appears to augment cisplatin induced cytotoxicity in liver cancer cells by inhibiting NF-kB and restoring IκB-α phosphorylation,[79] a synergism that is common to all NF-kB inhibitors[80] since cisplatin can itself promote NF-kB translocation (activation)[81][82] which prevents apoptosis.
In isolated HeLa cells, 10-80μM fucoxanthin appears to cause concentration-dependent cytotoxicity over 48 hours of incubation with an IC50 of 55.1+/-7.6μM associated with G0/G1 arrest and autophagy; it was said to be secondary to inhibition of mTOR/Akt signalling.[83]
Fucoxanthin shows synergism with Fish Oil, in which 6.9% of fish oil with 0.1% fucoxanthin in the diet is as potent as 0.2% fucoxanthin.[49] This may be due to increased bioavailability, as the inclusion of Medium Chain Triglycerides (MCTs) has also been shown to increase the efficacy of fucoxanthin via increased absorption.[22] Conjugated Linoleic Acid has also been shown to aid fucoxanthin's anti-obesity effects in rats.[43]
Fucoxanthin can also increase hepatic stores of docosahexaenoic acid (DHA) in the liver independent of fish oil supplementation.[48]
Coingestion of fucoxanthin with fatty acids, via increasing intestinal absorption of fucoxanthin and fucoxanthinol (a metabolite) increases the effects of fucoxanthin in the body since more gets into your body
Punicic Acid is a conjugated linoleic acid (structurally different from the standard Conjugated Linoleic Acid known as CLA) derived from Pomegranate. The two molecules have been shown to be synergistic in regards to suppressing adipocyte differentiation and related biomarkers such as: PPARy and C/EBPs, FOXO1 and FOXO3a, SIRT1, Fatty Acid Synthase, and AMPK/ACC phosphorylation.[57] All effects seen were conducive to either suppressing differentation or otherwise preventing lipid accumulation in adipocytes and the synergism was towards anti-obesity.[57] These results were seen in vitro, and are unrelated to increased bioavailability of fucoxanthin.
As assessed by the lone human study on the matter, there is benefit to combining Pomegranate Seed Oil and Fucoxanthin as this study used Xanthigen.[44] Fucoxanthin at 2.4mg raised metabolic rate by 6.39+/-0.17kJ/min at the end of the study while the same dose with Pomegranate extract (300mg) increased it by 7.03+/-0.33kJ/min (a 10% increase) while Pomegranate even at 1500mg had no effect on metabolic rate.[44]
Neither study disclosed interaction with companies invested in Xanthigen.
A relatively weak synergism, but a synergism none-the-less. Pomegranate Seed Oil and possibly Punicic Acid appear to increase the fat loss effects of Fucoxanthin
Despite being stored in the body for long periods (which may lead to overload symptoms in some molecules), toxicity has not been noted in mouse models.[19] When tested for its mutagenicity (ability to produce mutations in DNA), fucoxanthinol (the circulating metabolite of fucoxanthin) came back negative in all in vitro tests and oral dosages of 2,000mg/kg bodyweight were unable to cause short-term adverse effects.[84][19]
^ Maoka T. Carotenoids in marine animals. Mar Drugs. (2011)
^ Dembitsky VM, Maoka T. Allenic and cumulenic lipids. Prog Lipid Res. (2007)
^ Owens TG, Wold ER. Light-Harvesting Function in the Diatom Phaeodactylum tricornutum: I. Isolation and Characterization of Pigment-Protein Complexes. Plant Physiol. (1986)
^ Nagao R, et al. Comparison of oligomeric states and polypeptide compositions of fucoxanthin chlorophyll a/c-binding protein complexes among various diatom species. Photosynth Res. (2013)
^ Environmental Effects on Cell Composition.
^ a b c d e f Xia S, et al. Production, characterization, and antioxidant activity of fucoxanthin from the marine diatom Odontella aurita. Mar Drugs. (2013)
^ Lachnit T, et al. Compounds associated with algal surfaces mediate epiphytic colonization of the marine macroalga Fucus vesiculosus. FEMS Microbiol Ecol. (2013)
^ Imbs TI, et al. Isolation of Fucoxanthin and Highly Unsaturated Monogalactosyldiacylglycerol from Brown Alga Fucus evanescens C Agardh and In Vitro Investigation of Their Antitumor Activity. Mar Biotechnol (NY). (2013)
