No limiting role for glycogenin in determining maximal attainable glycogen levels in rat skeletal muscle

2000 ◽  
Vol 278 (3) ◽  
pp. E398-E404 ◽  
Author(s):  
Bo Falck Hansen ◽  
Wim Derave ◽  
Pia Jensen ◽  
Erik A. Richter

We examined whether the protein level and/or activity of glycogenin, the protein core upon which glycogen is synthesized, is limiting for maximal attainable glycogen levels in rat skeletal muscle. Glycogenin activity was 27.5 ± 1.4, 34.7 ± 1.7, and 39.7 ± 1.3 mU/mg protein in white gastrocnemius, red gastrocnemius, and soleus muscles, respectively. A similar fiber type dependency of glycogenin protein levels was seen. Neither glycogenin protein level nor the activity of glycogenin correlated with previously determined maximal attainable glycogen levels, which were 69.3 ± 5.8, 137.4 ± 10.1, and 80.0 ± 5.4 μmol/g wet wt in white gastrocnemius, red gastrocnemius, and soleus muscles, respectively. In additional experiments, rats were exercise trained by swimming, which resulted in a significant increase in the maximal attainable glycogen levels in soleus muscles (∼25%). This increase in maximal glycogen levels was not accompanied by an increase in glycogenin protein level or activity. Furthermore, even in the presence of very high glycogen levels (∼170 μmol/g wet wt), ∼30% of the total glycogen pool continued to be present as unsaturated glycogen molecules (proglycogen). Therefore, it is concluded that glycogenin plays no limiting role for maximal attainable glycogen levels in rat skeletal muscle.

2004 ◽  
Vol 97 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Kirk A. Abraham ◽  
Ronald L. Terjung

During contractions, there is a net efflux of phosphate from skeletal muscle, likely because of an elevated intracellular inorganic phosphate (Pi) concentration. Over time, contracting muscle could incur a substantial phosphate deficit unless Pi uptake rates were increased during contractions. We used the perfused rat hindquarter preparation to assess [32P]Pi uptake rates in muscles at rest or over a range of energy expenditures during contractions at 0.5, 3, or 5 Hz for 30 min. Pi uptake rates were reduced during contractions in a pattern that was dependent on contraction frequency and fiber type. In soleus and red gastrocnemius, [32P]Pi uptake rates declined by ∼25% at 0.5 Hz and 50–60% at 3 and 5 Hz. Uptake rates in white gastrocnemius decreased by 65–75% at all three stimulation frequencies. These reductions in Pi uptake are not likely confounded by changes in precursor [32P]Pi specific activity in the interstitium. In soleus and red gastrocnemius, declines in Pi uptake rates were related to energy expenditure over the contraction duration. These data imply that Pi uptake in skeletal muscle is acutely modulated during contractions and that decreases in Pi uptake rates, in combination with expected increases in Pi efflux, exacerbate the net loss of phosphate from the cell. Enhanced uptake of Pi must subsequently occur because skeletal muscle typically maintains a relatively constant total phosphate pool.


1955 ◽  
Vol 102 (6) ◽  
pp. 705-711 ◽  
Author(s):  
F. S. Robscheit-Robbins ◽  
G. H. Whipple

Normal red blood cells in dogs contain stroma in fairly uniform amounts. This red cell stroma is rich in proteins and lipides. Anemia due to blood loss causes an increase in stroma protein. The highest levels of stroma protein are found in the severe anemias. As the anemia is corrected by red cell regeneration, the stroma protein level falls to normal. Anemia due to blood destruction (phenylhydrazine) presents very high levels of stroma protein—almost double the increase noted in anemia due to blood loss. Hypoproteinemia added to anemia due to blood loss causes no significant change on the stroma protein level. Abscesses due to the subcutaneous injection of turpentine during the anemia cause slight decreases in the stroma protein levels. Chloroform poisoning has no effect on the stroma protein levels. The total lipides of the stroma are rather stable and are little influenced by anemia. In certain experiments with hemolytic anemia and with hypoproteinemia, there is a significant rise in total lipide figures.


2012 ◽  
Vol 113 (10) ◽  
pp. 1624-1634 ◽  
Author(s):  
Erin L. Seifert ◽  
Mark Bastianelli ◽  
Céline Aguer ◽  
Cynthia Moffat ◽  
Carmen Estey ◽  
...  

