Myofibrillar distribution of succinate dehydrogenase activity and lipid stores differs in skeletal muscle tissue of paraplegic subjects

2012 ◽  
Vol 302 (3) ◽  
pp. E365-E373 ◽  
Author(s):  
Richard A. M. Jonkers ◽  
Marlou L. Dirks ◽  
Christine I. H. C. Nabuurs ◽  
Henk M. De Feyter ◽  
Stephan F. E. Praet ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Succinate Dehydrogenase ◽  
Muscle Tissue ◽  
Muscle Fiber ◽  
Muscle Fibers ◽  
Oxidative Capacity ◽  
Skeletal Muscle Tissue ◽  
Whole Body ◽  
The Impact

Lack of physical activity has been related to an increased risk of developing insulin resistance. This study aimed to assess the impact of chronic muscle deconditioning on whole body insulin sensitivity, muscle oxidative capacity, and intramyocellular lipid (IMCL) content in subjects with paraplegia. Nine subjects with paraplegia and nine able-bodied, lean controls were recruited. An oral glucose tolerance test was performed to assess whole body insulin sensitivity. IMCL content was determined both in vivo and in vitro using1H-magnetic resonance spectroscopy and fluorescence microscopy, respectively. Muscle biopsy samples were stained for succinate dehydrogenase (SDH) activity to measure muscle fiber oxidative capacity. Subcellular distributions of IMCL and SDH activity were determined by defining subsarcolemmal and intermyofibrillar areas on histological samples. SDH activity was 57 ± 14% lower in muscle fibers derived from subjects with paraplegia when compared with controls ( P < 0.05), but IMCL content and whole body insulin sensitivity did not differ between groups. In muscle fibers taken from controls, both SDH activity and IMCL content were higher in the subsarcolemmal region than in the intermyofibrillar area. This typical subcellular SDH and IMCL distribution pattern was lost in muscle fibers collected from subjects with paraplegia and had changed toward a more uniform distribution. In conclusion, the lower metabolic demand in deconditioned muscle of subjects with paraplegia results in a significant decline in muscle fiber oxidative capacity and is accompanied by changes in the subcellular distribution patterns of SDH activity and IMCL. However, loss of muscle activity due to paraplegia is not associated with substantial lipid accumulation in skeletal muscle tissue.

scholarly journals Muscle Oxidative Capacity Is a Better Predictor of Insulin Sensitivity than Lipid Status

2003 ◽  
Vol 88 (11) ◽  
pp. 5444-5451 ◽  
Author(s):  
Clinton R. Bruce ◽  
Mitchell J. Anderson ◽  
Andrew L. Carey ◽  
David G. Newman ◽  
Arend Bonen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Citrate Synthase ◽  
Oxidative Capacity ◽  
Fatty Acyl ◽  
Whole Body ◽  
Before And After ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
Long Chain

Abstract We determined whole-body insulin sensitivity, long-chain fatty acyl coenzyme A (LCACoA) content, skeletal muscle triglyceride (TGm) concentration, fatty acid transporter protein content, and oxidative enzyme activity in eight patients with type 2 diabetes (TYPE 2); six healthy control subjects matched for age (OLD), body mass index, percentage of body fat, and maximum pulmonary O2 uptake; nine well-trained athletes (TRAINED); and four age-matched controls (YOUNG). Muscle biopsies from the vastus lateralis were taken before and after a 2-h euglycemic-hyperinsulinemic clamp. Oxidative enzyme activities, fatty acid transporters (FAT/CD36 and FABPpm), and TGm were measured from basal muscle samples, and total LCACoA content was determined before and after insulin stimulation. Whole-body insulin-stimulated glucose uptake was lower in TYPE 2 (P &lt; 0.05) than in OLD, YOUNG, and TRAINED. TGm was elevated in TYPE 2 compared with all other groups (P &lt; 0.05). However, both basal and insulin-stimulated skeletal muscle LCACoA content were similar. Basal citrate synthase activity was higher in TRAINED (P &lt; 0.01), whereas β-hydroxyacyl CoA dehydrogenase activity was higher in TRAINED compared with TYPE 2 and OLD. There was a significant relationship between the oxidative capacity of skeletal muscle and insulin sensitivity (citrate synthase, r = 0.71, P &lt; 0.001; β-hydroxyacyl CoA dehydrogenase, r = 0.61, P = 0.001). No differences were found in FAT/CD36 protein content between groups. In contrast, FABPpm protein was lower in OLD compared with TYPE 2 and YOUNG (P &lt; 0.05). In conclusion, despite markedly elevated skeletal muscle TGm in type 2 diabetic patients and strikingly different levels of whole-body glucose disposal, both basal and insulin-stimulated LCACoA content were similar across groups. Furthermore, skeletal muscle oxidative capacity was a better predictor of insulin sensitivity than either TGm concentration or long-chain fatty acyl CoA content.

scholarly journals Exercising for Insulin Sensitivity – Is There a Mechanistic Relationship With Quantitative Changes in Skeletal Muscle Mass?