^ a b c d e f Heo SJ, et al. Evaluation of anti-inflammatory effect of fucoxanthin isolated from brown algae in lipopolysaccharide-stimulated RAW 264.7 macrophages. Food Chem Toxicol. (2010)
^ a b Rajauria G, Abu-Ghannam N. Isolation and Partial Characterization of Bioactive Fucoxanthin from Himanthalia elongata Brown Seaweed: A TLC-Based Approach. Int J Anal Chem. (2013)
^ a b c d e f g h Kang SI, et al. Petalonia binghamiae extract and its constituent fucoxanthin ameliorate high-fat diet-induced obesity by activating AMP-activated protein kinase. J Agric Food Chem. (2012)
^ Quitain AT, et al. Supercritical Carbon Dioxide Extraction of Fucoxanthin from Undaria pinnatifida. J Agric Food Chem. (2013)
^ a b c d D'Orazio N, et al. Fucoxantin: a treasure from the sea. Mar Drugs. (2012)
^ a b ANALYSIS OF FUCOXANTHIN CONTENT AND PURIFICATION OF ALL-TRANS-FUCOXANTHIN FROM Turbinaria turbinata AND Sargassum plagyophyllum BY SiO2 OPEN COLUMN CHROMATOGRAPHY AND REVERSED PHASE-HPLC.
^ Garama D, Bremer P, Carne A. Extraction and analysis of carotenoids from the New Zealand sea urchin Evechinus chloroticus gonads. Acta Biochim Pol. (2012)
^ Kim SM, et al. A potential commercial source of fucoxanthin extracted from the microalga Phaeodactylum tricornutum. Appl Biochem Biotechnol. (2012)
^ Crupi P, et al. Determination of fucoxanthin isomers in microalgae (Isochrysis sp.) by high-performance liquid chromatography coupled with diode-array detector multistage mass spectrometry coupled with positive electrospray ionization. Rapid Commun Mass Spectrom. (2013)
^ Strand A, Herstad O, Liaaen-Jensen S. Fucoxanthin metabolites in egg yolks of laying hens. Comp Biochem Physiol A Mol Integr Physiol. (1998)
^ a b c Beppu F, et al. Single and repeated oral dose toxicity study of fucoxanthin (FX), a marine carotenoid, in mice. J Toxicol Sci. (2009)
^ Hu T, et al. Antioxidant activity of sulfated polysaccharide fractions extracted from Undaria pinnitafida in vitro. Int J Biol Macromol. (2010)
^ Nishino H, et al. Anti-neoplastic effect of halocynthiaxanthin, a metabolite of fucoxanthin. Anticancer Drugs. (1992)
^ a b c Maeda H, et al. Effect of medium-chain triacylglycerols on anti-obesity effect of fucoxanthin. J Oleo Sci. (2007)
^ Sangeetha RK, et al. Bioavailability and metabolism of fucoxanthin in rats: structural characterization of metabolites by LC-MS (APCI). Mol Cell Biochem. (2010)
^ Fucoxanthin restrains oxidative stress induced by retinol deficiency through modulation of Na(+)K(+)-ATPase [corrected.
^ a b c d e f g h i Hashimoto T, et al. Pharmacokinetics of fucoxanthinol in human plasma after the oral administration of kombu extract. Br J Nutr. (2012)
^ a b c d e f Hashimoto T, et al. The distribution and accumulation of fucoxanthin and its metabolites after oral administration in mice. Br J Nutr. (2009)
^ Sugawara T, et al. Esterification of xanthophylls by human intestinal Caco-2 cells. Arch Biochem Biophys. (2009)
^ a b c d e Matsumoto M, et al. Suppressive effects of the marine carotenoids, fucoxanthin and fucoxanthinol on triglyceride absorption in lymph duct-cannulated rats. Eur J Nutr. (2010)
^ a b Sugawara T, et al. Brown algae fucoxanthin is hydrolyzed to fucoxanthinol during absorption by Caco-2 human intestinal cells and mice. J Nutr. (2002)
^ a b Asai A, et al. Biotransformation of fucoxanthinol into amarouciaxanthin A in mice and HepG2 cells: formation and cytotoxicity of fucoxanthin metabolites. Drug Metab Dispos. (2004)
^ Das SK, Hashimoto T, Kanazawa K. Growth inhibition of human hepatic carcinoma HepG2 cells by fucoxanthin is associated with down-regulation of cyclin D. Biochim Biophys Acta. (2008)
^ a b Asai A, Yonekura L, Nagao A. Low bioavailability of dietary epoxyxanthophylls in humans. Br J Nutr. (2008)
^ Woo MN, et al. Anti-obese property of fucoxanthin is partly mediated by altering lipid-regulating enzymes and uncoupling proteins of visceral adipose tissue in mice. Mol Nutr Food Res. (2009)
