Resveratrol protects against hepatic insulin resistance in a rat's model of non‐alcoholic fatty liver disease by down‐regulation of <scp>GPAT</scp>‐1 and <scp>DGAT</scp>2 expression and inhibition of <scp>PKC</scp> membranous translocation

Badi, Rehab M.; Mostafa, Dalia G.; Khaleel, Eman F.; Satti, Huda H.

doi:10.1111/1440-1681.13074

Cited by 18 publications

(10 citation statements)

References 31 publications

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“…HFD feeding for six weeks induced a significant increase of both body weight gain, in accordance to juvenile obesity development, and biochemical parameters such as ALT and LDL, suggesting altogether an induced metabolic alteration in concordance with our previous results [ 24 ]. Besides, HFD diet group presented a remarkable increase in plasma insulin concentration and HOMA-IR index, which is closely linked to hepatic insulin resistance in NAFLD [ 37 ]. Additionally, HFD feeding also induced a gut microbiota imbalance at all taxonomic levels.…”

Section: Discussionmentioning

confidence: 99%

The Synbiotic Combination of Akkermansia muciniphila and Quercetin Ameliorates Early Obesity and NAFLD through Gut Microbiota Reshaping and Bile Acid Metabolism Modulation

et al. 2021

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Gut microbiota plays a key role in obesity and non-alcoholic fatty liver disease (NAFLD), so synbiotics could be a therapeutic alternative. We aim to evaluate a nutritional intervention together with the administration of the bacteria Akkermansia muciniphila and the antioxidant quercetin in an in vivo model of early obesity and NAFLD. 21-day-old rats were fed with control or high-fat diet for six weeks. Then, all animals received control diet supplemented with/without quercetin and/or A. muciniphila for three weeks. Gut microbiota, NAFLD-related parameters, circulating bile acids (BAs) and liver gene expression were analyzed. The colonization with A. muciniphila was associated with less body fat, while synbiotic treatment caused a steatosis remission, linked to hepatic lipogenesis modulation. The synbiotic promoted higher abundance of Cyanobacteria and Oscillospira, and lower levels of Actinobacteria, Lactococcus, Lactobacillus and Roseburia. Moreover, it favored elevated unconjugated hydrophilic BAs plasma levels and enhanced hepatic expression of BA synthesis and transport genes. A. muciniphila correlated with circulating BAs and liver lipid and BA metabolism genes, suggesting a role of this bacterium in BA signaling. Beneficial effects of A. muciniphila and quercetin combination are driven by gut microbiota modulation, the shift in BAs and the gut-liver bile flow enhancement.

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Section: Discussionmentioning

confidence: 99%

The Synbiotic Combination of Akkermansia muciniphila and Quercetin Ameliorates Early Obesity and NAFLD through Gut Microbiota Reshaping and Bile Acid Metabolism Modulation

et al. 2021

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“…Accumulating evidence has demonstrated that hepatic insulin resistance is the primary event in free fatty acid–induced whole-body insulin resistance. And muscle and adipose tissue insulin resistance may be the consequence of hepatic insulin resistance (Perry et al, 2014; Badi et al, 2019; Medak and Townsend, 2019). Recent evidence has shown that muscle- and adipose tissue–specific IR knockout mice only show muscle or adipose tissue insulin resistance, but total body glucose metabolism still remains normal (Perseghin, 2009).…”

Section: The Liver Is the First Organ To Develop Insulin Resistancementioning

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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“…However, subsequent gene deletion studies have shown that the formation of MPTP does not require ANT and VDAC, partly due to the presence of different subtypes of these putative pore components. Despite these observations, it is generally believed that Cyp-D is the main factor in the formation of MPTP (Zhou et al, 2019;Badi et al, 2019;Medak & Townsend, 2019).…”

Section: Discussionmentioning

confidence: 99%

Study on the protective effect of Lycopene on ischemia-reperfusion myocardium through Inhibiting the opening of mitochondrial MPTP and the activation of apoptotic pathway

Wang

Chen

2022

Food Sci. Technol

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Through in vitro experiments, the paper investigated whether Lycopene can mitigate cardiac ischemia/reperfusion injury, and further explored whether the underlying mechanism works by inhibiting the opening of MPTP.A hypoxia-reoxygenation model was established. CCK8 was employed to determine the viability of H9c2 cardiomyocytes. LDH was used to determine the degree of damage of H9c2 cardiomyocytes. Trypan blue staining was applied to determine the survival rate of H9c2 cardiomyocytes. Flow cytometry was used to determine the apoptosis rate of H9c2 cardiomyocytes. Rhodamine 123 staining method was applied to evaluate the changes of mitochondrial membrane potential of H9c2 cardiomyocytes. Western blot was employed to determine the protein expressions of related factors of MPTP downstream apoptosis pathway in H9c2 cardiomyocytes. Calcium induction method was used to evaluate the opening degree of MPTP of H9c2 cardiomyocytes. Western blot was applied to determine the protein expressions of the related factors regulating MPTP opening in H9c2 cardiomyocytes.The vitality of H9c2 cardiomyocytes in the Lycopene group was significantly improved, the LDH activity was significantly reduced, and the cell survival rate was significantly improved. The apoptosis rate was significantly reduced, and the membrane potential decreased significantly. The expression levels of Bax, cytochrome C, APAF-1, caspase 9 and caspase-3 proteins were significantly reduced. The sensitivity of MPTP opening was significantly decreased. Lycopene can effectively alleviate the hypoxia/reoxygenation injury of H9c2 cardiomyocytes. By up-regulating Bcl-2 and down-regulating Bax, Lycopene can inhibit the opening of mitochondrial MPTP and the activation of downstream apoptotic pathways, thereby reducing apoptosis.

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Resveratrol protects against hepatic insulin resistance in a rat's model of non‐alcoholic fatty liver disease by down‐regulation of GPAT‐1 and DGAT2 expression and inhibition of PKC membranous translocation

Cited by 18 publications

References 31 publications

The Synbiotic Combination of Akkermansia muciniphila and Quercetin Ameliorates Early Obesity and NAFLD through Gut Microbiota Reshaping and Bile Acid Metabolism Modulation

The Synbiotic Combination of Akkermansia muciniphila and Quercetin Ameliorates Early Obesity and NAFLD through Gut Microbiota Reshaping and Bile Acid Metabolism Modulation

Mitophagy in Hepatic Insulin Resistance: Therapeutic Potential and Concerns

Study on the protective effect of Lycopene on ischemia-reperfusion myocardium through Inhibiting the opening of mitochondrial MPTP and the activation of apoptotic pathway

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