Astaxanthin and liver health -
More oil red O-stained lipid droplets were observed in the liver tissue of the HFD and solvent groups than in the liver tissue of the ND group, resembling the percentage result of lipid droplets Figure 3E.
Conversely, ATX supplementation dose-dependently decreased the production of fatty droplets, in which the area of droplets was significantly lessened in the 0. These results confirmed that ATX prevented lipid accumulation and hepatic steatosis, conforming to the results of intrahepatic TG and TC levels.
As shown in the e-AT sections of HFD-induced mice Figures 3C,F , the mean adipocyte size increased almost Apoptotic cells were detected by green fluorescent TUNEL staining, and cell nuclei were stained blue DAPI.
Compared to that in the HFD group, the number of apoptotic cells stained green was reduced in a dose-dependent manner with ATX supplementation, and the apoptosis rates were decreased by To understand the mechanism s by which ATX modulates hepatic lipid metabolism in response to a high-fat diet, we analyzed the expression of genes related to lipogenesis and fatty acid β-oxidation in the liver by qRT—PCR.
These results indicated that consumption of a HFD contributed to fat synthesis and ultimately disturbed lipid metabolism; furthermore, high-dose ATX could improve the disorder of lipid metabolism by promoting cholesterol metabolism and inhibiting fat synthesis.
Figure 4. Astaxanthin significantly improved relative gene expression. B The heatmap of differential genes expression at the transcriptional level. C Regulatory effects of ATX supplementation on fatty acid and cholesterol metabolism in mice induced by HFD.
Data are shown as mean ± SD of triplicate. To explore how the hepatic lipidome is altered upon ATX intervention, RNA sequencing was used to accurately and quantitatively analyse liver transcriptional changes and lipid metabolism pathways in the liver in response to ATX supplementation.
A total of genes were differentially expressed in HFD-induced liver samples compared with ND-induced liver samples Supplementary Figures 2A,B. However, a total of differentially expressed genes, of which were increased and 53 were decreased, were identified in the 0.
We performed a comprehensive hepatic lipidomic analysis to evaluate whether differences in lipid content or composition may account for differences in hepatic lipid disorders between the HFD group and ATX group. A total of 1, lipid species were identified in liver samples, which belong to six primary classes of lipids, including glycerophospholipids GPs , glycerides GLs , fatty acyls FAs , sphingolipids SLs , sterol lipids STs , and prenol lipids PRs Supplementary Figure 3.
Based on the abovementioned results, we screened and 91 lipid biomarker candidates by applying volcano plots for such distinctions in ND vs. HFD and HFD vs. Figure 5.
Astaxanthin regulated lipid metabolites in HFD-fed mice. A OPLS-DA score plot left and permutation plot right. B Venn diagram depicting the overlap of significantly changed metabolites between experimental groups.
The volcano plot analysis of ND vs. HFD group C and HFD vs. Analysis of lipid metabolism pathway of ND vs. HFD E and HFD vs. G Heatmap of 34 significantly altered metabolites in ATX-treated HFD-fed mice.
Blue: downregulated metabolites. Red: upregulated metabolites. H The associated heatmap of significantly changed metabolites. According to the Venn diagram, we found that the accumulated lipid species were significantly different between the ND and HFD groups, while ATX intervention patently changed the levels of 91 lipid species, including 24 ordinary species, compared to the levels in HFD-fed alone Figure 5B.
Furthermore, in our present study, we found that 8 of the other 20 most relevant metabolites 3 BAs, 2 CARs, 2 BMP, and 1 TG were remarkably downregulated after ATX supplementation; however, there was no significant difference in the ND vs.
HFD group. We observed a significantly positive correlation among these 34 metabolite levels associated with lipid metabolism Figure 5H. Thus, these results indicated that the 22 metabolites, including 4 FFAs, 8 TGs, 2 DGs, 3 BAs, 2 CARs, and 2 BMPs, might be potential biomarkers accountable for alleviating the steatohepatitis induced by lipid disturbance.