^ a b c Yonekura L, et al. Keto-carotenoids are the major metabolites of dietary lutein and fucoxanthin in mouse tissues. J Nutr. (2010)
^ a b Tsuboi M, et al. Nitrocapsanthin and nitrofucoxanthin, respective products of capsanthin and fucoxanthin reaction with peroxynitrite. J Agric Food Chem. (2011)
^ a b c Liu CL, Lim YP, Hu ML. Fucoxanthin attenuates rifampin-induced cytochrome P450 3A4 (CYP3A4) and multiple drug resistance 1 (MDR1) gene expression through pregnane X receptor (PXR)-mediated pathways in human hepatoma HepG2 and colon adenocarcinoma LS174T cells. Mar Drugs. (2012)
^ Guengerich FP. Cytochrome P-450 3A4: regulation and role in drug metabolism. Annu Rev Pharmacol Toxicol. (1999)
^ Ransohoff RM, Perry VH. Microglial physiology: unique stimuli, specialized responses. Annu Rev Immunol. (2009)
^ Block ML, Zecca L, Hong JS. Microglia-mediated neurotoxicity: uncovering the molecular mechanisms. Nat Rev Neurosci. (2007)
^ Lull ME, Block ML. Microglial activation and chronic neurodegeneration. Neurotherapeutics. (2010)
^ a b Pangestuti R, et al. Fucoxanthin Ameliorates Inflammation and Oxidative Reponses in Microglia. J Agric Food Chem. (2013)
^ a b c d e f g Ha AW, Kim WK. The effect of fucoxanthin rich power on the lipid metabolism in rats with a high fat diet. Nutr Res Pract. (2013)
^ a b c d e f Hu X, et al. Combination of fucoxanthin and conjugated linoleic acid attenuates body weight gain and improves lipid metabolism in high-fat diet-induced obese rats. Arch Biochem Biophys. (2012)
^ a b c d e f g h i j Abidov M, et al. The effects of Xanthigen in the weight management of obese premenopausal women with non-alcoholic fatty liver disease and normal liver fat. Diabetes Obes Metab. (2010)
^ a b c d e f g h i j Maeda H, et al. Anti-obesity and anti-diabetic effects of fucoxanthin on diet-induced obesity conditions in a murine model. Mol Med Report. (2009)
^ a b c Nishikawa S, Hosokawa M, Miyashita K. Fucoxanthin promotes translocation and induction of glucose transporter 4 in skeletal muscles of diabetic/obese KK-A(y) mice. Phytomedicine. (2012)
^ a b Hosokawa M, et al. Fucoxanthin regulates adipocytokine mRNA expression in white adipose tissue of diabetic/obese KK-Ay mice. Arch Biochem Biophys. (2010)
^ a b Tsukui T, et al. Fucoxanthin and fucoxanthinol enhance the amount of docosahexaenoic acid in the liver of KKAy obese/diabetic mice. J Agric Food Chem. (2007)
^ a b Maeda H, et al. 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. J Agric Food Chem. (2007)
^ Maeda H, et al. Fucoxanthin from edible seaweed, Undaria pinnatifida, shows antiobesity effect through UCP1 expression in white adipose tissues. Biochem Biophys Res Commun. (2005)
^ Nicholls DG, Locke RM. Thermogenic mechanisms in brown fat. Physiol Rev. (1984)
^ a b Maeda H, et al. Seaweed carotenoid, fucoxanthin, as a multi-functional nutrient. Asia Pac J Clin Nutr. (2008)
^ Boss O, Farmer SR. Recruitment of brown adipose tissue as a therapy for obesity-associated diseases. Front Endocrinol (Lausanne). (2012)
^ a b Jeon SM, et al. Fucoxanthin-rich seaweed extract suppresses body weight gain and improves lipid metabolism in high-fat-fed C57BL/6J mice. Biotechnol J. (2010)
^ Park HJ, et al. Beneficial effects of Undaria pinnatifida ethanol extract on diet-induced-insulin resistance in C57BL/6J mice. Food Chem Toxicol. (2011)
^ a b c Yim MJ, et al. Suppressive effects of Amarouciaxanthin A on 3T3-L1 adipocyte differentiation through down-regulation of PPARγ and C/EBPα mRNA expression. J Agric Food Chem. (2011)
^ a b c d Lai CS, et al. Xanthigen suppresses preadipocyte differentiation and adipogenesis through down-regulation of PPARγ and C/EBPs and modulation of SIRT-1, AMPK, and FoxO pathways. J Agric Food Chem. (2012)
^ a b Maeda H, et al. Fucoxanthin and its metabolite, fucoxanthinol, suppress adipocyte differentiation in 3T3-L1 cells. Int J Mol Med. (2006)
^ Suppressive Effects of Amarouciaxanthin A on 3T3-L1 Adipocyte Differentiation through Down-regulation of PPARγ and C/EBPα mRNA Expression.
