scholarly journals Sarcolipin expression is not required for the mitochondrial enzymatic response to physical activity or diet

2017 ◽  
Vol 122 (5) ◽  
pp. 1276-1283
Author(s):  
Daniel Gamu ◽  
Anton Trinh ◽  
Val A. Fajardo ◽  
Eric Bombardier ◽  
A. Russell Tupling
Keyword(s):  
Exercise Training ◽  
Citrate Synthase ◽  
Oxidative Capacity ◽  
Metabolic Phenotype ◽  
High Fat ◽  
Muscle Oxidative Capacity ◽  
Plasmic Reticulum ◽  
Voluntary Running ◽  
Fat Feeding

In mice, transgenic manipulation of Ca2+-handling proteins is sufficient to alter the metabolic phenotype of muscle. We have previously shown that ablation of sarcolipin (SLN), a regulatory protein and uncoupler of sarco(endo)plasmic reticulum Ca2+-ATPases, leads to excessive diet-induced obesity and glucose intolerance in mice. However, it is unclear how loss of SLN per se affects muscle oxidative capacity and the ability of mitochondria to adapt to physiological stimuli, such as exercise training or calorie overload. To address this question, Sln−/− and wild-type (WT) littermates were given access to voluntary running wheels or underwent a treadmill training protocol for 8 wk. Furthermore, a separate group of mice were given a high-fat diet (42% kcal from fat for 8 wk) to determine whether the excessively obese phenotype of Sln−/− mice is associated with altered oxidative capacity. While voluntary running was insufficient to elicit mitochondrial adaptations, treadmill-trained mice showed significant increases ( P < 0.05) in the maximal activities of succinate dehydrogenase (+11%), citrate synthase (+12%), cytochrome oxidase (COX: +17%), along with increased protein expression of cytochrome c (+34%) and COX IV (+28%), which were irrespective of SLN expression. Lastly, no changes in the activities of mitochondrial marker enzymes existed with high-fat feeding, regardless of genotype. Together, these findings indicate that SLN is not required for the regulation of oxidative capacity in response to physiological stress, namely exercise or caloric surfeit. NEW & NOTEWORTHY Sarcolipin (SLN) has gained considerable attention for its uncoupling role of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA). Because of SLN’s ability to alter both cellular energy use and cytosolic [Ca2+], the potential exists for a regulatory role of mitochondrial biogenesis. Herein, we show skeletal muscle oxidative capacity to be unaltered in mice lacking SLN following exercise training or high-fat feeding. Our results contrast with published studies of SLN-overexpressing mice, possibly owing to supraphysiological uncoupling of SERCA.

Examining the Role of Ampk for Influencing Myocardial Serca2A Expression and Function in Response to High-Fat Feeding Or Exercise Training

2013 ◽  
Vol 29 (10) ◽  
pp. S361-S362
Author(s):  
S.E. Susser ◽  
M.P. Morrisette ◽  
A. Stammers ◽  
E. Zherebitskaya ◽  
T. Moffatt ◽  
...  
Keyword(s):  
Exercise Training ◽  
High Fat ◽  
And Function ◽  
Fat Feeding

scholarly journals Alterations in hepatic one-carbon metabolism and related pathways following a high-fat dietary intervention

2011 ◽  
Vol 43 (8) ◽  
pp. 408-416 ◽  
Author(s):  
Isabel Rubio-Aliaga ◽  
Baukje de Roos ◽  
Manuela Sailer ◽  
Gerard A. McLoughlin ◽  
Mark V. Boekschoten ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Carbon Metabolism ◽  
Dietary Intervention ◽  
Liver Steatosis ◽  
Oxidative Capacity ◽  
Blood Cholesterol ◽  
High Fat ◽  
One Carbon Metabolism ◽  
Fat Feeding