The KEGG database was used to perform pathway analysis of differentially expressed metabolites. The pathways were considerably disrupted in the HFD group, including glycerolipid metabolism, insulin resistance, cholesterol metabolism, fat digestion and absorption, and regulation of lipolysis in adipocytes, when compared with the ND group; however, 0.
Of the 8, OTUs visualized in the experimental groups, 4. In addition, the number of other OTUs in the ND group, HFD group and 0. The Goods coverage values had no obvious differences in each group Figure 6B. To assess community similarity among samples, we applied principal coordinates analysis PCoA to represent the relative abundance of OTUs in each community by two different analyses.
The PCoA plot showed that the structure and compositions of gut microbiota in the HFD group Axis 1, Figure 6. Astaxanthin regulated the gut microbiota.
A The Venn diagram. Data were analyzed using a one-way ANOVA and are expressed as the mean ± SD. C PCoA of unweighted UniFrac distance from beta diversity analysis.
D Phylum abundance graph genus levels. E Genus abundance graph. F Species taxonomy branch map based on LEfSe analysis.
G The heatmap of the 30 bacterial genera with the largest differences in abundance were selected, according to the unweighted UniFrac distance of the intestinal content samples. H Predicted the abundance map of MetaCyc secondary functional pathways. X-coordinate: the abundance of functional pathways, Y-coordinate: the MetaCyc secondary functional pathway.
I Analysis of differences in metabolic pathways left and species composition in different MetaCyc pathways right. At the phylum level, the taxonomic profiles of the gut microbiomes showed significant differences according to increasing ATX supplementation and developing obesity severity, within which Firmicutes , Bacteroidetes , and Proteobacteria were the dominant phyla.
At the genus level, the abundance of genera, including Bacteroides , Allobaculum , Desulfovibrio , Akkermansia , Oscillospira , Ruminococcus , Parabacteroides , Adlercreutzia , Alistipes , and Bilophila , was significantly altered by a high-fat diet compared with the normal diet and moderately inverted by 0.
Compared to the mice induced by HFD alone, the mice supplemented with ATX had significantly upregulated abundances of Akkermansia and Parabacteroides to Additionally, to explore high-dimensional biomarkers and identify significant differences at the species level, LEfSe with default parameters was used between the microbial communities compared.
The 65 most abundant OTUs were observed at the taxonomic level in the samples, among which beneficial bacteria were significantly reduced in the HFD group compared with the ND group, revealing a serious gut microbial disorder in HFD-fed mice Figure 6F.
Furthermore, 9 of the 30 most prevalent bacterial genera were upregulated and 21 bacterial genera were downregulated in the HFD-fed mice compared with the mice fed a normal diet, while these genera were partially promoted to their original relative abundance levels after ATX supplementation Figure 6G.
To characterize the functional role of the related abundant bacterial genera, we found 47 secondary functional pathways from the MetaCyc database of metabolic pathways that are relevant to lipometabolism, including the fatty acid and lipid biosynthesis pathway abundance value: 16, Obesity and obesity-related complications are classic health problems worldwide.
A long-term high-fat diet and an imbalance in energy expenditure are important causes for concern In both obese individuals and animal models of NASH, it could be characterized by excessive intracellular lipid accumulation combined with inflammation, which can ultimately progress into hepatic insulin resistance, mitochondrial dysfunction and cellular injury 27 , Emerging evidence shows that ATX, a natural functional food, has been used as a dietary supplement for treating obesity and liver injury and maintaining health 18 , Importantly, when compared to vitamin E, ATX was more effective at lipid peroxidation and preventing NASH.
In the present study, our results showed that ATX supplementation could prevent obesity and the development of NAFLD by meditating lipid metabolism and gut microbiota. Alternatively, ATX consumption also prevents oxidative stress in the liver and lipid peroxidation by improving antioxidant enzyme activity.
According to experimental results, dietary ATX not only significantly decreased body weight gain, adipose tissue weight, and serum TG, TC, and LDL-C levels but also ameliorated abnormal hepatic metabolism following the reduction of liver weight and hepatic TG and TC levels in HFD-induced mice.