^ Kanda H, et al. MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. J Clin Invest. (2006)
^ Nieto-Vazquez I, et al. Insulin resistance associated to obesity: the link TNF-alpha. Arch Physiol Biochem. (2008)
^ Koyama T. Extracts of marine algae show inhibitory activity against osteoclast differentiation. Adv Food Nutr Res. (2011)
^ a b Das SK, et al. Fucoxanthin induces apoptosis in osteoclast-like cells differentiated from RAW264.7 cells. J Agric Food Chem. (2010)
^ a b c d e f Sachindra NM, et al. Radical scavenging and singlet oxygen quenching activity of marine carotenoid fucoxanthin and its metabolites. J Agric Food Chem. (2007)
^ Nomura T, et al. Proton-donative antioxidant activity of fucoxanthin with 1,1-diphenyl-2-picrylhydrazyl (DPPH). Biochem Mol Biol Int. (1997)
^ Cytoprotective effect of fucoxanthin isolated from brown algae Sargassum siliquastrum against H2O2-induced cell damage.
^ a b c Rodrigues E, Mariutti LR, Mercadante AZ. Scavenging capacity of marine carotenoids against reactive oxygen and nitrogen species in a membrane-mimicking system. Mar Drugs. (2012)
^ Takashima M, et al. Capacity of fucoxanthin for scavenging peroxyl radicals and inhibition of lipid peroxidation in model systems. Free Radic Res. (2012)
^ Sies H. Strategies of antioxidant defense. Eur J Biochem. (1993)
^ Heo SJ, Jeon YJ. Protective effect of fucoxanthin isolated from Sargassum siliquastrum on UV-B induced cell damage. J Photochem Photobiol B. (2009)
^ a b Liu CL, Chiu YT, Hu ML. Fucoxanthin enhances HO-1 and NQO1 expression in murine hepatic BNL CL.2 cells through activation of the Nrf2/ARE system partially by its pro-oxidant activity. J Agric Food Chem. (2011)
^ Hine CM, Mitchell JR. NRF2 and the Phase II Response in Acute Stress Resistance Induced by Dietary Restriction. J Clin Exp Pathol. (2012)
^ a b Lee JY, et al. Hexane fraction from Laminaria japonica exerts anti-inflammatory effects on lipopolysaccharide-stimulated RAW 264.7 macrophages via inhibiting NF-kappaB pathway. Eur J Nutr. (2012)
^ Shiratori K, et al. Effects of fucoxanthin on lipopolysaccharide-induced inflammation in vitro and in vivo. Exp Eye Res. (2005)
^ a b Kim KN, et al. Fucoxanthin inhibits the inflammatory response by suppressing the activation of NF-κB and MAPKs in lipopolysaccharide-induced RAW 264.7 macrophages. Eur J Pharmacol. (2010)
^ Ishikawa C, et al. Anti-adult T-cell leukemia effects of brown algae fucoxanthin and its deacetylated product, fucoxanthinol. Int J Cancer. (2008)
^ Heo SJ, et al. Anti-inflammatory effect of fucoxanthin derivatives isolated from Sargassum siliquastrum in lipopolysaccharide-stimulated RAW 264.7 macrophage. Food Chem Toxicol. (2012)
^ a b c Kawashima T. A marine carotenoid, fucoxanthin, induces regulatory T cells and inhibits Th17 cell differentiation in vitro. Biosci Biotechnol Biochem. (2011)
^ Liu CL, Lim YP, Hu ML. Fucoxanthin enhances cisplatin-induced cytotoxicity via NFκB-mediated pathway and downregulates DNA repair gene expression in human hepatoma HepG2 cells. Mar Drugs. (2013)
^ Nakanishi C, Toi M. Nuclear factor-kappaB inhibitors as sensitizers to anticancer drugs. Nat Rev Cancer. (2005)
^ Sarkar FH, Li Y. Using chemopreventive agents to enhance the efficacy of cancer therapy. Cancer Res. (2006)
^ Yeh PY, et al. Involvement of nuclear transcription factor-kappa B in low-dose doxorubicin-induced drug resistance of cervical carcinoma cells. Biochem Pharmacol. (2003)
^ Hou LL, et al. Essential role of autophagy in fucoxanthin-induced cytotoxicity to human epithelial cervical cancer HeLa cells. Acta Pharmacol Sin. (2013)
^ Beppu F, et al. In vitro and in vivo evaluation of mutagenicity of fucoxanthin (FX) and its metabolite fucoxanthinol (FXOH). J Toxicol Sci. (2009)
Fucoxanthin Information
This page features 84 references. All factual claims are followed by specifically-applicable references. Click here to see the full set of research information and references for Fucoxanthin.
"Fucoxanthin," Examine.com, published on 1 September 2013, last updated on 16 August 2019, https://examine.com/supplements/fucoxanthin/


