Effects of a high-fat diet on energy metabolism and ROS production in rat liver

Vial, Guillaume; Dubouchaud, Hervé; Couturier, Karine; Cottet‐Rousselle, Cécile; Taleux, Nellie; Athias, Anne; Galinier, Anne; Casteilla, Louis; Leverve, Xavier

doi:10.1016/j.jhep.2010.06.044

Cited by 204 publications

(164 citation statements)

References 33 publications

(47 reference statements)

Supporting

Mentioning

140

Contrasting

Unclassified

Order By: Relevance

“…Previous findings in transgenic/knockout rodents have shown an inverse relationship between TEE and sensitivity for HFD-induced steatosis (32,35,40,43). Importantly, much like sedentary humans, we observed that REE of our caged animals represented the vast majority of TEE (Ͼ70%).…”

Section: Discussionsupporting

confidence: 67%

See 1 more Smart Citation

Intrinsic aerobic capacity impacts susceptibility to acute high-fat diet-induced hepatic steatosis

Morris¹,

Jackman

Johnson

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

PS, Thyfault JP. Intrinsic aerobic capacity impacts susceptibility to acute high-fat diet-induced hepatic steatosis. Am J Physiol Endocrinol Metab 307: E355-E364, 2014. First published June 24, 2014; doi:10.1152/ajpendo.00093.2014.-Aerobic capacity/fitness significantly impacts susceptibility for fatty liver and diabetes, but the mechanisms remain unknown. Herein, we utilized rats selectively bred for high (HCR) and low (LCR) intrinsic aerobic capacity to examine the mechanisms by which aerobic capacity impacts metabolic vulnerability for fatty liver following a 3-day high-fat diet (HFD). Indirect calorimetry assessment of energy metabolism combined with radiolabeled dietary food was employed to examine systemic metabolism in combination with ex vivo measurements of hepatic lipid oxidation. The LCR, but not HCR, displayed increased hepatic lipid accumulation in response to the HFD despite both groups increasing energy intake. However, LCR rats had a greater increase in energy intake and demonstrated greater daily weight gain and percent body fat due to HFD compared with HCR. Additionally, total energy expenditure was higher in the larger LCR. However, controlling for the difference in body weight, the LCR has lower resting energy expenditure compared with HCR. Importantly, respiratory quotient was significantly higher during the HFD in the LCR compared with HCR, suggesting reduced whole body lipid utilization in the LCR. This was confirmed by the observed lower whole body dietary fatty acid oxidation in LCR compared with HCR. Furthermore, LCR liver homogenate and isolated mitochondria showed lower complete fatty acid oxidation compared with HCR. We conclude that rats bred for low intrinsic aerobic capacity show greater susceptibility for dietary-induced hepatic steatosis, which is associated with a lower energy expenditure and reduced whole body and hepatic mitochondrial lipid oxidation. fatty liver; energy intake; fitness; obesity; energy expenditure LOW AEROBIC CAPACITY OR FITNESS is a powerful predictor of cardiovascular and all-cause mortality independent of other risk factors, including smoking, obesity, previous cardiovascular disease, and diabetes (18,19). Importantly, improving fitness also significantly increases survival in previously low-fit individuals (19). Aerobic capacity is also an independent predictor for the development of the metabolic syndrome and type 2 diabetes (12, 34). Low aerobic capacity is also a powerful predictor of nonalcoholic fatty liver disease (NA-FLD) prevalence (2) and negatively impacts lifestyle-based treatments for NAFLD (16). However, the mechanism(s) linking low aerobic capacity to metabolic disease processes remains unknown. In particular, there are limited data documenting the whole body and liver-specific energy metabolism phenotypes that exist between groups of differing aerobic capacities and how these different phenotypes may modulate susceptibility for NAFLD.NAFLD represents a spectrum of disease initially characterized by steatosis that may progress to hepatic in...

show abstract

Section: Discussionsupporting

confidence: 67%

“…Obesity and factors that modulate adiposity directly influence hepatic steatosis in human patients and rodent models (2,31,40). As such, the primary treatment for NAFLD is lifestyleinduced weight loss (33).…”

Section: Discussionmentioning

confidence: 99%

Intrinsic aerobic capacity impacts susceptibility to acute high-fat diet-induced hepatic steatosis

Morris¹,

Jackman

Johnson

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

show abstract

“…29) The levels of SIRT1 are induced under CR condition, 30) and SIRT1 transgenic mice display calorie restriction-resembled phenotypes. 31) Moreover, HFD is also associated with increased production of mitochondrial reactive oxygen species (ROS), 32) which are generated endogenously in the process of mitochondrial oxidative phosphorylation and responsible for oxidative damage. 33,34) The MnSOD, an important antioxidative enzyme, is reported to regulates ROS metabolism and detoxify mitochondrial ROS.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Protects against High-Fat Diet Induced Renal Pathological Damage and Cell Senescence by Activating SIRT1