No significant difference in the food efficiency ratio or serum HDL-C levels was observed in the HFD group with long-term ATX intake. From the physiological and biochemical profiles, ATX exhibited a better preventive effect on dyslipidaemia and abnormal liver function than our previous results Over the past decade, numerous pieces of evidence have shown that oxidative stress caused by a high-fat diet and specific products of ROS are involved in the development of obesity and fatty liver 31 , Thus, balancing the liver oxidative reaction is an important aspect of preventing the development of NAFLD.
Studies have shown that oxidative stress is closely related to endoplasmic reticulum ER stress in the development and progression of NAFLD and other diseases, while ATX can directly or indirectly moderate ER through antioxidant activity 33 , Interestingly, previous study has confirmed that ATX significantly reduced the levels of oxidative stress marker thiobarbituric acid-responsive substances TBARS in the liver of NASH mice In our results, both the ROS levels evaluated by the DHE probe and the levels of MDA measured, a lipid peroxidation product, were significantly increased in liver tissues in each experimental group.
HFD might have contributed to the increase in these oxidative stress indices and the decrease in antioxidant enzymes, including T-AOC, SOD, CAT, and GSH levels. Our results are consistent with previous studies showing that HFD seriously damaged the antioxidant defense system 32 , Regardless of the dose, the MDA levels of all ATX-supplemented groups were reduced, suggesting that ATX suppresses overproduction of ROS induced by obesity.
In addition, with dose-dependent increases of the ATX in the diet, the activities of antioxidant enzymes remarkedly improved and were close to normal levels in mice fed HFD. Multiple studies have confirmed that cell apoptosis induced by excessive endogenous cholesterol is associated with increased ROS in tissues 36 , As previously discussed, long-term HFD intake advanced total cholesterol and disturbed the oxidative balance in the liver, which was attributed to hepatocellular apoptosis.
Based on the TUNEL assay results, we found a large number of apoptotic liver cells in the HFD group, whereas ATX alleviated the degree of necrosis. Nevertheless, the precise intracellular mechanism responsible for this phenomenon was unclear in this study.
Moreover, the pathological results showed that ATX could effectively prevent fat accumulation and hepatic steatosis in a dose-dependent manner. Whether for obesity or the development of NAFLD, one of the root causes is the perturbation in lipid metabolism As reported in previous studies, excessive fat intake induced abnormal bile secretion and disturbed cholesterol levels In addition, FFAs usually trigger the accumulation of DGs and TGs by mediating insulin signal and sensitivity in liver tissue To demonstrate the function of ATX in lipid metabolism, lipidomic analysis revealed that the total levels of hepatic FFAs, TGs, and DGs were noticeably increased in HFD group mice, indicating that a high-fat diet partly supported our previous results.
Interestingly, our results suggested that ATX not only decreased the levels of FFAs and TGs but also specifically reduced the levels of BAs and acyl-carnitines, indicating that both cholesterol metabolism and fatty acid oxidation were improved in mouse livers. Moreover, SREBP1c , along with its downstream genes ACC , SCD1 and FAS , is an important component in the energy metabolic system and plays a key role in regulating the FFA and TG synthesis mentioned above 38 , According to transcriptome analysis, gene expression signatures were profoundly distinguished among the experimental groups.
Considering the degree and diversity of gene expression changes, only genes associated with the target pathway were screened in this study. AMPK , a key molecule in the regulation of biological energy metabolism, is involved in diabetes and metabolism-related diseases Peroxisome proliferator activated receptor PPARα and peroxisome proliferator-activated receptor gamma coactivator-1α PGC-1 play an important role in regulating the homeostasis of adipose tissue by jointly regulating the balance between fatty acid synthesis and oxidation The expression of PPARα , which is negatively correlated with the severity of NASH, is significantly reduced in NAFLD ATX alleviated the gene expression associated with EIF-2 signaling in NASH rather than improved the expression of gene related to mitochondrial dysfunction In present study, the results revealed that dietary 0.
As our previous manuscript shown, the interaction between PPARα and PGC-1α promoted the oxidation of fatty acids and inhibited the expression of SREBP1c to a certain extent During lipid metabolism, CPT-1 is a key rate-limiting enzyme that accelerates the entry and β-oxidation of long-chain fatty acids into mitochondria A high-fat diet suppresses the expression of PGC-1α , and the mitochondrial respiration rate decreases in the absence of PGC-1α , ultimately leading to a decrease in fatty acid oxidation capacity.