text:
Q: What advantages does Notification class give over simply sending email with Laravel 5.3? There was introduced a new notification class in Laravel 5.3 which allows pushing notifications to different channels. It does allow to quickly throw multiple lines and give a call to action and also allows sending notifications to multiple users with a single method call.
Are there any other advantages that I might have missed?

A: Notfications allow for emails, slack, sms, etc to be all applied in one place under a single notification, where Mailables are just mail.
Notification email does provide a dynamic template for composing an email using the MailMessage API, but it also allows you to just use a view of your choosing instead using (new MailMessage)->view('location.name')->....
As of v5.3.15 you can also now return Mailables instead of MailMessage from Notifications allowing for the use of a much more robust mail API that includes Cc, Bcc, etc.
So basically now you can get the best of both worlds when using Notifications now that you can implement Mailables within them instead of using MailMessage.

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text:
Q: Retrofit onResponse method not working, throws NullPointerException I'm trying to get data from web API, but something is wrong in my onResponse() method and I can't figure it out.
My JSON looks like this
  [
   "partner1",
   "partner2",
   "partner3",
     ...     ,
   "partner150"
  ]

I have Table partners (ActiveAndroid) in which I would like to save all partners from the API.
@Table(name = "Partners")
public class Partners extends Model {

    @Column(name = "Name")
    String name;

    public Partners() {}

    public Partners(String name) {
        this.name = name;
    }
}

Here is my POJO model class:
public class Partners extends ArrayList<String> {

@SerializedName("partners")
@Expose
public List<String> partners = new ArrayList<String>();

public List<String> getPartners() {
    return partners;
}

public void setName(List<String> partners) {
    this.partners = partners;
}

}
This is my interface
public interface APIService {

        @GET("Partners")
        Call<Partners> getPartners();
}

This is my APIHelper class
public class APIHelper {

    public static final String PARTNERS_URL = "https://part-of-link.com/partners.json/";

    public static APIService apiService;

    public static APIService getApiService() {
        if (apiService == null) {
            Retrofit retrofit = new Retrofit.Builder().baseUrl(PARTNERS_URL)
                    .addConverterFactory(GsonConverterFactory.create()).build();
            apiService = retrofit.create(APIService.class);
        }
        return apiService;
    }
}

And this is Fragment where I have a Button on which I would like to implement thw onClick() method to get the data from the API and save it into the Partners table.
public class DownloadMain extends Fragment implements Callback<Partners> {

    private Button dloadPartners;
    private Call<Partners> callPartners;
    public static APIService apiService;

    public DownloadMain() {}

    public DownloadMain newInstance() { return new DownloadMain(); }

    @Override
    public void onCreate(Bundle savedInstanceState) {
        super.onCreate(savedInstanceState);
    }

    @Override
    public View onCreateView(LayoutInflater inflater, ViewGroup container,
                             Bundle savedInstanceState) {

        View view = inflater.inflate(R.layout.download_main, container, false);

        dloadPartners = (Button) view.findViewById(R.id.downloadPartners);
        dloadPartners.setOnClickListener(btnListener);

        callPartners = APIHelper.getApiService().getPartners();
        callPartners.enqueue(this);

        return view;
    }

    Button.OnClickListener btnListener = (new View.OnClickListener() {
        @Override
        public void onClick(View v) {
            APIHelper helper = new APIHelper();
            apiService = helper.getApiService();

