Gut Microbiome and Metabolomics Study of Selenium-Enriched Kiwifruit Regulating Hyperlipidemia in Mice Induced by a High-Fat Diet

He, Kan; Gao, Qian; Su, Jinxing; Shang, Hai; Meng, Xia; Jiang, Shangquan; Liu, Dahai; Huang, Bei

doi:10.1021/acs.jafc.3c00108

Cited by 5 publications

(3 citation statements)

References 51 publications

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“…Selenium was able to maintain the anti-oxidative stress function of glutathione peroxidation and selenoprotein P ( 49 ). Guo et al ( 50 ) fed selenium nanoparticles (SeNPs) 50 μg/d in apolipoprotein E-deficient (ApoE) mice, and showed that it was able to alleviate hyperlipidemia in ApoE mice by regulating cholesterol metabolism through antioxidant selenoenzymes/selenoproteins and reducing oxidative stress, and additionally metabolomics selenium-enriched kiwifruit was also found to be able to treat hyperlipidemia ( 51 ). Carotenoids (Crt) act as antioxidants in lipid-rich environments ( 52 ), mainly through (i) electron transfer between free radicals (R-) and Crt, leading to the formation of Crt radical cation (Crt-+) or Crt radical anion (Crt-); and (ii) radical adducts (R-), leading to the formation of Crt radical cation (Crt-+) or Crt radical anion (Crt-).…”

Section: Discussionmentioning

confidence: 99%

Linear association of compound dietary antioxidant index with hyperlipidemia: a cross-sectional study

Zhou,

Li,

et al. 2024

Front. Nutr.

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BackgroundThere is growing evidence that antioxidant-rich diets may prevent hyperlipidemia. However, the relationship between the Composite Dietary Antioxidant Index (CDAI) and hyperlipidemia is unclear. The CDAI is a composite score reflecting the antioxidant content of an individual’s diet, and this study aimed to investigate the relationship between CDAI and hyperlipidemia.MethodsThe study used the 2003–2018 National Health and Nutrition Examination Survey (NHANES) database for cross-sectional analyses and included 27,626 participants aged 20 years and older. The CDAI, which includes vitamins A, C, and E, zinc, selenium, and carotenoids, was calculated based on dietary intake reported in a 24-h recall interview. Hyperlipidemia was defined by the National Cholesterol Education Program (NCEP). Covariates included age, sex, race, education, marriage, household poverty-to-income ratio (PIR), glomerular filtration rate (eGFR), body mass index (BMI), energy, carbohydrates, total fat, cholesterol, smoking, alcohol consumption, hypertension, diabetes mellitus, coronary heart disease, and lipid-lowering medications. The association between CDAI and hyperlipidemia was explored through multiple logistic regression analyses and smoothed curve fitting. We also performed subgroup analyses and interaction tests to verify the relationship’s stability.ResultsAfter adjusting for potential confounders, CDAI was negatively associated with the risk of developing hyperlipidemia (OR 0.98, 95% CI 0.96–0.99, p < 0.01). The results of weighted regression models stratified by quartiles of CDAI (−8.664 ≤ Q1 ≤ −2.209, −2.209 < Q2 ≤ −0.002, −0.002 < Q3 ≤ 2.774, 2.774 < Q4 ≤ 124.284), fully adjusted for confounding variables, indicated that compared with the bottom quartile (Q1) of the CDAI, Q2, Q3, and Q4 of participants had a lower advantage ratio (Q2: OR 0.91, 95% CI 0.78–1.06, p < 0.21; Q3: OR 0.85, 95% CI 0.73–1.00, p < 0.05; and Q4: OR 0.77, 95% CI 0.64–0.94, p < 0.01), which was confirmed by a test for trend (p < 0.05). Smoothed curve fit analysis showed linearity (p for non-linear = 0.0912). In summary, there is a linear negative relationship between CDAI and the risk of developing hyperlipidemia. Subgroup analyses by age, sex, ethnicity, education level, marriage, tobacco status, alcoholic drinking, body mass index (BMI), hypertension, and diabetes did not indicate strong interactions.ConclusionIn this large cross-sectional study, there was a linear negative association between CDAI and hyperlipidemia among US adults. Therefore increase antioxidant rich foods in your life as a prevention of hyperlipidemia.

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Section: Discussionmentioning

confidence: 99%

Linear association of compound dietary antioxidant index with hyperlipidemia: a cross-sectional study

Zhou,

Li,

et al. 2024

Front. Nutr.

