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Title
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Combined consumption of beef-based cooked mince and sucrose stimulates oxidative stress, cardiac hypertrophy, and colonic outgrowth of desulfovibrionaceae in rats
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Author
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Abstract
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| Scope High consumption of red meat and sucrose increases the epidemiological risk for chronic diseases. Mechanistic hypotheses include alterations in oxidative status, gut microbial composition, fat deposition and low‐grade inflammation. Methods and results For two weeks, 40 rats consumed a diet high in white or red meat (chicken‐based or beef‐based cooked mince respectively), and containing corn starch or sucrose in a 2 × 2 factorial design. Lard was mixed with lean chicken or beef to obtain comparable dietary fatty acid profiles. Beef (vs. chicken)‐fed rats had higher lipid oxidation products (malondialdehyde, 4‐hydroxy‐2‐nonenal and hexanal) in stomach content and blood, and lower blood glutathione. Sucrose (vs. corn starch)‐fed rats showed increased blood lipid oxidation products and glutathione peroxidase activity, higher liver weight and malondialdehyde concentrations, and mesenterial and retroperitoneal fat accumulation. Beef‐sucrose‐fed rats had increased cardiac weight, suggesting pathophysiological effects on the cardiovascular system. The colonic microbiome of beef‐sucrose‐fed rats showed an outgrowth of the sulfate‐reducing family of the Desulfovibrionaceae, partly in expense of the Lactobacillus genus, indicating intestinal dysbiosis. Blood C‐reactive protein, a marker for inflammation, was not different among groups. Conclusions Consumption of a cooked beef‐based meat product with sucrose increased oxidative stress parameters and promoted cardiac hypertrophy and intestinal dysbiosis. |
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Language
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English
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Source (journal)
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Molecular nutrition and food research. - Weinheim
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Publication
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Weinheim
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2019
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ISSN
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1613-4125
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DOI
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10.1002/MNFR.201800962
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Volume/pages
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63
:2
(2019)
, 11 p.
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Article Reference
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1800962
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ISI
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000456706100004
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Pubmed ID
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30379400
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Medium
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E-only publicatie
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Full text (Publisher's DOI)
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Full text (open access)
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Full text (publisher's version - intranet only)
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