            Call<Partners> call = apiService.getPartners();
            call.enqueue(new Callback<Partners>() {
                @Override
                public void onResponse(Call<Partners> call, Response<Partners> response) {

        Call<Partners> call = apiService.getPartners();
        call.enqueue(new Callback<Partners>() {
            @Override
            public void onResponse(Call<Partners> call, Response<Partners> response) {

               List<String> partners =  response.body().getPartners();
                Log.d(TAG, "Number of partners received: " + partners.size());
                }

                @Override
                public void onFailure(Call<Partners> call, Throwable t) {
                    Toast.makeText(getActivity(), "FAIL!!!", Toast.LENGTH_SHORT).show();
                }
            });
        }
    });
    @Override
    public void onResponse(Call<Partners> call, Response<Partners> response) {

    }

    @Override
    public void onFailure(Call<Partners> call, Throwable t) {

    }
}

Here the onResponse() method throws me an error: Attempt to invoke virtual method 'java.util.List com.example...pojo.Partners.getPartners()' on a null object reference
What I want is to get all partners from web and save it into my Partners table on button click.
I can't find solution to this error so if someone could help me I've would be grateful.
Question: Could anybody guide me and tell me what is wrong and help me to fix this?

A: Firstly, Java naming conventions. Partner represents a single entity, not plural of Partners. - Change your classname to reflect that. It's also confusing for us because your question has two classes of the same name. For your use case, making a class that extends an Arraylist is unnecessary.

Secondly, please learn proper JSON-to-Java conversions. Your JSON is simply an Array of Strings - the object extending the Arraylist is again unnecessary.
If you want to keep the ActiveAndroid model object and use it for Retrofit, the JSON needs to look like this for a List<Partner>
[
   {"name": "partner1"},
   {"name": "partner2"}
]

And for the current Partners class that extends an Arraylist with an inner Arraylist, something like this (which isn't valid JSON)
[
  "partners" : [
      "partner1",
      "partner2"
  ]
]

So, again, you don't need the class that extends the Arraylist.

And finally, try to understand the "flow" of a Retrofit method usage.
You get a Call object of a certain type, you enqueue it to start the HTTP request, then you define a Callback with two actions for when the request succeeds and errors.
Now, see that you've implemented the Callback on the Fragment?
public class DownloadMain extends Fragment implements Callback<Partners>

But you need to use that - you have those two empty methods for onResponse and onError at the bottom of the Fragment class... That's where you should implement what happens when Retrofit is done, and that's where the code goes when you have this line in onCreateView
callPartners.enqueue(this);

But since those methods are empty, nothing happens on that call. Meanwhile the other enqueue methods have unnecessary Callback implementations, when you could just use this
Additionally, no offense, but you seem to just be copy-pasting code around without knowing what's happening... Notice how you make a second, unnecessary API call.
// Call 1
Call<Partners> call = apiService.getPartners();
call.enqueue(new Callback<Partners>() {
    @Override
    public void onResponse(Call<Partners> call, Response<Partners> response) {
        // Call 2, despite having a response
        Call<Partners> call = apiService.getPartners();
        call.enqueue(new Callback<Partners>() {
            @Override
            public void onResponse(Call<Partners> call, Response<Partners> response) {

With all these above problems, I'm not too surprised Retrofit would error out, but the problem can be avoided by first fixing the Retrofit Model, then be sure to check if response.body() is null before you attempt to use it.

If you do it all correctly, the only line of code in the onClick, needs to just be this.
callPartners.enqueue(DownloadMain.this);

A: In the button click listener, the apiService is not initialised, although you are calling helper.getApiService();. So apiService instance is null, when calling Call call = apiService.getPartners();. hence NullPointerException.
Initialise apiService.
@Override
public void onClick(View v) {
    APIHelper helper = new APIHelper();
    apiService = helper.getApiService();

    Call<Partners> call = apiService.getPartners();

A: Seems like your JSON response is just an array of strings, so I think you can do away with the POJOs and instead do this:
public interface APIService {

    @GET("Partners")
    Call<List<String>> getPartners();
}

while replacing every type parameter where you declared Partners with List<String> for example, replace all Call<Partners> with Call<List<String>>


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text:
Limulatys reliquus är en snäckart som beskrevs av Tom Iredale 1936. Limulatys reliquus ingår i släktet Limulatys och familjen Haminoeidae. Inga underarter finns listade i Catalogue of Life.