Obesity frequently leads to insulin resistance and the development of hepatic steatosis. To characterize the molecular changes that promote hepatic steatosis, transcriptomics, proteomics, and metabolomics technologies were applied to liver samples from C57BL/6J mice obtained from two independent intervention trials. After 12 wk of high-fat feeding the animals became obese, hyperglycemic, and insulin resistant, had elevated levels of blood cholesterol and VLDL, and developed hepatic steatosis. Nutrigenomic analysis revealed alterations of key metabolites and enzyme transcript levels of hepatic one-carbon metabolism and related pathways. The hepatic oxidative capacity and the lipid milieu were significantly altered, which may play a key role in the development of insulin resistance. Additionally, high choline levels were observed after the high-fat diet. Previous studies have linked choline levels with insulin resistance and hepatic steatosis in conjunction with changes of certain metabolites and enzyme levels of one-carbon metabolism. The present results suggest that the coupling of high levels of choline and low levels of methionine plays an important role in the development of insulin resistance and liver steatosis. In conclusion, the complexities of the alterations induced by high-fat feeding are multifactorial, indicating that the interplay between several metabolic pathways is responsible for the pathological consequences.

scholarly journals Human skeletal muscle metabolic responses to 6 days of high‐fat overfeeding are associated with dietary n‐3PUFA content and muscle oxidative capacity

2020 ◽  
Vol 8 (16) ◽  
Author(s):  
Sophie L. Wardle ◽  
Lindsay S. Macnaughton ◽  
Chris McGlory ◽  
Oliver C. Witard ◽  
James R. Dick ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Oxidative Capacity ◽  
Metabolic Responses ◽  
High Fat ◽  
Muscle Oxidative Capacity

Capillary tortuosity in rat soleus muscle is not affected by endurance training

1989 ◽  
Vol 256 (4) ◽  
pp. H1110-H1116 ◽  
Author(s):  
D. C. Poole ◽  
O. Mathieu-Costello ◽  
J. B. West
Keyword(s):  
Exercise Training ◽  
Citrate Synthase ◽  
Metabolic Response ◽  
Oxidative Capacity ◽  
Treadmill Running ◽  
Female Rats ◽  
Capillary Length ◽  
Direct Function ◽  
Musculus Soleus ◽  
Muscle Changes

The total capillary length available for blood-tissue transfer is determined by the number and orientation of the capillaries. Therefore, whether capillary tortuosity changes with exercise training has important implications for peripheral gas exchange. To determine the effects of exercise training on capillary orientation and capillary length per volume of muscle fiber [Jv(c,f)] female rats were trained by treadmill running (30 m/min, up to 60 min/day, 5 days/wk) for 4 wk. Muscles from control and trained rats were perfusion fixed at sarcomere lengths (l) ranging from 1.59 to 2.15 microns, and morphometric techniques were used to estimate capillary orientation and Jv(c,f). Training increased (P less than 0.05) musculus soleus oxidative capacity 35% [as estimated from citrate synthase activity: 24.7 +/- 1.4 to 34.7 +/- 1.0 (SE) mumol.g-1.min-1], capillary-to-fiber ratio 30% (2.17 +/- 0.06 to 2.83 +/- 0.05), and Jv(c,f) 32% (1,886 +/- 73 to 2,496 +/- 180 mm-2). Capillary tortuosity (as determined from comparisons of transverse and longitudinal sections) was a direct function of l in control and trained rats and contributed 17-73% of capillary length above that estimated from capillary counts on transverse sections. We conclude that capillary tortuosity in m. soleus is unchanged by training. Therefore, Jv(c,f) increases as a consequence of increased capillary number. M. soleus citrate synthase activity is best correlated with Jv(c,f) and not with capillary counts on transverse sections. We hypothesize that training-induced muscle changes of capillary geometry improve O2 delivery to skeletal muscle and may therefore alter the metabolic response (e.g., lactate accumulation) to exercise after training.(ABSTRACT TRUNCATED AT 250 WORDS)

Artificial selection for high-capacity endurance running is protective against high-fat diet-induced insulin resistance

2007 ◽  
Vol 293 (1) ◽  
pp. E31-E41 ◽  
Author(s):  
Robert C. Noland ◽  
John P. Thyfault ◽  
Sarah T. Henes ◽  
Brian R. Whitfield ◽  
Tracey L. Woodlief ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Weight Gain ◽  
High Fat Diet ◽  
Oxidative Capacity ◽  
Male Rats ◽  
High Fat ◽  
Endurance Running ◽  
Muscle Oxidative Capacity ◽  
Obesity And Diabetes