2021 ◽  
Vol 12 ◽  
Author(s):  
Jasmine Paquin ◽  
Jean-Christophe Lagacé ◽  
Martin Brochu ◽  
Isabelle J. Dionne
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Homeostasis ◽  
Metabolic Health ◽  
Whole Body ◽  
Future Research ◽  
Level Of Evidence ◽  
Exercise Interventions ◽  
Quantitative Changes ◽  
The Impact

Skeletal muscle (SM) tissue has been repetitively shown to play a major role in whole-body glucose homeostasis and overall metabolic health. Hence, SM hypertrophy through resistance training (RT) has been suggested to be favorable to glucose homeostasis in different populations, from young healthy to type 2 diabetic (T2D) individuals. While RT has been shown to contribute to improved metabolic health, including insulin sensitivity surrogates, in multiple studies, a universal understanding of a mechanistic explanation is currently lacking. Furthermore, exercised-improved glucose homeostasis and quantitative changes of SM mass have been hypothesized to be concurrent but not necessarily causally associated. With a straightforward focus on exercise interventions, this narrative review aims to highlight the current level of evidence of the impact of SM hypertrophy on glucose homeostasis, as well various mechanisms that are likely to explain those effects. These mechanistic insights could provide a strengthened rationale for future research assessing alternative RT strategies to the current classical modalities, such as low-load, high repetition RT or high-volume circuit-style RT, in metabolically impaired populations.

scholarly journals Hsp60 in Skeletal Muscle Fiber Biogenesis and Homeostasis: From Physical Exercise to Skeletal Muscle Pathology

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 224 ◽  
Author(s):  
Antonella Marino Gammazza ◽  
Filippo Macaluso ◽  
Valentina Di Felice ◽  
Francesco Cappello ◽  
Rosario Barone
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fiber ◽  
Pathological Condition ◽  
Treatment Options ◽  
Muscle Fibers ◽  
Mitochondrial Protein ◽  
Oxidative Capacity ◽  
Skeletal Muscle Fiber ◽  
Muscle Pathology ◽  
Skeletal Muscle Fibers

Hsp60 is a molecular chaperone classically described as a mitochondrial protein with multiple roles in health and disease, participating to the maintenance of protein homeostasis. It is well known that skeletal muscle is a complex tissue, rich in proteins, that is, subjected to continuous rearrangements, and this homeostasis is affected by many different types of stimuli and stresses. The regular exercise induces specific histological and biochemical adaptations in skeletal muscle fibers, such as hypertrophy and an increase of mitochondria activity and oxidative capacity. The current literature is lacking in information regarding Hsp60 involvement in skeletal muscle fiber biogenesis and regeneration during exercise, and in disease conditions. Here, we briefly discuss the functions of Hsp60 in skeletal muscle fibers during exercise, inflammation, and ageing. Moreover, the potential usage of Hsp60 as a marker for disease and the evaluation of novel treatment options is also discussed. However, some questions remain open, and further studies are needed to better understand Hsp60 involvement in skeletal muscle homeostasis during exercise and in pathological condition.

scholarly journals Expression of macrophage genes within skeletal muscle correlates inversely with adiposity and insulin resistance in humans

2018 ◽  
Vol 43 (2) ◽  
pp. 187-193 ◽  
Author(s):  
Dongmei Liu ◽  
Flor Elisa Morales ◽  
Heidi. B. IglayReger ◽  
Mary K. Treutelaar ◽  
Amy E. Rothberg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Weight Loss ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Muscle Tissue ◽  
Skeletal Muscle Tissue ◽  
Obese Patients ◽  
Weight Loss Intervention