Källor

Snäckor
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text:
Federal Judge Hands Quotient Major Win in Coupon Fraud Case
A federal judge has handed Quotient a sweeping victory in a lawsuit against a couple that the company had accused of fraudulently printing and selling coupons from Coupons.com, Quotient's flagship consumer site.
Magistrate Judge Nathanael Cousins of the United States District Court, Northern District of California, handed Quotient a complete victory in its suit against the so-called "coupon fairies," who sold Quotient's coupons on Instagram under various usernames.
The court issued a permanent injunction against the defendants, enjoining them from using the Quotient Promotions Network, selling Quotient's coupons, and using or selling the means by which they improperly obtained Quotient's coupons. In addition, the court awarded Quotient more than $113,000 for damages, attorney fees and other costs.
"We have demonstrated our commitment to aggressively fight those who commit coupon fraud," said Steven Boal, CEO of Quotient.
This decision stems from a lawsuit filed in October 2016 by Quotient against a defendant then known only by Instagram usernames. After successfully identifying the real names of the defendants, Quotient amended and served its complaint and fought off a baseless motion to dismiss the case, leading ultimately to this victory. Quotient accused the couple of violating the Computer Fraud and Abuse Act, known as the CFAA, along with other allegations. The defendants have 30 days to appeal the ruling.
This is a second win for Quotient this year. In a separate lawsuit, the company was able to enjoin another coupon fairy from accessing or selling Quotient's coupons.
— The Quotient News Team
Posted in Digital Coupons, Intellectual Property, Legal, Technology
Technology Brands Solutions

