scholarly journals Relative lipid oxidation associates directly with mitochondrial fusion phenotype and mitochondria-sarcoplasmic reticulum interactions in human skeletal muscle

2020 ◽  
Vol 318 (6) ◽  
pp. E848-E855 ◽  
Author(s):  
Mauricio Castro-Sepulveda ◽  
Sebastian Jannas-Vela ◽  
Rodrigo Fernández-Verdejo ◽  
Daniela Ávalos-Allele ◽  
German Tapia ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Lipid Oxidation ◽  
Vastus Lateralis ◽  
Whole Body ◽  
Body Lipid ◽  
Cellular Mechanisms ◽  
Muscle Lipid ◽  
Skeletal Muscle Biopsy ◽  
Skeletal Muscle Lipid

Disturbances in skeletal muscle lipid oxidation might induce ectopic fat deposition and lipotoxicity. Nevertheless, the cellular mechanisms that regulate skeletal muscle lipid oxidation have not been fully determined. We aimed to determine whether there was an association between relative whole body lipid oxidation and mitochondrial size or mitochondria-sarcoplasmic reticulum interactions in the skeletal muscle. Twelve healthy men were included [mean (standard deviation), 24.7 (1.5) yr old, 24.4 (2.6) kg/m2]. The respiratory quotient (RQ) was used to estimate relative lipid oxidation at rest and during exercise (50% maximal oxygen consumption, 600 kcal expended). A skeletal muscle biopsy was obtained from the vastus lateralis at rest. Transmission electron microscopy was used to determine mitochondrial size and mitochondria-sarcoplasmic reticulum interactions (≤50 nm of distance between organelles). Protein levels of fusion/fission regulators were measured in skeletal muscle by Western blot. Resting RQ and exercise RQ associated inversely with intermyofibrillar mitochondrial size ( r = −0.66 and r = −0.60, respectively, P < 0.05). Resting RQ also associated inversely with the percentage of intermyofibrillar mitochondria-sarcoplasmic reticulum interactions ( r = −0.62, P = 0.03). Finally, intermyofibrillar mitochondrial size associated inversely with lipid droplet density ( r = −0.66, P = 0.01) but directly with mitochondria fusion-to-fission ratio ( r = 0.61, P = 0.03). Our results show that whole body lipid oxidation is associated with skeletal muscle intermyofibrillar mitochondrial size, fusion phenotype, and mitochondria-sarcoplasmic-reticulum interactions in nondiabetic humans.

Contributions of working muscle to whole body lipid metabolism are altered by exercise intensity and training

2007 ◽  
Vol 292 (1) ◽  
pp. E107-E116 ◽  
Author(s):  
Anne L. Friedlander ◽  
Kevin A. Jacobs ◽  
Jill A. Fattor ◽  
Michael A. Horning ◽  
Todd A. Hagobian ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Lipid Oxidation ◽  
Exercise Intensity ◽  
Whole Body ◽  
Body Lipid ◽  
Muscle Lipid ◽  
Before And After ◽  
Net Uptake ◽  
Leg Muscle ◽  
Male Subjects

To evaluate the contribution of working muscle to whole body lipid oxidation, we examined the effects of exercise intensity and endurance training (9 wk, 5 days/wk, 1 h, 75% V̇o2 peak) on whole body and leg free fatty acid (FFA) kinetics in eight male subjects (26 ± 1 yr, means ± SE). Two pretraining trials [45 and 65% V̇o2 max (45UT, 65UT)] and two posttraining trials [65% of pretraining V̇o2 peak (ABT), and 65% of posttraining V̇o2 peak (RLT)] were performed using [1-13C]palmitate infusion and femoral arteriovenous sampling. Training increased V̇o2 peak by 15% (45.2 ± 1.2 to 52.0 ± 1.8 ml·kg−1·min−1, P < 0.05). Muscle FFA fractional extraction was lower during exercise (EX) compared with rest regardless of workload or training status (≈20 vs. 48%, P < 0.05). Two-leg net FFA balance increased from net release at rest (≈−36 μmol/min) to net uptake during EX for 45UT (179 ± 75), ABT (236 ± 63), and RLT (136 ± 110) ( P < 0.05), but not 65UT (51 ± 127). Leg FFA tracer measured uptake was higher during EX than rest for all trials and greater during posttraining in RLT (716 ± 173 μmol/min) compared with pretraining (45UT 450 ± 80, 65UT 461 ± 72, P < 0.05). Leg muscle lipid oxidation increased with training in ABT (730 ± 163 μmol/min) vs. 65UT (187 ± 94, P < 0.05). Leg muscle lipid oxidation represented ∼62 and 30% of whole body lipid oxidation at lower and higher relative intensities, respectively. In summary, training can increase working muscle tracer measured FFA uptake and lipid oxidation for a given power output, but both before and after training the association between whole body and leg lipid metabolism is reduced as exercise intensity increases.