Elevated oxidative capacity, such as occurs via endurance exercise training, is believed to protect against the development of obesity and diabetes. Rats bred both for low (LCR)- and high (HCR)-capacity endurance running provide a genetic model with inherent differences in aerobic capacity that allows for the testing of this supposition without the confounding effects of a training stimulus. The purpose of this investigation was to determine the effects of a high-fat diet (HFD) on weight gain patterns, insulin sensitivity, and fatty acid oxidative capacity in LCR and HCR male rats in the untrained state. Results indicate chow-fed LCR rats were heavier, hypertriglyceridemic, less insulin sensitive, and had lower skeletal muscle oxidative capacity compared with HCR rats. Upon exposure to an HFD, LCR rats gained more weight and fat mass, and their insulin resistant condition was exacerbated, despite consuming similar amounts of metabolizable energy as chow-fed controls. These metabolic variables remained unaltered in HCR rats. The HFD increased skeletal muscle oxidative capacity similarly in both strains, whereas hepatic oxidative capacity was diminished only in LCR rats. These results suggest that LCR rats are predisposed to obesity and that expansion of skeletal muscle oxidative capacity does not prevent excess weight gain or the exacerbation of insulin resistance on an HFD. Elevated basal skeletal muscle oxidative capacity and the ability to preserve liver oxidative capacity may protect HCR rats from HFD-induced obesity and insulin resistance.

Increased mitochondrial content rescues in vivo muscle oxidative capacity in long‐term high‐fat‐diet‐fed rats

2009 ◽  
Vol 24 (5) ◽  
pp. 1354-1364 ◽  
Author(s):  
N. M. A. Van den Broek ◽  
J. Ciapaite ◽  
H. M. M. L. De Feyter ◽  
S. M. Houten ◽  
R. J. A. Wanders ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Oxidative Capacity ◽  
High Fat ◽  
Mitochondrial Content ◽  
Muscle Oxidative Capacity

The role of androgens in the regulation of muscle oxidative capacity following aerobic exercise training

2017 ◽  
Vol 42 (9) ◽  
pp. 1001-1007 ◽  
Author(s):  
Michael L. Rossetti ◽  
Bradley S. Gordon
Keyword(s):  
Cytochrome C ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Therapeutic Option ◽  
Oxidative Capacity ◽  
The Body ◽  
Aerobic Exercise Training ◽  
Peroxisome Proliferator ◽  
Muscle Oxidative Capacity ◽  
Androgen Depletion

Reduced production or bioavailability of androgens, termed hypogonadism, occurs in a variety of pathological conditions. While androgens target numerous tissues throughout the body, hypogonadism specifically reduces the ability of skeletal muscle to produce adenosine triphosphate aerobically, i.e., muscle oxidative capacity. This has important implications for overall health as muscle oxidative capacity impacts a number of metabolic processes. Although androgen replacement therapy is effective at restoring muscle oxidative capacity in hypogonadal individuals, this is not a viable therapeutic option for all who are experiencing hypogonadism. While aerobic exercise may be a viable alternative to increase muscle oxidative capacity, it is unknown whether androgen depletion affects this adaptation. To determine this, sham and castrated mice were randomized to remain sedentary or undergo 8 weeks of aerobic treadmill exercise training. All mice were fasted overnight prior to sacrifice. Though exercise increased markers of muscle oxidative capacity independent of castration (cytochrome c oxidase subunit IV and cytochrome c), these measures were lower in castrated mice. This reduction was not due to a difference in peroxisome proliferator activated receptor gamma coactivator 1 alpha protein content, as expression was increased to a similar absolute value in sham and castrated animals following exercise training. However, markers of BCL2/Adenovirus E1B 19 kDa Interacting Protein 3 (BNIP3)-mediated mitophagy were increased by castration independent of exercise. Together, these data show that exercise training can increase markers of muscle oxidative capacity following androgen depletion. However, these values are reduced by androgen depletion likely due in part to elevated BNIP3-mediated mitophagy.

scholarly journals Pharmacological Modulation of Dopamine Receptor D2-Mediated Transmission Alters the Metabolic Phenotype of Diet Induced Obese and Diet Resistant C57Bl6 Mice