Zhang

et al. 2016

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Obesity-related renal diseases have been a worldwide issue. Effective strategy that prevents high fat-diet induced renal damage is of great significance. Resveratrol, a natural plant polyphenol, is famous for its antioxidant activity, cardioprotective effects and anticancer properties. However whether resveratrol can play a role in the treatment of renal diseases is unknown. In this study, we added resveratrol in normal glucose or high glucose medium and provide evidences that resveratrol protects against high-glucose triggered oxidative stress and cell senescence. Moreover, mice were fed with standard diet, standard diet plus resveratrol, high-fat diet or high-fat diet plus resveratrol for 3 months, and results show that resveratrol treatment prevents high-fat diet induced renal pathological damage by activating SIRT1, a key member in the mammalian sirtuin family that response to calorie restriction life-extension method. This research confirms the potential role of resveratrol in the treatment of renal diseases and may provide an effective and convenient method to mimic the beneficial effects of calorie restriction.

show abstract

“…Previous studies have demonstrated the prejudicial effects of HFD on fat and metabolic performance. [24][25][26][27] The absence of alterations in food intake indicates that the difference in fat mass was not induced by decreased appetite and was probably caused by changes in metabolic regulation. 13 Previous studies also showed a beneficial metabolic role of Ang-(1-7) in body fat mass.…”

Section: Discussionmentioning

confidence: 99%

Oral Formulation of Angiotensin-(1–7) Improves Lipid Metabolism and Prevents High-Fat Diet–Induced Hepatic Steatosis and Inflammation in Mice

et al. 2013

View full text Add to dashboard Cite

Abstract-Angiotensin (Ang)-(1-7) has been described as an important tool on treating and preventing metabolic disorders. In this study, we aimed to evaluate the effect of an oral formulation of Ang-(1-7) included in hydroxypropylβ-cyclodextrin (HPβCD/Ang- [1][2][3][4][5][6][7]) on hepatic function, steatosis, and on liver inflammatory markers expression in mice treated with a high-fat diet. Male FVB/N mice were divided into 4 groups and fed for 60 days, with each group receiving 1 of the following diets: standard diet+HPβCD, standard diet+Ang-(1-7)/HPβCD, high-fat diet+HPβCD, or highfat diet+Ang-[1-7]/HPβCD. Body weight, food intake, and blood parameters, such as total cholesterol, triglyceride, alaninetransaminases, and aspartate transaminases, were evaluated. Immunohistochemical analyses were performed for inflammatory markers tumor necrosis factor-α and interleukin-6. Expression of angiotensin converting enzyme, angiotensin-converting enzyme-2, interleukin-1β, tumor necrosis factor-α, interleukin-6, transforming growth factor-β, acetyl-CoA carboxylase, carbohydrate-responsive element-binding protein, peroxisome proliferator-activated receptor-γ, and sterol regulatory element-binding proteins-1c was evaluated by quantitative real-time polymerase chain reaction. The major findings of our study included reduced liver fat mass and weight, decreased plasma total cholesterol, triglyceride, and alaninetransaminase enzyme levels in the oral Ang-(1-7)-treated groups compared with the control groups. These results were accompanied by a significant reduction in tumor necrosis factor-α and interleukin-6 mRNA expression in the liver. Analyses of liver adipogenesis-related genes by quantitative real-time polymerase chain reaction showed that acetyl-CoA carboxylase, peroxisome proliferator-activated receptor-γ, and sterol regulatory element-binding proteins1c mRNA expression were significantly suppressed. In conclusion, we observed that treatment with Ang-(1-7) improved metabolism and decreased proinflammatory profile and fat deposition in liver of mice. The renin-angiotensin system (RAS) is now recognized to play an important role in the development of cardiovascular and metabolic disorders. [10][11][12][13] The RAS consists primarily of an enzymatic cascade in which angiotensinogen is converted to angiotensin (Ang) I and subsequently to Ang II by the actions of renin and Ang-converting enzyme (ACE), respectively. 14 Ang-(1-7) is formed mainly from Ang II by ACE-2 and indirectly from Ang I.14 The ACE-2/Ang-(1-7)/Mas axis has been suggested as an important counter-regulatory arm in the RAS with effects opposing those of ACE/Ang II/Ang II receptor, type 1. 13Recent studies showed an important participation of RAS in the nonalcoholic fatty liver disease (NAFLD) development and progression. The Ang II has been implicated as a major player in the altered hepatic lipid metabolism observed in NAFLD. Genetic disruption of several RAS components in rodent models results in a protection from high-fat diet (HFD)-induced obesity. [15...

show abstract

Effects of a high-fat diet on energy metabolism and ROS production in rat liver

Cited by 204 publications

References 33 publications

Intrinsic aerobic capacity impacts susceptibility to acute high-fat diet-induced hepatic steatosis

Intrinsic aerobic capacity impacts susceptibility to acute high-fat diet-induced hepatic steatosis

Resveratrol Protects against High-Fat Diet Induced Renal Pathological Damage and Cell Senescence by Activating SIRT1

Oral Formulation of Angiotensin-(1–7) Improves Lipid Metabolism and Prevents High-Fat Diet–Induced Hepatic Steatosis and Inflammation in Mice

Contact Info

Product

Resources

About