Abstract
PurposeExtra virgin olive oil (EVOO) and flaxseed oil (FO) contain a variety of constituents beneficial for chronic inflammation and cardio-metabolic derangement. However, little is known about the impact of EVOO and FO on dysbiosis of gut microbiota, intestinal immunity, and barrier. We, therefore, aimed to assess the impact of EVOO and FO on gut microbiota, mucosal immunity, barrier integrity, and metabolic health in mice.MethodsC57BL/6 J mice were exposed to a low-fat (LF), lard (HF), high fat-extra virgin olive oil (HF-EVOO), or high fat-flaxseed oil (HF-FO) diet for 10 weeks. Gut microbiota assessment was undertaken using 16S rRNA sequencing. Levels of mRNA for genes involved in intestinal inflammation and barrier maintenance in the intestine and bacterial infiltration in the liver were measured by qPCR.ResultsHF-EVOO or HF-FO mice showed greater diversity in gut microbiota as well as a lower abundance of the Firmicutes phylum in comparison with HF mice (P < 0.05). The qPCR analyses revealed that mRNA level of FoxP3, a transcription factor, and IL-10, an inducer of regulatory T cells, was significantly elevated in the intestines of mice-fed HF-EVOO in comparison with mice-fed HF (P < 0.05). The mRNA level of the antimicrobial peptide, RegӀӀӀγ, was markedly elevated in the intestines of HF-EVOO and HF-FO compared with HF group (P < 0.05).ConclusionsOur data suggest that the consumption of EVOO or FO can beneficially impact gut microbiota, enhance gut immunity, and assist in the preservation of metabolic health in mice.
Highlights
Metabolic health can be described as the body’s ability to successfully balance fuel oxidation and fuel availability in an endocrine-influenced environment [1]
The present study clearly demonstrates that mice-fed HFEVOO and HF-flaxseed oil (FO) exhibited a variety of beneficial effects on markers of health
HF-Extra virgin olive oil (EVOO)- and HFFO-fed mice exemplified a significantly positive impact on blood glucose compared to HF-fed mice
Summary
Metabolic health can be described as the body’s ability to successfully balance fuel oxidation and fuel availability in an endocrine-influenced environment [1]. Low-grade, sustained systemic inflammation, considered to lie at the heart of metabolic dysfunction, is strongly linked to the consumption of obesogenic diets high in pro-inflammatory-saturated fats [2, 3]. Chronic intake of diets high in saturated fats leads to inevitable weight gain, but can compromise intestinal barrier function, causing metabolic endotoxemia, inducing systemic inflammation partly through toll-like receptor (TLR) signaling [4]. A number of mechanisms employed by the mucosal immune system aim to assist in the protection of gut barrier and preservation of host defense. The adaptive immune system plays a fundamental role in modulating the local gut environment and composition of microbiota, with key players such as intestinal regulatory T (Treg) cells, aiding mucosal tolerance, and enforcing commensalism [6, 7]
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