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
J. E. de Leeuw van Weenen ◽  
E. T. Parlevliet ◽  
J. P. Schröder-van der Elst ◽  
S. A. van den Berg ◽  
K. Willems van Dijk ◽  
...  
Keyword(s):  
Dopamine Receptor ◽  
High Fat Diet ◽  
Metabolic Phenotype ◽  
High Fat ◽  
Voluntary Activity ◽  
Insulin Resistant ◽  
Dopamine Receptor D2 ◽  
Dopaminergic Tone ◽  
Haloperidol Treatment ◽  
Fat Feeding

High fat feeding induces a variety of obese and lean phenotypes in inbred rodents. Compared to Diet Resistant (DR) rodents, Diet Induced Obese (DIO) rodents are insulin resistant and have a reduced dopamine receptor D2 (DRD2) mediated tone. We hypothesized that this differing dopaminergic tone contributes to the distinct metabolic profiles of these animals. C57Bl6 mice were classified as DIO or DR based on their weight gain during 10 weeks of high fat feeding. Subsequently DIO mice were treated with the DRD2 agonist bromocriptine and DR mice with the DRD2 antagonist haloperidol for 2 weeks. Compared to DR mice, the bodyweight of DIO mice was higher and their insulin sensitivity decreased. Haloperidol treatment reduced the voluntary activity and energy expenditure of DR mice and induced insulin resistance in these mice. Conversely, bromocriptine treatment tended to reduce bodyweight and voluntary activity, and reinforce insulin action in DIO mice. These results show that DRD2 activation partly redirects high fat diet induced metabolic anomalies in obesity-prone mice. Conversely, blocking DRD2 induces an adverse metabolic profile in mice that are inherently resistant to the deleterious effects of high fat food. This suggests that dopaminergic neurotransmission is involved in the control of metabolic phenotype.

scholarly journals Relationships between maximal muscle oxidative capacity and blood lactate removal after supramaximal exercise and fatigue indexes in humans

2004 ◽  
Vol 97 (6) ◽  
pp. 2132-2138 ◽  
Author(s):  
C. Thomas ◽  
P. Sirvent ◽  
S. Perrey ◽  
E. Raynaud ◽  
J. Mercier
Keyword(s):  
Blood Lactate ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Oxidative Capacity ◽  
Slow Phase ◽  
Vastus Lateralis Muscle ◽  
Supramaximal Exercise ◽  
Muscle Oxidative Capacity ◽  
S Cycling ◽  
Lactate Removal

The present study investigated whether blood lactate removal after supramaximal exercise and fatigue indexes measured during continuous and intermittent supramaximal exercises are related to the maximal muscle oxidative capacity in humans with different training status. Lactate recovery curves were obtained after a 1-min all-out exercise. A biexponential time function was then used to determine the velocity constant of the slow phase (γ2), which denoted the blood lactate removal ability. Fatigue indexes were calculated during all-out (FIAO) and repeated 10-s cycling sprints (FISprint). Biopsies were taken from the vastus lateralis muscle, and maximal ADP-stimulated mitochondrial respiration ( Vmax) was evaluated in an oxygraph cell on saponin-permeabilized muscle fibers with pyruvate + malate and glutamate + malate as substrates. Significant relationships were found between γ2 and pyruvate + malate Vmax ( r = 0.60, P < 0.05), γ2 and glutamate + malate Vmax ( r = 0.66, P < 0.01), and γ2 and citrate synthase activity ( r = 0.76, P < 0.01). In addition, γ2, glutamate + malate Vmax, and pyruvate + malate Vmax were related to FIAO (γ2 − FIAO: r = 0.85; P < 0.01; glutamate + malate Vmax − FIAO: r = 0.70, P < 0.01; and pyruvate + malate Vmax − FIAO: r = 0.63, P < 0.01) and FISprint (γ2 − FISprint: r = 0.74, P < 0.01; glutamate + malate Vmax − FISprint: r = 0.64, P < 0.01; and pyruvate + malate Vmax − FISprint: r = 0.46, P < 0.01). In conclusion, these results suggested that the maximal muscle oxidative capacity was related to blood lactate removal ability after a 1-min all-out test. Moreover, maximal muscle oxidative capacity and blood lactate removal ability were associated with the delay in the fatigue observed during continuous and intermittent supramaximal exercises in well-trained subjects.

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