The impact of a short-term high-fat diet on mitochondrial respiration, reactive oxygen species production, and dynamics in oxidative and glycolytic skeletal muscles of young rats

Leduc‐Gaudet, Jean‐Philippe; Reynaud, Olivier; Chabot, F.; Mercier, Julien; Andrich, David E.; St-Pierre, David H.; Gouspillou, Gilles

doi:10.14814/phy2.13548

Cited by 41 publications

(30 citation statements)

References 35 publications

(99 reference statements)

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“…The overexpression of PGC1α also promoted a fiber-type switch from a glycolytic toward a more oxidative phenotype in mice ( Lin et al, 2002 ). In line with our previous work ( Leduc-Gaudet et al, 2018 ), we could not observe any difference in the expression of PGC1α, suggesting that mitochondrial biogenesis is not altered in SOL or EDL muscles in response to our short-term HFD. Overexpression of PPARγ was also observed in the SOL muscle.…”

Section: Discussionsupporting

confidence: 93%

“…Our results show that larger LDs were observed in SOL, but not in EDL muscles; these discrepancies could be explained by differences in the experimental model, namely by the age and the species tested. Further, we have recently reported that 14 days of HFD significantly increase palmitic acid utilization while altering the expression of genes involved in the regulation of mitochondrial dynamics in both oxidative and glycolytic muscles of young rats ( Leduc-Gaudet et al, 2018 ). Interestingly our results obtained with the same model show a decline in ambulatory activity in response to the short-term HFD ( Andrich et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

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Altered Lipid Metabolism Impairs Skeletal Muscle Force in Young Rats Submitted to a Short-Term High-Fat Diet

et al. 2018

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Obesity and ensuing disorders are increasingly prevalent in young populations. Prolonged exposure to high-fat diets (HFD) and excessive lipid accumulation were recently suggested to impair skeletal muscle functions in rodents. We aimed to determine the effects of a short-term HFD on skeletal muscle function in young rats. Young male Wistar rats (100–125 g) were fed HFD or a regular chow diet (RCD) for 14 days. Specific force, resistance to fatigue and recovery were tested in extensor digitorum longus (EDL; glycolytic) and soleus (SOL; oxidative) muscles using an ex vivo muscle contractility system. Muscle fiber typing and insulin signaling were analyzed while intramyocellular lipid droplets (LD) were characterized. Expression of key markers of lipid metabolism was also measured. Weight gain was similar for both groups. Specific force was decreased in SOL, but not in EDL of HFD rats. Muscle resistance to fatigue and force recovery were not altered in response to the diets. Similarly, muscle fiber type distribution and insulin signaling were not influenced by HFD. On the other hand, percent area and average size of intramyocellular LDs were significantly increased in the SOL of HFD rats. These effects were consistent with the increased expression of several mediators of lipid metabolism in the SOL muscle. A short-term HFD impairs specific force and alters lipid metabolism in SOL, but not EDL muscles of young rats. This indicates the importance of clarifying the early mechanisms through which lipid metabolism affects skeletal muscle functions in response to obesogenic diets in young populations.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Altered Lipid Metabolism Impairs Skeletal Muscle Force in Young Rats Submitted to a Short-Term High-Fat Diet

et al. 2018

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“…Mitochondrial respiratory function was increased in both the soleus and gastrocnemius with HFD. This is in contrast to our hypothesis, but some studies have also reported an increase in mitochondrial function with HFD [14,15,39]. While two studies have observed a decrease in mitochondrial respiratory function with HFD [11,12].…”

Section: Discussionsupporting

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Changes in insulin resistance do not occur in parallel with changes in mitochondrial content and function in male rats

