Fat intake reverses the beneficial effects of low caloric intake on skeletal muscle mitochondrial H2O2 production

Garait, Blandine; Couturier, Karine; Servais, Stéphane; Letexier, Dominique; Perrin, David; Batandier, Cécile; Rouanet, Jean‐Louis; Sibille, Brigitte; Rey, Benjamin; Leverve, Xavier; Favier, R.

doi:10.1016/j.freeradbiomed.2005.06.026

Cited by 39 publications

(34 citation statements)

References 39 publications

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“…characteristics of the metabolic syndrome (see Frisard and Ravussin 13 for a recent review) suggests that the Lou/C strain might represent an appropriate model for examining the impact of caloric intake on mitochondrial properties (oxidative phosphorylation efficiency, ROS production) in relation to fat metabolism and insulin sensitivity. This suggestion is somewhat supported by our recent data 1,14,15 showing that the intriguing phenotype of Lou/C rats cannot be easily reproduced in Wistar rats by adjusting food intake (pairfeeding) since Lou/C rats displayed a lower visceral adiposity 1,14 as compared to pair-fed Wistar (WPF) rats. Furthermore, we found that H 2 O 2 generation was reduced in skeletal muscle mitochondria of Lou/C compared with Wistar rats, 15 and this localized adaptation in H 2 O 2 production can be reversed by allowing this peculiar strain to switch on a high-fat intake owing to their strong preference for fat.…”

Section: Introductionmentioning

confidence: 66%

“…This suggestion is somewhat supported by our recent data 1,14,15 showing that the intriguing phenotype of Lou/C rats cannot be easily reproduced in Wistar rats by adjusting food intake (pairfeeding) since Lou/C rats displayed a lower visceral adiposity 1,14 as compared to pair-fed Wistar (WPF) rats. Furthermore, we found that H 2 O 2 generation was reduced in skeletal muscle mitochondria of Lou/C compared with Wistar rats, 15 and this localized adaptation in H 2 O 2 production can be reversed by allowing this peculiar strain to switch on a high-fat intake owing to their strong preference for fat. 2,3,8,15 Collectively, these data suggest that Lou/C rats display specific mitochondrial properties permitting to oxidize fatty acids to a greater extent.…”

Section: Introductionmentioning

confidence: 66%

“…Furthermore, we found that H 2 O 2 generation was reduced in skeletal muscle mitochondria of Lou/C compared with Wistar rats, 15 and this localized adaptation in H 2 O 2 production can be reversed by allowing this peculiar strain to switch on a high-fat intake owing to their strong preference for fat. 2,3,8,15 Collectively, these data suggest that Lou/C rats display specific mitochondrial properties permitting to oxidize fatty acids to a greater extent.…”

Section: Introductionmentioning

confidence: 81%

“…Experiment 2. In this experiment, Lou/C rats had the choice between the standard chow (UAR A04) and a high-fat diet, 15 both of which were provided ad libitum in stainless steel hanging cages. Body weight and food intake were recorded thrice weekly and fresh food was provided at the same time to ensure minimal disturbance to the animals' food behavior.…”

Section: Animals and Experimental Designmentioning

confidence: 99%

“…The second objective of the study was to evaluate the impact of high-fat diet on these properties, since we recently found that the reduced oxidative stress evidenced in skeletal muscle from Lou/C rats is lost in skeletal muscle mitochondria when fat proportion in the diet is increased. 15 …”

Section: Introductionmentioning

confidence: 99%

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Liver mitochondrial properties from the obesity-resistant Lou/C rat

et al. 2008

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Objective: The first objective was to evaluate the influence of caloric intake on liver mitochondrial properties. The second objective was aimed at determining the impact of increasing fat intake on these properties. Design: Lou/C rats, displaying an inborn low caloric intake and resistant to diet-induced obesity, were compared to Wistar rats fed either ad libitum or pair-fed. An additional group of Lou/C rats were allowed to increase their fat intake by adjusting their diet from a standard high carbohydrate low-fat diet to a high-fat carbohydrate-free diet. Measurements: Hydrogen peroxide (H 2 O 2 ) generation, oxygen consumption rate (J O2 ), membrane potential (DC), activity of respiratory chain complexes, cytochrome contents, oxidative phosphorylation efficiency (OPE) and uncoupling protein 2 (UCP2) expression were determined in liver mitochondria. Results: H 2 O 2 production was higher in Lou/C than Wistar rats with glutamate/malate and/or succinate, octanoyl-carnitine, as substrates. These mitochondrial features cannot be mimicked by pair-feeding Wistar rats and remained unaltered by increasing fat intake. Enhanced H 2 O 2 production by mitochondria from Lou/C rats is due to an increased reverse electron flow through the respiratory-chain complex I and a higher medium-chain acyl-CoA dehydrogenase activity. While J O 2 was similar over a large range of DC in both strains, Lou/C rats were able to sustain higher membrane potential and respiratory rate. In addition, mitochondria from Lou/C rats displayed a decrease in OPE that cannot be explained by increased expression of UCP2 but rather to a slip in proton pumping by cytochrome oxidase. Conclusions: Liver mitochondria from Lou/C rats display higher reactive oxygen species (ROS) generation but to deplete upstream electron-rich intermediates responsible for ROS generation, these animals increased intrinsic uncoupling of cytochrome oxidase. It is likely that liver mitochondrial properties allowed this strain of rat to display higher insulin sensitivity and resist diet-induced obesity.

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Section: Introductionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 81%

Section: Animals and Experimental Designmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Liver mitochondrial properties from the obesity-resistant Lou/C rat

et al. 2008

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Polarographic Oxygen Sensors, the Oxygraph, and High‐Resolution Respirometry to Assess Mitochondrial Function

Gnaiger

2008

Drug‐Induced Mitochondrial Dysfunction

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Introduction 2. Polarographic oxygen sensor and traditional oxygraphy 3. High-resolution respirometry: the Oxygraph-2k 3.1. Calibration of polarographic oxygen sensors and oxygen concentration in respiration media at air saturation 3.2. From oxygraph slopes to respiratory flux corrected for background effects 4. Phosphorylation control protocol with intact cells 4.1. Titration steps of the PC protocol 4.2. Experimental example for the PC protocol 4.3. Flux control ratios from the PC protocol 5. Intact cells, permeabilized cells and tissue, or isolated mitochondria 5.1. Intact cells 5.2. Permeabilized cells and tissue 5.3. Isolated mitochondria 6. Titration protocols in permeabilized cells, permeabilized tissue preparations, and isolated mitochondria 7. Multisensor applications Drug-Induced Mitochondrial Dysfunction, Edited by James Dykens and Yvonne Will

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Caloric Restriction and Oxidative Stress

Škrha

2011

Oxidative Stress in Vertebrates and Invertebrates

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Fat intake reverses the beneficial effects of low caloric intake on skeletal muscle mitochondrial H2O2 production

Cited by 39 publications

References 39 publications

Liver mitochondrial properties from the obesity-resistant Lou/C rat

Liver mitochondrial properties from the obesity-resistant Lou/C rat

Polarographic Oxygen Sensors, the Oxygraph, and High‐Resolution Respirometry to Assess Mitochondrial Function

Caloric Restriction and Oxidative Stress

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