Abstract:We isolated and characterized tilapia-head chondroitin sulfate (TH-CS) and explored its biological activity and mechanisms of action as an oral supplement for nonalcoholic fatty liver disease (NAFLD) induced by a high-fat diet (HFD) in mice. The results showed that treatment with TH-CS for 8 weeks alleviated the development of NAFLD, as evidenced by the notable improvement in liver damage, blood lipid accumulation and insulin resistance (IR). Meanwhile, TH-CS treatment reduced the expression of proinflammatory… Show more
“…These results suggest that the increased liver weights and macrovesicular fatty change of the hepatocytes in the HFrD group were caused by the accumulation of triglycerides in the liver. In other words, the daily consumption of excessive fructose for 4 weeks induced a typical NAFLD-like situation, as seen in other reports (12,33,34). In this study, periportal vacuolation in the hepatocytes was observed in the HFrD group after 4-weeks consumption (Table II).…”
Background/Aim: The habitual consumption of excessive fructose is associated with the onset and progression of lifestyle-related diseases, such as nonalcoholic fatty liver disease (NAFLD). In this study, we investigated the physiological changes observed when consuming a diet containing excessive fructose on the viewpoints of hepatotoxicity biological markers using a rat model and explored the biomarker candidates that could detect the effects of excessive fructose intake at an early stage. Materials and Methods: Male rats were fed 63% high fructose diet (HFrD) ad libitum and their blood samples were collected before and at 1, 2, 3, and 4 weeks after allocation. The plasma biochemical parameters, hepatotoxic enzyme activities including alkaline phosphatase (ALP) isozymes were analyzed. Results: HFrD consumption for 4-weeks created NAFLD-like symptoms, including elevated plasma lipid parameters and hepatotoxicity markers, as well as fat accumulation in the liver compared with rats consuming a control diet. Alanine aminotransferase (ALT) and glutamate dehydrogenase (GLDH) were increased from the 3 rd and 2 nd weeks, respectively, but no changes were observed on ALP activity. However, the daily consumption of the HFrD increased the plasma activities of liver-type ALP isozyme, and decreased plasma small intestinaltype ALP isozyme soon after the start of feeding. Conclusion: ALP isozyme analysis in combination with GLDH and ALT activities in the plasma samples could be a useful tool to detect the physiological changes induced by excessive fructose intake at an early stage of the development of NAFLD.
“…These results suggest that the increased liver weights and macrovesicular fatty change of the hepatocytes in the HFrD group were caused by the accumulation of triglycerides in the liver. In other words, the daily consumption of excessive fructose for 4 weeks induced a typical NAFLD-like situation, as seen in other reports (12,33,34). In this study, periportal vacuolation in the hepatocytes was observed in the HFrD group after 4-weeks consumption (Table II).…”
Background/Aim: The habitual consumption of excessive fructose is associated with the onset and progression of lifestyle-related diseases, such as nonalcoholic fatty liver disease (NAFLD). In this study, we investigated the physiological changes observed when consuming a diet containing excessive fructose on the viewpoints of hepatotoxicity biological markers using a rat model and explored the biomarker candidates that could detect the effects of excessive fructose intake at an early stage. Materials and Methods: Male rats were fed 63% high fructose diet (HFrD) ad libitum and their blood samples were collected before and at 1, 2, 3, and 4 weeks after allocation. The plasma biochemical parameters, hepatotoxic enzyme activities including alkaline phosphatase (ALP) isozymes were analyzed. Results: HFrD consumption for 4-weeks created NAFLD-like symptoms, including elevated plasma lipid parameters and hepatotoxicity markers, as well as fat accumulation in the liver compared with rats consuming a control diet. Alanine aminotransferase (ALT) and glutamate dehydrogenase (GLDH) were increased from the 3 rd and 2 nd weeks, respectively, but no changes were observed on ALP activity. However, the daily consumption of the HFrD increased the plasma activities of liver-type ALP isozyme, and decreased plasma small intestinaltype ALP isozyme soon after the start of feeding. Conclusion: ALP isozyme analysis in combination with GLDH and ALT activities in the plasma samples could be a useful tool to detect the physiological changes induced by excessive fructose intake at an early stage of the development of NAFLD.
“…AMPK serves as a regulator for both anabolic and catabolic pathways. Activated AMPK decreases lipogenesis in the liver by inhibiting SREBP-1c expression [49,50]. PPAR-α is a nuclear hormone receptor involved in the regulation of lipid metabolism and inflammation.…”
Food-borne bioactive peptides have shown promise in preventing and mitigating alcohol-induced liver injury. This study was the first to assess the novel properties of Mactra chinenesis peptides (MCPs) in mitigating acute alcoholic liver injury in mice, and further elucidated the underlying mechanisms associated with this effect. The results showed that MCPs can improve lipid metabolism by modulating the AMPK signaling pathway, decreasing fatty acid synthase activity, and increasing carnitine palmitoyltransferase 1a activity. Meanwhile, MCPs ameliorate inflammation by inhibiting the NF-κB activation, leading to reduced levels of pro-inflammatory cytokines (tumor necrosis factor-α and interleukin-1β). Additionally, a 16S rDNA sequencing analysis revealed that MCPs can restore the balance of gut microbiota and increase the relative abundance of beneficial bacteria. These findings suggest that supplementation of MCPs could attenuate alcohol intake-induced acute liver injury, and, thus, may be utilized as a functional dietary supplement for the successful treatment and prevention of acute liver injury.
“…Western blotting analysis was performed based on previous study 29 . The total protein concentration in the supernatant of mice brain tissue homogenates was quantified using the BCA protein assay kit (Jiancheng Bioengineering Institute, Nanjing, China).…”
Section: Methodsmentioning
confidence: 99%
“…Western blotting analysis was performed based on previous study. 29 The total protein concentration in the supernatant of mice brain tissue homogenates was quantified using the BCA protein assay kit (Jiancheng Bioengineering Institute, Nanjing, China). An equal amount of denatured protein from each brain tissue sample was separated by sodium dodecyl sulfate polyacrylamide-gel electrophoresis and transferred to polyvinylidene fluoride membranes.…”
BackgroundCognitive impairment (CI) is a significant public health concern, and bioactive peptides have shown potential as therapeutic agents. However, information about their synergistic effects on cognitive function is still limited. Here, we investigated the synergistic effects of Tilapia Head Protein Hydrolysate (THPH) and Walnut Protein Hydrolysate (WPH) in mitigating CI induced by scopolamine in mice.ResultsThe results showed that the combined supplementation of THPH and WPH (mass ratio, 1:1) was superior to either individual supplement in enhancing spatial memory and object recognition abilities in CI mice, and significantly lessened brain injury in CI mice by alleviating neuronal damage, reducing oxidative stress, and stabilizing the cholinergic system. In addition, the combined supplementation was found to be more conducive to remodeling the gut microbiota structure in CI mice, not only remarkably reducing the ratio of Firmicutes to Bacteroidota, but specifically enriching the genus Roseburia. On the other hand, the combined supplementation regulated the disorders of sphingolipid and amino acid metabolism in CI mice, particularly upregulating glutathione and histidine metabolism, and displayed a stronger ability to increase the expression of genes and proteins related to the BDNF/TrkB/CrEB signaling pathway in the brain.ConclusionThese findings demonstrated that tilapia head and walnut‐derived protein hydrolysates exerted synergistic effects in ameliorating CI, which was achieved through modulation of gut microbiota, serum metabolic pathways, and BDNF signaling pathways.This article is protected by copyright. All rights reserved.
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