Dietary cholesterol induces hepatic inflammation and blunts mitochondrial function in the liver of high-fat-fed mice

Li, Songpei; Zeng, Xiaomei; Zhou, Xin; Wang, Hao; Jo, Eunjung; Robinson, Stephen R.; Xu, Aimin; Ye, Ji-Ming

doi:10.1016/j.jnutbio.2015.08.021

Cited by 26 publications

(34 citation statements)

References 57 publications

(70 reference statements)

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“…This line of view is confirmed by a recent report highlighting the crucial role of dietary cholesterol in delivering the “second hit” for NASH onset, in context of moderate dietary fat administration (45% of total calories from fat) [77]. In this study, addition of a moderate level of cholesterol in HF elicits the onset of hepatocellular damage and inflammation through activation of the inflammasomes response, while neither dietary cholesterol nor HF alone produced the NASH phenotype.…”

Section: Mechanisms Of Mitochondrial Oxidative Stress Damagesupporting

confidence: 83%

“…In this study, addition of a moderate level of cholesterol in HF elicits the onset of hepatocellular damage and inflammation through activation of the inflammasomes response, while neither dietary cholesterol nor HF alone produced the NASH phenotype. Importantly, addition of cholesterol to HF resulted in blunted adaptation of mitochondrial metabolism to HF and markedly reduced mitochondrial biogenesis, effects paralleled by a decrease in PGC-1 α and TFAM expression levels [77]. Moreover, while hepatic inflammation recovered after removal of excess dietary cholesterol, mitochondrial functions remained hampered alongside elevated NRLP3 inflammasome protein levels, indicating slow recovery dynamics from mitochondrial damage.…”

Section: Mechanisms Of Mitochondrial Oxidative Stress Damagementioning

confidence: 99%

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PPARs and Mitochondrial Metabolism: From NAFLD to HCC

2016

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Metabolic related diseases, such as type 2 diabetes, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD), are widespread threats which bring about a significant burden of deaths worldwide, mainly due to cardiovascular events and cancer. The pathogenesis of these diseases is extremely complex, multifactorial, and only partially understood. As the main metabolic organ, the liver is central to maintain whole body energetic homeostasis. At the cellular level, mitochondria are the metabolic hub connecting and integrating all the main biochemical, hormonal, and inflammatory signaling pathways to fulfill the energetic and biosynthetic demand of the cell. In the liver, mitochondria metabolism needs to cope with the energetic regulation of the whole body. The nuclear receptors PPARs orchestrate lipid and glucose metabolism and are involved in a variety of diseases, from metabolic disorders to cancer. In this review, focus is placed on the roles of PPARs in the regulation of liver mitochondrial metabolism in physiology and pathology, from NAFLD to HCC.

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Section: Mechanisms Of Mitochondrial Oxidative Stress Damagesupporting

confidence: 83%

Section: Mechanisms Of Mitochondrial Oxidative Stress Damagementioning

confidence: 99%

PPARs and Mitochondrial Metabolism: From NAFLD to HCC

2016

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“…According to previous studies, PVE may produce oxidative stress through tumor necrosis factor-α (8-10) and interleukin-6 (10). Deposition of free fatty acids supposedly induces hepatocyte damage due to oxidative stress (11)(12)(13)(14). On the basis of the current results, it appears a useful prospective application to focus on excessive oxidative stress when performing PVE in patients with NASH.…”

Section: Discussionmentioning

confidence: 81%

Oxidative stress induced by portal vein embolization in fatty liver: Experimental study of a nonalcoholic steatohepatitis model

