2019
DOI: 10.1016/j.freeradbiomed.2019.07.002
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Hydroxytyrosol prevents PM2.5-induced adiposity and insulin resistance by restraining oxidative stress related NF-κB pathway and modulation of gut microbiota in a murine model

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Cited by 59 publications
(51 citation statements)
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“…These mediators enhance the expression of thermogenic markers that stimulate mitochondrial FAO and energy expenditure, pointing to BAT as a crucial anti-obesity target [ 43 ]. This contention is further supported by data showing that HT prevents visceral adipogenesis and decreased metabolic activity in BAT and WAT, induced by the exposure to fine particulate matter in mice [ 44 ]. The contribution of EPA to the induction of a healthy adipocyte phenotype may also involve its direct binding to PPAR-γ, whose expression and activity are diminished by HFD and partially rescued by EPA.…”
Section: Discussionmentioning
confidence: 70%
See 1 more Smart Citation
“…These mediators enhance the expression of thermogenic markers that stimulate mitochondrial FAO and energy expenditure, pointing to BAT as a crucial anti-obesity target [ 43 ]. This contention is further supported by data showing that HT prevents visceral adipogenesis and decreased metabolic activity in BAT and WAT, induced by the exposure to fine particulate matter in mice [ 44 ]. The contribution of EPA to the induction of a healthy adipocyte phenotype may also involve its direct binding to PPAR-γ, whose expression and activity are diminished by HFD and partially rescued by EPA.…”
Section: Discussionmentioning
confidence: 70%
“…The EPA plus HT protocol also improved the pro-inflammatory status of WAT in HFD-fed mice in an additive manner. Possible mechanisms involved include: (i) disruption of the SFA inflammatory signal in Toll-like receptor 4 that activate NF-κB, (ii) PPAR-γ activation that interferes with the translocation of NF-κB to the nucleus, (iii) binding to GPR120 and prevention of NF-κB activation, (iv) decreased pro-inflammatory adipokine expression and macrophage accumulation, promoting repolarization towards the M2 anti-inflammatory phenotype by SPMs [ 9 , 66 , 67 ] and (v) preservation of WAT n-3 LCPUFAs and downregulation of NF-κB by HT [ 13 , 44 ].…”
Section: Discussionmentioning
confidence: 99%
“…Research has shown 4-Hydroxytyrosol to be beneficial for metabolic and cardiovascular disorders. It also reduces liver and serum 4-HNE levels and alleviates PM 2.5 -induced, adiposity, and insulin resistance in adult female C57BL/6j mice by mitigating oxidative stress as well as restraining NF-κB activation and gut microbiota [111]. Additionally, there is evidence that 4-hydroxytyrosol significantly reduces 4-HNE expression in red blood cells from hyperlipemic patients and protects red blood cells against 4-HNE toxicity [112].…”
Section: Improvement Of Energy Metabolism Disordermentioning
confidence: 99%
“…The main MUFA in OO, oleic acid, is more resistant to oxidation than PUFAs. Phenolic compounds also show substantial antioxidant capacity [ 73 , 74 , 75 ], as is the case of HxT, which has demonstrated remarkable antioxidant potential in both in vitro and animal experiments—for a review, see [ 67 , 76 , 77 ]—as well as in healthy volunteers [ 78 ]. The free radical scavenging potential of HxT has been recognized by the European Food Safety Authority [ 79 ].…”
Section: Effect On General Mechanisms Of Diseasementioning
confidence: 99%
“…There are a wealth of experimental studies, principally with cell cultures or rodent models, showing a role for polyphenols, mainly HxT, in improving MetS features [ 96 , 97 ], including some key ones such as adiposity and insulin resistance [ 77 ].…”
Section: Impact On Metabolic Syndrome and Its Componentsmentioning
confidence: 99%