Genders

Kuang

et al. 2020

Preprint

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AbstractAims/hypothesisTo investigate if there is a causal relationship between changes in insulin resistance and mitochondrial respiratory function and content in rats fed a high fat diet (HFD) with or without concurrent exercise training. We hypothesised that provision of a high fat diet (HFD) would increase insulin resistance and decrease mitochondrial characteristics (content and function), and that exercise training would improve both mitochondrial characteristics and insulin resistance in rats fed a HFD.MethodsMale Wistar rats were given either a chow diet or a high fat diet (HFD) for 12 weeks. After 4 weeks of the dietary intervention, half of the rats in each group began eight weeks of interval training. In vivo glucose and insulin tolerance was assessed, as was ex vivo glucose uptake in epitrochlearis muscle. Mitochondrial respiratory function was assessed in permeabilised soleus and white gastrocnemius (WG) muscles. Mitochondrial content was determined by measurement of citrate synthase (CS) activity and protein expression of components of the electron transport system (ETS).ResultsHFD rats had impaired glucose and insulin tolerance. HFD did not change CS activity in the soleus; however, it did increase CS activity in WG (Chow 5.9 ± 0.5, HFD 7.2 ± 0.7 mol h-1 kg protein-1). Protein expression of components of the ETS and mitochondrial respiratory function (WG Chow 65.2 ± 8.4, HFD 88.6 ± 8.7 pmol O2 s-1 mg-1) were also increased by HFD. Exercise training improved glucose and insulin tolerance in the HFD rats. Exercise training did not alter CS activity in either muscle. Mitochondrial respiratory function was increased with exercise training in the chow fed animals in soleus muscle, but not in WG. This exercise effect was absent in the HFD animals. Mitochondrial characteristics did not consistently correlate with insulin or glucose tolerance.Conclusions/interpretationHFD induced insulin resistance, but it did not negatively affect any of the measured mitochondrial characteristics. Exercise training improved insulin resistance, but without changes in mitochondrial respiration and content. The lack of an association between mitochondrial characteristics and insulin resistance was reinforced by the absence of strong correlations between these measures. Our results suggest that defects in mitochondrial respiration and content are not responsible for insulin resistance in HFD rats.

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“…We also observed that subjecting mice to an HFD did not alter mitochondrial bioenergetics. This could be due to subjecting our mice to a short-term high fat feeding regiment, which has previously been shown to have little impact on mitochondrial bioenergetics (19). We also observed that mitochondria from GRX2 heterozygotes contained higher PDH levels, which could also account for the increase in muscle fuel metabolism.…”

Section: Discussionmentioning

confidence: 75%

Deletion of the Glutaredoxin-2 Gene Protects Mice from Diet-Induced Weight Gain, Which Correlates with Increased Mitochondrial Respiration and Proton Leaks in Skeletal Muscle

Young

Gardiner

Kuksal

et al. 2019

Antioxidants & Redox Signaling

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Aims: The aim of this study was to determine whether deleting the gene encoding glutaredoxin-2 (GRX2) could protect mice from diet-induced weight gain. Results: Subjecting wild-type littermates to a high fat diet (HFD) induced a significant increase in overall body mass, white adipose tissue hypertrophy, lipid droplet accumulation in hepatocytes, and higher circulating insulin and triglyceride levels. In contrast, GRX2 heterozygotes (GRX2 +/-) fed an HFD had a body mass, white adipose tissue weight, and hepatic and circulating lipid and insulin levels similar to littermates fed a control diet. Examination of the bioenergetics of muscle mitochondria revealed that this protective effect was associated with an increase in respiration and proton leaks. Muscle mitochondria from GRX2 +/mice had a *2to 3-fold increase in state 3 (phosphorylating) respiration when pyruvate/malate or succinate served as substrates and a *4-fold increase when palmitoyl-carnitine was being oxidized. Proton leaks were *2to 3-fold higher in GRX2 +/muscle mitochondria. Treatment of mitochondria with either guanosine diphosphate, genipin, or octanoyl-carnitine revealed that the higher rate of O 2 consumption under state 4 conditions was associated with increased leaks through uncoupling protein-3 and adenine nucleotide translocase. GRX2 +/mitochondria also had better protection from oxidative distress. Innovation: For the first time, we demonstrate that deleting the Grx2 gene can protect from diet-induced weight gain and the development of obesity-related disorders. Conclusions: Deleting the Grx2 gene protects mice from diet-induced weight gain. This effect was related to an increase in muscle fuel combustion, mitochondrial respiration, proton leaks, and reactive oxygen species handling.

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The impact of a short-term high-fat diet on mitochondrial respiration, reactive oxygen species production, and dynamics in oxidative and glycolytic skeletal muscles of young rats

Cited by 41 publications

References 35 publications

Altered Lipid Metabolism Impairs Skeletal Muscle Force in Young Rats Submitted to a Short-Term High-Fat Diet

Altered Lipid Metabolism Impairs Skeletal Muscle Force in Young Rats Submitted to a Short-Term High-Fat Diet

Changes in insulin resistance do not occur in parallel with changes in mitochondrial content and function in male rats

Deletion of the Glutaredoxin-2 Gene Protects Mice from Diet-Induced Weight Gain, Which Correlates with Increased Mitochondrial Respiration and Proton Leaks in Skeletal Muscle

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