In present study, our results found 0. A previous study confirmed that the suppression of SCD-1 could effectively attenuate HFD-induced insulin resistance and hepatic steatosis However, we did not examine the effects of SCD-1 knockdown or overexpression on liver lipid metabolism in mice, which should be addressed in future studies.
Cholesterol 7α-hydroxylase CYP7A1 and cytochrome P 27A1 CYP27A1 , two important rate-limiting enzymes, play major roles in maintaining the balance of cholesterol and bile acid in the bile acid biosynthetic pathway in the liver The decrease in serum cholesterol is due to a decrease in its de novo synthesis in the liver and an increase in the conversion to bile acids.
LXRα , as nuclear receptors, regulates the transcription of CYP7A1 , which is related to regulation of cholesterol and bile acids metabolisms Our data showed that a HFD could downregulate LXRα , CYP7A1 , and CYP27A1 expression, while high-dose ATX supplementation could upregulate them, indicating that ATX could eliminate excess cholesterol in liver tissue by stimulating the conversion of cholesterol to bile acids.
Besides, the expression of CYP7A1 and CYP27A1 is regulated by the intestinal flora The characteristic role of diet in obesity and metabolic disorders is that diet has become an important factor in regulating the gut environment. Both long-term and short-term dietary interventions will induce changes in the structure and function of intestinal microbes Briefly, liver metabolites mainly affect the composition of gut microbes and the integrity of the intestinal barrier, while gut microbiota regulate the synthesis of bile acids, glucose and lipid metabolism in the liver Noticeably, many recent studies have shown that functional foods and natural health products, directly or indirectly, prevent obesity and metabolic diseases by improving intestinal diversity 25 , In the current study, mice fed a HFD exhibited lower diversity and gut microbiota disturbance; however, ATX had a salutary effect on promoting gut microbiota and improving diversity.
Moreover, the increase in Actinobacteria and Verrucomicrobia at the phylum level indicated that ATX effectively activated functional bacteria. Astaxanthin treatment had the greatest impact on Allobaculum and Akkermansia at the genus level.
The relative abundance of Allobaculum is associated with hormone secretion, SCFA production, serum HDL-C concentration, and intestinal barrier integrity, which is usually found in higher relative abundances in healthy individuals in prior studies 54 , In addition, Akkermansia , an intestinal symbiont colonizing the mucosal layer, is considered to be a functional probiotic that is closely related to fat increase, secondary bile acid biosynthesis and IR In this study, the relative abundance of Allobaculum and Akkermansia in the 0.
In addition, ATX significantly decreased the abundance of Desulfovibrio , a pathogenic bacterium that induces lipopolysaccharide Lactobacillus , Clostridum , and Bifidobacterium are closely associated with cholesterol metabolism, and the abundance of Bifidobacterium is positively correlated with the level of high-density lipoprotein HDL Surprisingly, further screening found that ATX, in contrast to chalk and cheese from our previous research, promoted Butyricimonas , Lactobacillus , Clostridum , and Bifidobacterium in the current results.
As the results shown, 0. Another interesting finding in this study was the promotion of Butyricimonas , a probiotic that produces butyric acid metabolites, after ATX supplementation, which contributed to alleviating systemic obesity and gut inflammation.
Moreover, butyrate can restore intestinal mucosal injury induced by a high-fat diet and reduce nonalcoholic steatohepatitis Thus, according to the increase in these functional probiotics, ATX supplementation could effectively prevent the microbial dysbiosis induced by HFD.
All in all, when compared to our previous study, we found that the preventive effect of ATX is better than its therapeutic effect whether from the physiological and biochemical level, from the metabolic level or from the multi-omics and pathological level.
In conclusion, the current study shows that ATX has a better preventive effect on the development of obesity and NAFLD induced by HFD when compared with prognosis treatment. Both physiological and biochemical profiles demonstrate that long-term consumption of ATX effectively prevents body weight gain, dyslipidaemia and abnormal liver function.