et al. 2018

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The present study aimed to investigate whether excessive oxidative stress production or reduction of antioxidative stress potential may occur following portal vein embolization (PVE) in an experimental animal nonalcoholic steatohepatitis (NASH) model. A NASH rabbit model (n=11) was established by feeding of a fat diet for 4 weeks, and a normal diet rabbit model (n=11) was prepared as a control. The oxidative status of NASH was examined by measuring derivatives of reactive oxygen metabolites (d-ROM) for oxidative stress and biological antioxidative potential (BAP) for antioxidative potential in the NASH model and normal group. Additionally, oxidative status of PVE after 2 weeks was assessed by measuring d-ROM and BAP in the NASH and normal liver models. Oxidative status in a PVE+NASH model was also detected. In the process of NASH creation (fat diet for 4 weeks), total cholesterol was increased in the NASH group (P<0.0001). In the NASH group, PVE induced an increase in serum aspartate transaminase (P=0.0318). At 4 weeks after initiation of the fat diet, a decrease in BAP was determined as statistically significant (P<0.0001). In normal liver, d-ROM production was stimulated in the Sham group after 2 weeks (P=0.0152), but BAP was not altered (P=0.6119). In NASH liver, d-ROM production was stimulated in PVE and Sham groups (P<0.0001 and P=0.0189, respectively), but BAP did not change (P>0.05). In conclusion, decrease of antioxidant potential may promote NASH progression. Additionally, PVE appeared to cause a surge in oxidative stress in NASH liver.

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“…To explore the effects of CoQ 10 on the antioxidant defense mechanism under the circumstance of oxidative stress in our study, therefore, we applied a CoQ 10 supplement to the rats fed a high cholesterol diet. Since involvement of oxidative stress induced by high cholesterol in the pathological damage of the heart, liver and arteries has been well studied, it can be hypothesized that feeding 1-2% cholesterol to rats might lead to an increase in cholesterol-mediated tissue damage occurred by lipid peroxidation [15][16][17].…”

Section: Introductionmentioning

confidence: 99%

The effects of coenzyme Q10 supplement on blood lipid indices and hepatic antioxidant defense system in SD rats fed a high cholesterol diet

et al. 2019

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A total of 24 SD rats were allotted to four treatment groups such as the control (CON), 1% of cholesterol diet (CHO), 0.5% of coenzyme Q 10 (COQ) and 1% of cholesterol plus 0.5% of coenzyme Q 10 (CHCQ) groups to determine the effects of coenzyme Q 10 (CoQ 10 ) on the antioxidant defense system in rats. The body weight, weight gain, liver weight and abdominal fat pads were unaffected by 0.5% of CoQ 10 supplement in the rats. The level of triglyceride and HDL-cholesterol levels in the blood was significantly increased (p < 0.05) by the 1% of cholesterol supplement (CHO), whereas 0.5% of CoQ 10 supplement (COQ) did not alter these blood lipid indices. In the mRNA expression, there was a significant effect (P < 0.05) of the CoQ 10 supplement on the mRNA expression of superoxide dismutase (SOD), although the mRNA expression of glutathione peroxidase (GPX) and glutathione S-transferase (GST) was unaffected by cholesterol or the CoQ 10 supplement. Similar to mRNA expression of SOD, its activity was also significantly increased (P < 0.05) by CoQ 10 , but not by the cholesterol supplement effect. The activities hepatic GPX and GST were unaffected by CoQ 10 and cholesterol supplements in rats. Lipid peroxidation in the CHO group resulted in a significant (p < 0.05) increase compared with that in the other groups, indicating that the CoQ 10 supplement to 1% of cholesterol-fed rats alleviated the production of lipid peroxidation in the liver. In conclusion, 0.5% of the CoQ 10 supplement resulted in positive effects on the hepatic antioxidant defense system without affecting blood lipid indices in 1% of cholesterol fed rats.

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Dietary cholesterol induces hepatic inflammation and blunts mitochondrial function in the liver of high-fat-fed mice

Cited by 26 publications

References 57 publications

PPARs and Mitochondrial Metabolism: From NAFLD to HCC

PPARs and Mitochondrial Metabolism: From NAFLD to HCC

Oxidative stress induced by portal vein embolization in fatty liver: Experimental study of a nonalcoholic steatohepatitis model

The effects of coenzyme Q10 supplement on blood lipid indices and hepatic antioxidant defense system in SD rats fed a high cholesterol diet

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