Lycopene ameliorates systemic inflammation-induced synaptic dysfunction <i>via</i> improving insulin resistance and mitochondrial dysfunction in the liver–brain axis

Wang, Jia; Zou, Qianhui; Suo, Yao; Tan, Xiao Di; Tian, Yuan; Liu, Zhigang; Liu, Xuebo

doi:10.1039/c8fo02460j

Cited by 45 publications

(25 citation statements)

References 57 publications

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“…[54] LPS-induced neuroinflammation was reported to cause cognitive impairment and nervous-system damage in mice. [55] Interestingly, the mRNA expression fluctuations of Bdnf and inflammatory cytokines showed almost opposite trends under HFD, which suggests that inflammatory cytokines could represent a major factor related to the decrease of Bdnf levels. Furthermore, HFD induces inflammation in the central nervous system, which further leads to cognitive impairments and decreases the expression of PSD-95 and BDNF.…”

Section: Discussionmentioning

confidence: 98%

Methionine Restriction Regulates Cognitive Function in High‐Fat Diet‐Fed Mice: Roles of Diurnal Rhythms of SCFAs Producing‐ and Inflammation‐Related Microbes

Wang

Ren

Hui

et al. 2020

Molecular Nutrition Food Res

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Scope Methionine restriction (MR) is known to potently alleviate inflammation and improve gut microbiome in obese mice. The gut microbiome exhibits diurnal rhythmicity in composition and function, and this, in turn, drives oscillations in host metabolism. High‐fat diet (HFD) strongly altered microbiome diurnal rhythmicity, however, the role of microbiome diurnal rhythmicity in mediating the improvement effects of MR on obesity‐related metabolic disorders remains unclear. Methods and results 10‐week‐old male C57BL/6J mice are fed a low‐fat diet or HFD for 4 weeks, followed with a full diet (0.86% methionine, w/w) or a methionine‐restricted diet (0.17% methionine, w/w) for 8 weeks. Analyzing microbiome diurnal rhythmicity at six time points, the results show that HFD disrupts the cyclical fluctuations of the gut microbiome in mice. MR partially restores these cyclical fluctuations, which lead to time‐specifically enhance the abundance of short‐chain fatty acids producing bacteria, increases the acetate and butyric, and dampens the oscillation of inflammation‐related Desulfovibrionales and Staphylococcaceae over the course of 1 day. Notably, MR, which protects against systemic inflammation, influences brain function and synaptic plasticity. Conclusion MR could serve as a potential nutritional intervention for attenuating obesity‐induced cognitive impairments by balancing the circadian rhythm in microbiome‐gut‐brain homeostasis.

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Section: Discussionmentioning

confidence: 98%

Methionine Restriction Regulates Cognitive Function in High‐Fat Diet‐Fed Mice: Roles of Diurnal Rhythms of SCFAs Producing‐ and Inflammation‐Related Microbes

Wang

Ren

Hui

et al. 2020

Molecular Nutrition Food Res

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“…Conversely, a number of NRF2-activating compounds have shown beneficial effects in MS model systems. NRF2 activation by resveratrol, lycopene, quercetin, and ferulic acid has been shown to reduce LPS-induced neurotoxicity, improve synaptic and mitochondrial function, and reduce inflammatory markers as well as gliosis (Chen et al., 2017; Khan et al., 2018; Rehman et al., 2019; Wang et al., 2019). In the EAE model, DMF treatment increased NRF2 activation in neurons and glial cells and improved disease score ratings, an effect that was lost with NRF2 deletion (Linker et al., 2011).…”

Section: Nrf2 and Msmentioning

confidence: 99%

NRF2 as a Therapeutic Target in Neurodegenerative Diseases

2020

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Increased reactive oxygen species production and oxidative stress have been implicated in the pathogenesis of numerous neurodegenerative conditions including among others Alzheimer's disease, Parkinson's disease, Huntington's disease, Friedrich's ataxia, multiple sclerosis, and stroke. The endogenous antioxidant response pathway protects cells from oxidative stress by increasing the expression of cytoprotective enzymes and is regulated by the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2). In addition to regulating the expression of antioxidant genes, NRF2 has also been shown to exert anti-inflammatory effects and modulate both mitochondrial function and biogenesis. This is because mitochondrial dysfunction and neuroinflammation are features of many neurodegenerative diseases as well NRF2 has emerged as a promising therapeutic target. Here, we review evidence for a beneficial role of NRF2 in neurodegenerative conditions and the potential of specific NRF2 activators as therapeutic agents.

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“…In the initial study, a decreased number of mitochondria have been found in insulin-resistant skeletal muscle cells, suggesting that mitochondrial function is impaired in insulin-resistant skeletal muscle cells (Perreault et al, 2018). As research progresses, hepatic fatty acid–induced mitochondrial dysfunction has also been proved to play an important role in the development of hepatic insulin resistance (Wang et al, 2017b; Wang et al, 2018; Wang et al, 2019b). Recently, it has been widely recognized that mitochondrial autophagy (mitophagy), a catabolic process, can selectively remove damaged mitochondria by autophagolysosomes to maintain mitochondrial function and energy metabolism (Redmann et al, 2018; Li et al, 2018a).…”

Section: Introductionmentioning

confidence: 99%

Mitophagy in Hepatic Insulin Resistance: Therapeutic Potential and Concerns

Nie

Huang

et al. 2019

Front. Pharmacol.

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Metabolic syndrome, characterized by central obesity, hypertension, and hyperlipidemia, increases the morbidity and mortality of cardiovascular disease, type 2 diabetes, nonalcoholic fatty liver disease, and other metabolic diseases. It is well known that insulin resistance, especially hepatic insulin resistance, is a risk factor for metabolic syndrome. Current research has shown that hepatic fatty acid accumulation can cause hepatic insulin resistance through increased gluconeogenesis, lipogenesis, chronic inflammation, oxidative stress and endoplasmic reticulum stress, and impaired insulin signal pathway. Mitochondria are the major sites of fatty acid β-oxidation, which is the major degradation mechanism of fatty acids. Mitochondrial dysfunction has been shown to be involved in the development of hepatic fatty acid–induced hepatic insulin resistance. Mitochondrial autophagy (mitophagy), a catabolic process, selectively degrades damaged mitochondria to reverse mitochondrial dysfunction and preserve mitochondrial dynamics and function. Therefore, mitophagy can promote mitochondrial fatty acid oxidation to inhibit hepatic fatty acid accumulation and improve hepatic insulin resistance. Here, we review advances in our understanding of the relationship between mitophagy and hepatic insulin resistance. Additionally, we also highlight the potential value of mitophagy in the treatment of hepatic insulin resistance and metabolic syndrome.

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Lycopene ameliorates systemic inflammation-induced synaptic dysfunction via improving insulin resistance and mitochondrial dysfunction in the liver–brain axis

Abstract: Lycopene supplementation effectively attenuated systemic inflammation-induced synaptic dysfunction through ameliorating insulin resistance, mitochondrial dysfunction and inflammatory response in the mouse liver–brain axis.

Cited by 45 publications

References 57 publications

Methionine Restriction Regulates Cognitive Function in High‐Fat Diet‐Fed Mice: Roles of Diurnal Rhythms of SCFAs Producing‐ and Inflammation‐Related Microbes

Methionine Restriction Regulates Cognitive Function in High‐Fat Diet‐Fed Mice: Roles of Diurnal Rhythms of SCFAs Producing‐ and Inflammation‐Related Microbes

NRF2 as a Therapeutic Target in Neurodegenerative Diseases

Mitophagy in Hepatic Insulin Resistance: Therapeutic Potential and Concerns

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