Background: Wine aged in oak barrels will incorporate polyphenols inherent in the staves, suggesting that wine stored in these wooden containers will introduce oak compounds into the human body after consumption.

Objective: The purpose of the present study is to test whether consumption of these oak compounds could favorably influence metabolism in mice fed an obesogenic diet.

Methods: C57BL/6  male mice ( = 8) were fed diets for 10 wk as follows: low-fat (LF), high-fat (HF), and HF containing 0.17% of oak tannin (HF+OT). A second 10-wk study was completed; mice were provided LF, HF, and HF diets supplemented with 7.0% of concentrates made from oaked wine (HF+OWC) or unoaked wine (HF+UWC). Physiological parameters were measured during the feeding trial and serum markers and hepatic gene expression measured from samples obtained at necropsy.

Results: Intake of HF+OT significantly reduced body-weight gain (18.4 ± 1.2 g in HF vs. 13.2 ± 1.4 g in HF+OT,  < 0.05). Serum resistin concentrations were lower in HF+OT mice compared with HF mice (301 ± 10.1 pg/mL in HF+OT vs. 374 ± 10.9 pg/mL in HF;  < 0.05). Hepatic lipid accumulation and expression of glutathione--transferase-m2 () and NAD(P)H:quinone oxidoreductase () mRNAs were significantly decreased in HF+OT compared with HF mice ( < 0.05). When compared with HF-fed mice, intake of both OWC and UWC decreased body-weight gain ( < 0.05), with no significant impact on food consumption. Fasting glucose concentrations, serum insulin, and hepatic lipid accumulation were reduced in HF+OWC-fed mice compared with HF+UWC-fed mice ( < 0.05). Furthermore, hepatic glutathione--transferase-a1 () mRNA levels were significantly reduced in OWC-supplemented (0.25 ± 0.08) compared with UWC-supplemented (1.71 ± 0.24) mice ( < 0.05).

Conclusions: In this mouse model of metabolic disease, intake of OTs and a concentrate made from an oaked wine had a potent impact on alleviating HF-induced metabolic syndrome. Thus, intake of OTs, provided passively in oaked wine or as a dietary supplement, may act as an agent to attenuate the markers of metabolic syndrome.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7101168PMC
http://dx.doi.org/10.1093/cdn/nzaa033DOI Listing

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