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“…Dietary Zn, on the other hand, protects intestinal health by promoting intestinal mucosal integrity and enhancing proteins associated with barrier function (occludin and zonula occludens) [ 62 ]. He et al reported that Se-enriched kiwifruit significantly increased the abundance of beneficial bacteria in the intestine by regulating the digestion and absorption of metabolic pathways to maintain the health of mice [ 63 ]. Hou et al also noted that supplementation with high doses of Zn amino acids (120 mg/kg) enriched and regulated the balance of intestinal flora and promoted healthy growth of calves [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

Selenium- and/or Zinc-Enriched Egg Diet Improves Oxidative Damage and Regulates Gut Microbiota in D-Gal-Induced Aging Mice

Liu,

Wang,

Wan

et al. 2024

Nutrients

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Eggs, with their high nutritional value, are great carriers for enriching nutrients. In this study, selenium- and/or zinc-enriched eggs (SZE) were obtained and their effects on ameliorating oxidative stress injury, alleviating cognitive impairment, and maintaining intestinal flora balance in a D-gal-induced aging mice model were investigated. As determined by the Y-maze test, SZE restored the learning and memory abilities and increased the Ach level and AChE activity of aging mice (p < 0.05). Meanwhile, supplementation of low-dose SZE increased antioxidant levels and decreased inflammation levels (p < 0.05). High-dose SZE increased anti-inflammatory levels but were less effective than low dose. Additionally, SZE maintained the intestinal flora balance and significantly increased the ratio of Firmicutes and Bacteroidota. Blautia, as a probiotic, was negatively correlated with pro-inflammatory factors and positively correlated with antioxidant levels (p < 0.05). These results suggest that SZE might improve organ damage and cognitive function by attenuating oxidative stress and inflammatory response and maintaining healthy gut flora.

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“…Chronic nutrient overload, particularly high levels of dietary fat, is commonly attributed as the primary cause of imbalanced lipid metabolism. , Notably, dyslipidemia resulting from a high-fat diet (HFD) can lead to the accumulation of excessive lipids in non-adipose tissues, a condition known as ectopic lipid deposition (ELD) . Renal tubules, being energy-demanding and metabolically active, are susceptible to ELD, which can trigger lipotoxic damage to intrinsic renal tubular cells, compromising renal reabsorption and excretion. − Emerging studies have highlighted that renal tubular ELD is a common pathological feature of chronic kidney disease (CKD), which affects more than 850 million people globally and nearly one-third of the elderly, posing a serious threat to human health. , It is generally believed that the pathophysiology of renal tubular ELD is associated with maladaptive oxidative stress, excessive inflammatory responses, and aberrant lipid metabolism, but the underlying pathogenesis of renal tubular ELD is still not fully clear. , Lipogenesis and lipolysis are the main pathways involved in renal tubular lipid metabolism, where they play a crucial role in regulating the renal tubular lipid profile to maintain the normal physiological functions of the tubules .…”

Section: Introductionmentioning

confidence: 99%

Tea Polysaccharide Ameliorates High-Fat Diet-Induced Renal Tubular Ectopic Lipid Deposition via Regulating the Dynamic Balance of Lipogenesis and Lipolysis

Kuang,

Li,

Qian

et al. 2024

J. Agric. Food Chem.

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Renal tubular ectopic lipid deposition (ELD) plays a significant role in the development of chronic kidney disease, posing a great threat to human health. The present work aimed to explore the intervention effect and potential molecular mechanism of a purified tea polysaccharide (TPS3A) on renal tubular ELD. The results demonstrated that TPS3A effectively improved kidney function and slowed the progression of tubulointerstitial fibrosis in high-fat-diet (HFD)-exposed ApoE −/− mice. Additionally, TPS3A notably suppressed lipogenesis and enhanced lipolysis, as shown by the downregulation of lipogenesis markers (SREBP-1 and FAS) and the upregulation of lipolysis markers (HSL and ATGL), thereby reducing renal tubular ELD in HFD-fed ApoE −/− mice and palmitic-acid-stimulated HK-2 cells. The AMPK-SIRT1-FoxO1 axis is a core signal pathway in regulating lipid deposition. Consistently, TPS3A significantly increased the levels of phosphorylated-AMPK, SIRT1, and deacetylation of Ac-FoxO1. However, these effects of TPS3A on lipogenesis and lipolysis were abolished by AMPK siRNA, SIRT1 siRNA, and FoxO1 inhibitor, resulting in exacerbated lipid deposition. Taken together, TPS3A shows promise in ameliorating renal tubular ELD by inhibiting lipogenesis and promoting lipolysis through the AMPK-SIRT1-FoxO1 signaling pathway.

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Gut Microbiome and Metabolomics Study of Selenium-Enriched Kiwifruit Regulating Hyperlipidemia in Mice Induced by a High-Fat Diet

Cited by 5 publications

References 51 publications

Linear association of compound dietary antioxidant index with hyperlipidemia: a cross-sectional study

Linear association of compound dietary antioxidant index with hyperlipidemia: a cross-sectional study

Selenium- and/or Zinc-Enriched Egg Diet Improves Oxidative Damage and Regulates Gut Microbiota in D-Gal-Induced Aging Mice

Tea Polysaccharide Ameliorates High-Fat Diet-Induced Renal Tubular Ectopic Lipid Deposition via Regulating the Dynamic Balance of Lipogenesis and Lipolysis

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