Subsequently, pathological analysis indicated that ATX relieves liver steatosis, as well as oxidative stress and apoptosis caused by excessive fatty acids. Moreover, ATX improves hepatic lipid metabolism and increases gut probiotics, confirming that some metabolites might be positively correlated with specific bacteria to maintain body health through the liver-gut axis.
This study provides scientific evidence for the functional effects of ATX on obesity prevention. However, our research still has some limitations.
Future studies should focus on verifying the role of different pathways in the regulation of lipid metabolism at the protein level and exploring the molecular mechanism of liver oxidative stress and apoptosis through fatty acids mediated by ATX.
The data presented in the study are deposited in the DRYAD repository, accession number: doi: The animal study was reviewed and approved by Institutional Animal Care and Use Committee of Shanxi Agricultural University.
MW and WX: conceptualization and methodology. MW, WX, JY, YL, CJ, CZ, JX, and RL: validation and investigation. MW: formal analysis, writing—original draft preparation, visualization, and project administration. HC: resources, writing—review, editing, supervision, and funding acquisition.
All authors have read and agreed to the published version of the manuscript. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.
Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Supplementary Figure 1 Evaluation of TUNEL reagent on cell apoptosis.
A The positive result of is indicated by the green marked spots in the sample. B Apoptosis rate of each treatment. Values are expressed as mean ± SD of triplicate. Supplementary Figure 2 The screened genes and Volcano plot of ND vs. Adaptive immune responses triggered by oxidative stress contribute to hepatic inflammation in NASH.
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For more information, please see our University Websites Privacy Notice. February 17, Sheila Foran - UConn Communications. A pigment that gives shrimp and flamingoes their color may help control and prevent non-alcoholic fatty liver disease.
A pigment known as astaxanthin, which gives shrimp and flamingoes their color, shows promise in the control and prevention of non-alcoholic fatty liver disease, a UConn nutritionist finds. Consider the bright plumage of the iconic flamingo. The rich color of a Sockeye salmon. The more subtle colors of cooked shrimp.
Their varying shades of pink come through the food chain starting with a substance called astaxanthin — a carotenoid pigment found in a type of algae called Haematococcus pluvialis.
And for Ji-Young Lee, associate professor in the Department of Nutritional Sciences, astaxanthin also plays a key role in her research on the control and prevention of non-alcoholic fatty liver disease NAFLD.
As NAFLD progresses, it moves from inflammation and the accumulation of scar tissue, called fibrosis, to the late-stage scarring of cirrhosis, which hardens tissue and prevents the liver from working properly.
Over time, the organ shuts down completely; in some cases, the disease is a precursor to cancer.
Our websites may use cookies Astaxanthln personalize and enhance your experience. Snd continuing Fat burner for toning changing your heatlh settings, Wild salmon preparation agree / Fasting and Emotional Well-being this collection. For more information, please see our University Websites Privacy Notice. February 17, Sheila Foran - UConn Communications. A pigment that gives shrimp and flamingoes their color may help control and prevent non-alcoholic fatty liver disease. A pigment known as astaxanthin, which gives shrimp and flamingoes their color, shows promise in the control and prevention of non-alcoholic fatty liver disease, a UConn nutritionist finds. Volume 8, Number 10, Octoberpages Astaxanthij as a Potential Protector of Wild salmon preparation Function: A Review. a Endurance training for rowers Wild salmon preparation Clinic, Tokyo, Japan b Division ,iver Community and Family Medicine, Anv Medical University, Tochigi, / Fasting and Emotional Well-being c Corresponding Author: Jui-Tung Chen, J. Chen Clinic, Akasaka, Akasaka-Kaikan B1F, Minato-Ku, TokyoJapan. Protecting against liver damage, such as non-alcoholic fatty liver disease, is currently considered to be important for the prevention of adverse conditions, such as cardiovascular and cancerous diseases. Liver damage often occurs in relation to oxidative stress with metabolic disorders, including cellular lipid accumulation. Here, we briefly review astaxanthin as a potential protector against liver damage.
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