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text:
Batucada Surgiu Independent
Jazz vocalist Kris Russell was born in Sacramento, but her musical heart has long been in Brazil amidst the muses and magic of Bossa Nova. Following up her two previous Rio-flavored Smooth Jazz singles, Kris celebrates the recent 60th anniversary of the genre's birth with "Batucada Surgiu" (pronounced "bot-ooh-ka-da sir-joo") - A high octane, English/Portuguese world dance party of a song credited to Kris Russell and the Mystery Jazz Ensemble. Her percussive, keyboard and trumpet driven six-piece band lays an empowering foundation for her to explore the mystical and fiery energies created by Brazilian composers Marcos K. Valle and his brother Paulo Valle.
Batucada Surgiu entered the Radio Indie Alliance Singles TOP 20 at Number 12 for the week of June 7th 2019
'Down in Brazil' reached #6 on BDS Billboard's SmoothJazz most added chart for radio on May 15, 2017
'Down in Brazil' reached RadioWaves Prime Movers Chart for 5/12/2017 to 5/18/2017
'Down in Brazil' reached the RadioWaves SmoothJazz/Fusion Chart at #69 for the weeks of 6/9/2017 to 6/15/2017, 6/16/2017 to 6/22/2017
And also made that same chart for 6/23/2017 to 6/29/2017
'Down in Brazil' made #5 on the Groove Jazz Chart for most increased play for Radio on June 12th 2017
Kris Russell and the Mystery Jazz Ensemble's single "Down in Brazil" ...Winner of a Bronze Medal for 2017 ( Global Music Awards)
JAZZ VOCALIST KRIS RUSSELL RELEASES NEW SINGLE, 'DOWN IN BRAZIL,' ALONG WITH NEW TRISTEZA FRAGRANCE
12:38 ET
LAS VEGAS, May 15, 2017 /PRNewswire/ -- Jazz Vocalist Kris Russell will release her newest single titled 'Down in Brazil,' a contemporary bossa nova with music and lyrics written by Jazz singer and award winning artist and composer Michael Franks, with a new arrangement by Kris Russell and the Mystery Jazz Ensemble. It will be featured on SmoothJazz.com, Global Radio and other radio stations in the USA and around the world on May 15, 2017.
Kris is excited and eager to build on the momentum from her first single released last year, a sophisticated, sultry, symphonic bossa nova with arrangement by Richard Rome, of Cole Porter's classic Jazz Standard, 'I Concentrate On You.' With the introduction of this newest single, Kris endeavored to record a more contemporary sound and song from a contemporary artist, yet still include the sound and instrumentation of traditional bossa nova that she loves so much.
Jazz Vocalist Kris Russell Releases New Single, 'Down in Brazil,' Along With New Tristeza lll Fragrance
Brazil, with its pulsating, rhythmic sounds, incredible food, gorgeous sandy beaches, unique smells, vibrant colors and beautiful music, inspired Kris to create her newest CD 'Down in Brazil,' and also inspired her to design her new trademark signature perfume that she is releasing at the same time as her new single for family, friends and fans. The perfume's name was inspired by a recording Sergio Mendez did of the classic Brazilian song 'Tristeza,' which in Portuguese means 'no more sadness.'
"It's impossible to listen to the Brazilian classic song 'Tristeza' and remain unhappy and sad. It's a beautiful uplifting song, so inspirational and filled with such joy and happiness," says Kris.
Her Tristeza lll fragrance and new single will be available on her website at www.krisrusselljazz.com and other social media sites. The fragrance will be available in a 10-milliliter roll on as an eau de parfum, along with her music. The signature perfume will be available on her site in beautiful 2 oz. bottles as well, and will be sold at her live music performances.
After reading the master perfumer Roja Dove's classic, "The Essence of Perfume," Kris began designing beautiful perfumes and will create one just for you if you like, as she just wants share her passion and art. Details will be available soon on her website! "Creating perfume is a skill as well as an art, just as creating and performing music is a skill and art, and I'm excited to be creating and sharing with everyone some of the art and the music I love!"
She also has created a new music video which will be released on smoothjazz.com along with the CD, and on YouTube at Down in Brazil.
RADIO QUOTES:
About the new single "Down in Brazil.....Paul Peters in the United Kingdom a.o. with shows on Forest FM, Abby 109 and syndicated radio stations worldwide says, "Great....my late partner , who's show I now present would have played this....So I must." 7/1/2017
Q 108 Kingston Radio in Canada likes and spins 'Down in Brazil' and says, "What a beautiful voice...takes me back to the Golden Era of Jazz."
Jeff Moses of WJMX Smooth Jazz Boston Global Radio says, quote "Your music is always Brilliant and Stellar!"
Billy Stritch, "Kris Russell is always a memorable addition to our cast-party open mike nights in Las Vegas. Her lightly swinging style lights up the stage and I always love playing for her."
"I'm always excited to see Kris Russell when I bring Cast Party NYC to Las Vegas! But then.....she sings.....and everyone is over-the-moon! Kris brings such a great taste and an inherent understanding of the lyrics. Brava Kris!" Jim Caruso Host of Jim Caruso's Cast Party
REVIEW FOR 'DOWN IN BRAZIL'
Las Vegas based singer Kris Russell grew up in Sacramento with a passionate love of ballads, swing, cool jazz, bebop and traditional jazz inspired by the likes of Julie London, Rosemary Clooney, Peggy Lee, and Ella Fitzgerald.
Continuing to establish herself as a timeless contemporary jazz vocalist in her own right, she follows her debut single "I Concentrate On You" with a sultry, soulful and exotic twist on Michael Franks' travelogue classic "Down in Brazil." Russell's lighthearted, freewheeling version is fortified with a seamless blend of Fender Rhodes, acoustic guitar and smoky sax. Book your ticket now and venture "Down in Brazil" with this talented songstress! Jonathan Widran
I CONCENTRATE ON YOU MUSIC AND LYRICS BY COLE PORTER KRIS RUSSELL'S FIRST RELEASE:
"I Concentrate On You," music and lyrics by Cole Porter, vocals by Kris Russell, and arrangement by Richard Rome was played in the USA, Europe and around the globe on Smooth Jazz Global Radio and was also featured on their Radar Chart for the months of Aug. Sept. and Oct. of 2016. www.SmoothJazz.com
For the week of Aug 19-Aug 26 2016 "I Concentrate On You" made the number #10 spot out of 100 on the Radio Waves Prime Movers Jazz Chart!
Kris Russell' s newest release "I Concentrate On You", Music and Lyrics by Cole Porter was included on TM Century's Gold Hit Disc #HC201635 August 26th 2016.
KRIS RUSSELL I Concentrate On You - Kris Russell
Growing up in a family of musicians and entertainers, vocalist Kris Russell was inspired by great female jazz singers, studied the styles of legendary Brazilian artists and has had a long passion for the works of Cole Porter. The veteran live performer draws from all of these influences on her debut single "I Concentrate on You," a lush, intimate and inviting twist on the Porter classic, a delightful intro to a truly gifted and versatile singer! ~JONATHAN WIDRAN
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