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Ameliorative effects of functional crude-chalaza hydrolysates on the hepatosteatosis development induced by a high-fat diet.

ABSTRACT: Approximately 400 metric tons of egg chalazae, a byproduct in the liquid-egg processing plant, are produced yearly but always regarded as a waste in Taiwan. Our team successfully developed a crude egg chalaza hydrolysate by protease-A digestion (CCH-A). Free branched-chain amino acids, 3-aminoisobutyric acid, and β-alanine, and anserine were assayed in the CCH-A used in this study. Besides, the in vitro bile-acid binding ability and inhibitory lipase activity of CCH-As were demonstrated. Then, high-fat diet feeding for 10 wk caused hyperlipidemia, insulin resistance, and hepatosteatosis in hamsters (P < 0.05). However, CCH-A co-treatment decreased serum/liver triglyceride levels and lipid accumulation in livers by increasing daily fecal lipid/bile-acid outputs, upregulating fatty-acid β oxidation, and downregulating fatty-acid biosynthesis in livers (P < 0.05). CCH-A co-treatment also amended insulin resistance, augmented hepatic antioxidant capacity, and decreased liver damages and inflammatory responses (P < 0.05). Taken together, our results do not only demonstrate the hepatoprotective effects of CCH-As against a chronic high-fat dietary habit, achieving effects similar to Simvastatin, but also decrease the environmental burden of handling chalazae in the liquid-egg industry.

SUBMITTER: Chen JW

PROVIDER: S-EPMC7921881 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature

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Ameliorative effects of functional crude-chalaza hydrolysates on the hepatosteatosis development induced by a high-fat diet.

Chen Jr-Wei JW Lin Yi-Ling YL Samuel Wu Yi-Hsieng YH Wang Sheng-Yao SY Chou Chung-Hsi CH Chen Yi-Chen YC

Poultry science 20210120 4

Approximately 400 metric tons of egg chalazae, a byproduct in the liquid-egg processing plant, are produced yearly but always regarded as a waste in Taiwan. Our team successfully developed a crude egg chalaza hydrolysate by protease-A digestion (CCH-A). Free branched-chain amino acids, 3-aminoisobutyric acid, and β-alanine, and anserine were assayed in the CCH-A used in this study. Besides, the in vitro bile-acid binding ability and inhibitory lipase activity of CCH-As were demonstrated. Then, h ...[more]

PMID: 33647717

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Project description:IntroductionEpidemiological studies linking dietary fat intake and obesity to breast cancer risk have produced inconsistent results. This may be due to the difficulty of dissociating fat intake from obesity, and/or the lack of defined periods of exposure in these studies. The pubertal mammary gland is highly sensitive to cancer-causing agents. We assessed how high fat diet (HFD) affects inflammation, proliferative, and developmental events in the pubertal gland, since dysregulation of these can promote mammary tumorigenesis. To test the effect of HFD initiated during puberty on tumorigenesis, we utilized BALB/c mice, for which HFD neither induces obesity nor metabolic syndrome, allowing dissociation of HFD effects from other conditions associated with HFD.MethodsPubertal BALB/c mice were fed a low fat diet (12% kcal fat) or a HFD (60% kcal fat), and subjected to carcinogen 7,12-dimethylbenz[a]anthracene (DMBA)-induced tumorigenesis.ResultsHFD elevated mammary gland expression of inflammatory and growth factor genes at 3 and 4 weeks of diet. Receptor activator of nuclear factor kappa-B ligand (RANKL), robustly induced at 4 weeks, has direct mitogenic activity in mammary epithelial cells and, as a potent inducer of NF-?B activity, may induce inflammatory genes. Three weeks of HFD induced a transient influx of eosinophils into the mammary gland, consistent with elevated inflammatory factors. At 10 weeks, prior to the appearance of palpable tumors, there were increased numbers of abnormal mammary epithelial lesions, enhanced cellular proliferation, increased growth factors, chemokines associated with immune-suppressive regulatory T cells, increased vascularization, and elevated M2 macrophages. HFD dramatically reduced tumor latency. Early developing tumors were more proliferative and were associated with increased levels of tumor-related growth factors, including increased plasma levels of HGF in tumor-bearing animals. Early HFD tumors also had increased vascularization, and more intra-tumor and stromal M2 macrophages.ConclusionsTaken together in this non-obesogenic context, HFD promotion of inflammatory processes, as well as local and systemically increased growth factor expression, are likely responsible for the enhanced tumorigenesis. It is noteworthy that although DMBA mutagenesis is virtually random in its targeting of genes in tumorigenesis, the short latency tumors arising in animals on HFD showed a unique gene expression profile, highlighting the potent overarching influence of HFD.

Project description:BACKGROUNDS:The incidence of nonalcoholic fatty liver disease (NAFLD) is rapidly increasing due to the prevalence of obesity. NAFLD is a major risk factor of hepatocellular carcinoma (HCC). Even with successful surgical removal, the presence of NAFLD is associated with an increased recurrence of HCC. Despite the extensive study of NAFLD, its underlying mechanism(s) remains essentially unknown and there are no FDA-approved drugs for its treatment. Alterations in microRNA (miR) expression have been observed in human fatty livers. However, regulatory mechanism(s) of miRNA biogenesis and their role in regulating the development of NAFLD is poorly described. METHODS:We used immunohistochemistry, luciferase assays and immunoblotting to study the regulatory mechanism of miR-378 biogenesis. Wild-type mice kept on a high fat diet (HFD) were injected with miR-378 inhibitors or a mini-circle expression system containing miR-378 to study loss and gain-of functions of miR-378. RESULTS:miR-378 was significantly increased in fatty livers of dietary obese mice and human hepatoma HepG2 cells with accumulated lipid. Further studies identified NRF1 (Nuclear receptor factor 1), a key regulator of fatty acid oxidation (FAO), as a direct target of miR-378. Overexpression of miR-378 impaired FAO and promoted lipid accumulation in murine hepatoma Hepa1-6 cells. In contrast, knockdown of miR-378 using its ASO (anti-sense oligo) improved FAO and reduced intracellular lipid content in Hepa1-6 cells. Liver-specific expression of miR-378 impaired FAO, which subsequently promoted the development of hepatosteatosis. Antagonizing miR-378 via injecting miR-378-ASO into HFD-treated mice led to increased expression of Nrf1, improved FAO and decreased hepatosteatosis. Additional knockdown of up-regulated Nrf1 offset the effects of miR-378-ASO, suggesting that Nrf1 mediated the inhibitory effect of miR-378-ASO on hepatosteatosis. Furthermore, Nrf1 was identified as a transcriptional repressor of miR-378. Ablation of Nrf1 using its shRNA in livers led to increased miR-378, which subsequently resulted in reduced FAO and elevated hepatic lipid content. CONCLUSIONS:These findings identified a negative feedback loop between miR-378 and Nrf1 that promotes the pathogenesis of hepatosteatosis, and suggests the use of miR-378 as a potential therapeutic target for NAFLD.

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Ameliorative effects of functional crude-chalaza hydrolysates on the hepatosteatosis development induced by a high-fat diet.

Publications

Ameliorative effects of functional crude-chalaza hydrolysates on the hepatosteatosis development induced by a high-fat diet.

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