Exercise capacity and performance strongly associate with metabolic and biophysical characteristics of skeletal muscle, factors that also relate to overall disease risk. Despite its importance, the exact mechanistic features that connect aerobic metabolism with health status are unknown. To explore this, we applied artificial selection of rats for intrinsic (i.e., untrained) aerobic treadmill running to generate strains of low- and high-capacity runners (LCR and HCR, respectively), subsequently shown to diverge for disease risk. Concurrent breeding of LCR and HCR per generation allows the lines to serve as reciprocal controls for unknown environmental changes. Here we provide the first direct evidence in mitochondria isolated from skeletal muscle that intrinsic mitochondrial capacity is higher in HCR rats. Maximal phosphorylating respiration was ∼40% greater in HCR mitochondria, independent of substrate and without altered proton leak or major changes in protein levels or muscle fiber type, consistent with altered control of phosphorylating respiration. Unexpectedly, H2O2 emission was ∼20% higher in HCR mitochondria, due to greater reduction of more harmful reactive oxygen species to H2O2; indeed, oxidative modification of mitochondrial proteins was lower. When the higher mitochondrial yield was considered, phosphorylating respiration and H2O2 emission were 70–80% greater in HCR muscle. Greater capacity of HCR muscle for work and H2O2 signaling may result in enhanced and more immediate cellular repair, possibly explaining lowered disease risks.


2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Jaume Padilla ◽  
Nathan T Jenkins ◽  
Jeffrey S Martin ◽  
Jacqueline M Crissey ◽  
Shawn B Bender ◽  
...  

2021 ◽  
Author(s):  
Yu Han ◽  
Lauren Z. Li ◽  
Nikhitha L. Kastury ◽  
Cody T. Thomas ◽  
Maggie P. Y. Lam ◽  
...  

RNA and protein levels correlate only partially and some transcripts are better correlated with their protein counterparts than others. This suggests that in aging and disease studies, some transcriptomics markers may carry more information in predicting protein-level changes. Here we applied a computational data analysis workflow to predict which transcriptomic changes are more likely relevant to protein-level regulation in striated muscle aging. The protein predictability of each transcript is estimated from existing large proteogenomics data sets, then transferred to new total RNA sequencing data comparing skeletal muscle and cardiac muscle in young adult (~4 months) mice vs. early aging (~20 months) mice. Aging cardiac and skeletal muscles both invoke transcriptomic changes in innate immune system and mitochondria pathways but diverge in extracellular matrix processes. On an individual gene level, we identified 611 age-associated signatures in skeletal and cardiac muscles at 10% FDR, including a number of myokine and cardiokine encoding genes. We estimate that about 48% of the aging-associated transcripts may predict protein levels well (r ≥ 0.5). In parallel, a comparison of the identified aging-regulated genes with public human transcriptomics data showed that only 35-45% of the identified genes show an age-dependent expression in corresponding human tissues. Finally, integrating both protein predictability and human translatability from multiple data sources, we nominate 134 prioritized aging signatures that are predicted to correlate strongly with protein levels and that show age-dependent expression in humans. These prioritized gene signatures may hold promise to understanding heart and skeletal muscle physiology in human and mouse aging.


2007 ◽  
Vol 39 (Supplement) ◽  
pp. S286
Author(s):  
Matthew J. Wessner ◽  
Paticia S. Sexton ◽  
William L. Sexton

2000 ◽  
Vol 279 (4) ◽  
pp. H1540-H1547 ◽  
Author(s):  
T. L. Haas ◽  
M. Milkiewicz ◽  
S. J. Davis ◽  
A. L. Zhou ◽  
S. Egginton ◽  
...  

Proteolysis of the capillary basement membrane is a hallmark of inflammation-mediated angiogenesis, but it is undetermined whether proteolysis plays a critical role in the process of activity-induced angiogenesis. Matrix metalloproteinases (MMPs) constitute the major class of proteases responsible for degradation of basement membrane proteins. We observed significant elevations of mRNA and protein levels of both MMP-2 and membrane type 1 (MT1)-MMP (2.9 ± 0.7- and 1.5 ± 0.1-fold above control, respectively) after 3 days of chronic electrical stimulation of rat skeletal muscle. Inhibition of MMP activity via the inhibitor GM-6001 prevented the growth of new capillaries as assessed by the capillary-to-fiber ratio (1.34 ± 0.08 in GM-6001-treated muscles compared with 1.69 ± 0.03 in control 7-day-stimulated muscles). This inhibition correlated with a significant reduction in the number of capillaries with observable breaks in the basement membrane, as assessed by electron microscopy (0.27 ± 0.27% in GM-6001-treated muscles compared with 3.72 ± 0.65% in control stimulated muscles). Proliferation of capillary-associated cells was significantly elevated by 2 days and remained elevated throughout 14 days of stimulation. Capillary-associated cell proliferation during muscle stimulation was not affected by MMP inhibition (80.3 ± 9.3 nuclei in control and 63.5 ± 8.5 nuclei in GM-6001-treated animals). We conclude that MMP proteolysis of capillary basement membrane proteins is a critical component of physiological angiogenesis, and we postulate that capillary-associated proliferation precedes and occurs independently of endothelial cell sprout formation.


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