scholarly journals Perilipin 3 Differentially Regulates Skeletal Muscle Lipid Oxidation in Active, Sedentary, and Type 2 Diabetic Males

2015 ◽  
Vol 100 (10) ◽  
pp. 3683-3692 ◽  
Author(s):  
Jeffrey D. Covington ◽  
Robert C. Noland ◽  
R. Caitlin Hebert ◽  
Blaine S. Masinter ◽  
Steven R. Smith ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lipid Oxidation ◽  
Muscle Lipid ◽  
Skeletal Muscle Lipid ◽  
Type 2 Diabetic

scholarly journals One Week of Bed Rest Leads to Substantial Muscle Atrophy and Induces Whole-Body Insulin Resistance in the Absence of Skeletal Muscle Lipid Accumulation

Diabetes ◽  
2016 ◽  
Vol 65 (10) ◽  
pp. 2862-2875 ◽  
Author(s):  
Marlou L. Dirks ◽  
Benjamin T. Wall ◽  
Bas van de Valk ◽  
Tanya M. Holloway ◽  
Graham P. Holloway ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Lipid Accumulation ◽  
Bed Rest ◽  
Whole Body ◽  
Muscle Lipid ◽  
Skeletal Muscle Lipid

scholarly journals Skeletal Muscle Lipid Content and Insulin Resistance: Evidence for a Paradox in Endurance-Trained Athletes

2001 ◽  
Vol 86 (12) ◽  
pp. 5755-5761 ◽  
Author(s):  
Bret H. Goodpaster ◽  
Jing He ◽  
Simon Watkins ◽  
David E. Kelley
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Lipid Content ◽  
Vastus Lateralis ◽  
Positive Association ◽  
Oxidative Capacity ◽  
Fat Free Mass ◽  
Muscle Lipid ◽  
Quantitative Image ◽  
Skeletal Muscle Lipid

We examined the hypothesis that an excess accumulation of intramuscular lipid (IMCL) is associated with insulin resistance and that this may be mediated by the oxidative capacity of muscle. Nine sedentary lean (L) and 11 obese (O) subjects, 8 obese subjects with type 2 diabetes mellitus (D), and 9 lean, exercise-trained (T) subjects volunteered for this study. Insulin sensitivity (M) determined during a hyperinsulinemic (40 mU·m−2min−1) euglycemic clamp was greater (P &lt; 0.01) in L and T, compared with O and D (9.45 ± 0.59 and 10.26 ± 0.78 vs. 5.51 ± 0.61 and 1.15 ± 0.83 mg·min−1kg fat free mass−1, respectively). IMCL in percutaneous vastus lateralis biopsy specimens by quantitative image analysis of Oil Red O staining was approximately 2-fold higher in D than in L (3.04 ± 0.39 vs. 1.40 ± 0.28% area as lipid; P &lt; 0.01). IMCL was also higher in T (2.36 ± 0.37), compared with L (P &lt; 0.01). The oxidative capacity of muscle determined with succinate dehydrogenase staining of muscle fibers was higher in T, compared with L, O, and D (50.0 ± 4.4, 36.1 ± 4.4, 29.7 ± 3.8, and 33.4 ± 4.7 optical density units, respectively; P &lt; 0.01). IMCL was negatively associated with M (r = −0.57, P &lt; 0.05) when endurance-trained subjects were excluded from the analysis, and this association was independent of body mass index. However, the relationship between IMCL and M was not significant when trained individuals were included. There was a positive association between the oxidative capacity and M among nondiabetics (r = 0.37, P &lt; 0.05). In summary, skeletal muscle of trained endurance athletes is markedly insulin sensitive and has a high oxidative capacity, despite having an elevated lipid content. In conclusion, the capacity for lipid oxidation may be an important mediator of the association between excess muscle lipid accumulation and insulin resistance.

Regulation of skeletal muscle energy/nutrient-sensing pathways during metabolic adaptation to fasting in healthy humans

2014 ◽  
Vol 307 (10) ◽  
pp. E885-E895 ◽  
Author(s):  
Marjolein A. Wijngaarden ◽  
Leontine E. H. Bakker ◽  
Gerard C. van der Zon ◽  
Peter A. C. 't Hoen ◽  
Ko Willems van Dijk ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Lipid Oxidation ◽  
Energy Homeostasis ◽  
Nutrient Sensing ◽  
Whole Body ◽  
Metabolic Adaptation ◽  
Protein Kinase Activity ◽  
Short Term ◽  
Muscle Energy

During fasting, rapid metabolic adaptations are required to maintain energy homeostasis. This occurs by a coordinated regulation of energy/nutrient-sensing pathways leading to transcriptional activation and repression of specific sets of genes. The aim of the study was to investigate how short-term fasting affects whole body energy homeostasis and skeletal muscle energy/nutrient-sensing pathways and transcriptome in humans. For this purpose, 12 young healthy men were studied during a 24-h fast. Whole body glucose/lipid oxidation rates were determined by indirect calorimetry, and blood and skeletal muscle biopsies were collected and analyzed at baseline and after 10 and 24 h of fasting. As expected, fasting induced a time-dependent decrease in plasma insulin and leptin levels, whereas levels of ketone bodies and free fatty acids increased. This was associated with a metabolic shift from glucose toward lipid oxidation. At the molecular level, activation of the protein kinase B (PKB/Akt) and mammalian target of rapamycin pathways was time-dependently reduced in skeletal muscle during fasting, whereas the AMP-activated protein kinase activity remained unaffected. Furthermore, we report some changes in the phosphorylation and/or content of forkhead protein 1, sirtuin 1, and class IIa histone deacetylase 4, suggesting that these pathways might be involved in the transcriptional adaptation to fasting. Finally, transcriptome profiling identified genes that were significantly regulated by fasting in skeletal muscle at both early and late time points. Collectively, our study provides a comprehensive map of the main energy/nutrient-sensing pathways and transcriptomic changes during short-term adaptation to fasting in human skeletal muscle.

Intramyocellular fat storage in metabolic diseases

2016 ◽  
Vol 26 (1) ◽  
Author(s):  
Claire Laurens ◽  
Cedric Moro
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Metabolic Diseases ◽  
Recent Literature ◽  
Lipid Storage ◽  
Muscle Lipid ◽  
The Past ◽  
Skeletal Muscle Lipid ◽  
Ectopic Lipid Storage

AbstractOver the past decades, obesity and its metabolic co-morbidities such as type 2 diabetes (T2D) developed to reach an endemic scale. However, the mechanisms leading to the development of T2D are still poorly understood. One main predictor for T2D seems to be lipid accumulation in “non-adipose” tissues, best known as ectopic lipid storage. A growing body of data suggests that these lipids may play a role in impairing insulin action in metabolic tissues, such as liver and skeletal muscle. This review aims to discuss recent literature linking ectopic lipid storage and insulin resistance, with emphasis on lipid deposition in skeletal muscle. The link between skeletal muscle lipid content and insulin sensitivity, as well as the mechanisms of lipid-induced insulin resistance and potential therapeutic strategies to alleviate lipotoxic lipid pressure in skeletal muscle will be discussed.

scholarly journals The effect of short-term fasting on liver and skeletal muscle lipid, glucose, and energy metabolism in healthy women and men

2011 ◽  
Vol 53 (3) ◽  
pp. 577-586 ◽  
Author(s):  
Jeffrey D. Browning ◽  
Jeannie Baxter ◽  
Santhosh Satapati ◽  
Shawn C. Burgess
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Short Term ◽  
Muscle Lipid ◽  
Healthy Women ◽  
Skeletal Muscle Lipid
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