Local inflammation in obese adipose tissue has been shown to contribute to insulin resistance; however, the role of macrophage infiltration within skeletal muscle is still debatable. This study aimed to evaluate the association of skeletal muscle macrophage gene expression with adiposity levels and insulin sensitivity in obese patients. Twenty-two nondiabetic obese patients and 23 healthy lean controls were included. Obese patients underwent a 3-month weight loss intervention. Macrophage gene expression in skeletal muscle (quantitative real-time polymerase chain reaction), body composition (dual-energy X-ray absorptiometry), and insulin sensitivity (homeostatic model assessment (HOMA) and oral glucose tolerance test) were compared between groups and their associations were analyzed. To validate skeletal muscle findings, we repeated the analyses with macrophage gene expression in adipose tissue. Expression levels of macrophage genes (CD68, CD11b, CD206, CD16, CD40, and CD163) were lower in skeletal muscle tissue of obese versus lean participants. Macrophage gene expression was also found to be inversely associated with adiposity, fasting insulin, and HOMA (r = −0.4 ∼ −0.6, p < 0.05), as well as positively associated with insulin sensitivity (r = 0.4 ∼ 0.8, p < 0.05). On the other hand, adipose tissue macrophage gene expression showed higher levels in obese versus lean participants, presenting a positive association with adiposity levels. Macrophage gene expression, in both skeletal and adipose tissue samples, was only minimally affected by the weight loss intervention. In contrast with the established positive relationship between adiposity and macrophage gene expression, an unexpected inverse correlation between these 2 variables was observed in skeletal muscle tissue. Additionally, muscle macrophage gene expression was inversely correlated with insulin resistance.

Aligned and electrically conductive 3D collagen scaffolds for skeletal muscle tissue engineering

2021 ◽  
Author(s):  
Ivan M Basurto ◽  
Mark T Mora ◽  
Gregg M Gardner ◽  
George Christ ◽  
Steven R Caliari
Keyword(s):  
Skeletal Muscle ◽  
Tissue Engineering ◽  
Muscle Tissue ◽  
Muscle Fibers ◽  
Three Dimensional ◽  
Skeletal Muscle Tissue ◽  
Collagen Scaffolds ◽  
Electrically Conductive ◽  
Normal Movement ◽  
3D Collagen

Skeletal muscle is characterized by its three-dimensional (3D) anisotropic architecture composed of highly aligned and electrically-excitable muscle fibers that enable normal movement. Biomaterial-based tissue engineering approaches to repair skeletal muscle...

scholarly journals Extracellular matrix: an important regulator of cell functions and skeletal muscle development

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Weiya Zhang ◽  
Yuan Liu ◽  
Hong Zhang
Keyword(s):  
Skeletal Muscle ◽  
Extracellular Matrix ◽  
Connective Tissue ◽  
Muscle Tissue ◽  
Muscle Fiber ◽  
Muscle Development ◽  
Skeletal Muscle Tissue ◽  
Skeletal Muscle Development ◽  
Comprehensive Overview ◽  
Cell Functions

AbstractExtracellular matrix (ECM) is a kind of connective tissue in the cell microenvironment, which is of great significance to tissue development. ECM in muscle fiber niche consists of three layers: the epimysium, the perimysium, and the endomysium (basal lamina). These three layers of connective tissue structure can not only maintain the morphology of skeletal muscle, but also play an important role in the physiological functions of muscle cells, such as the transmission of mechanical force, the regeneration of muscle fiber, and the formation of neuromuscular junction. In this paper, detailed discussions are made for the structure and key components of ECM in skeletal muscle tissue, the role of ECM in skeletal muscle development, and the application of ECM in biomedical engineering. This review will provide the reader with a comprehensive overview of ECM, as well as a comprehensive understanding of the structure, physiological function, and application of ECM in skeletal muscle tissue.

scholarly journals SKELETAL MUSCLE POSTTRAUMATIC REGENERATION RESPONSE TO HUMIC PELOID MEDICATION

2019 ◽  
Vol 16 (32) ◽  
pp. 96-107
Author(s):  
Galina N SUVOROVA ◽  
Natalia N VOLOGDINA ◽  
Nadezhda P AVVAKUMOV ◽  
Maria Y KRIVOPALOVA
Keyword(s):  
Skeletal Muscle ◽  
Humic Acids ◽  
Muscle Tissue ◽  
Muscle Fibers ◽  
Skeletal Muscle Tissue ◽  
Control Group ◽  
Acid Extraction ◽  
Zinc Ions ◽  
Posttraumatic Regeneration ◽  
Regeneration Response

One of the relevant tasks of current morphology is the investigation of tissue regenerative potential and research for new medications that improve recovery process efficiency. Nowadays, clinical specialists focus on medications that are based on natural compounds. However, such medication influence on the processes that occur within the injured tissues is still not identified. The purpose of this study was to investigate skeletal muscle tissue posttraumatic regeneration response to humic peloid medication, based on humic acids modified by Zinc ions. Humic acid extraction was carried out by means of patent procedure. The study included laboratory Wistar rats with hyperextension of front femur muscle. The preparations were studied by means of light and electronic microscopy and autoradiography. Histologic preparations evaluation showed that under peloid medication exposure the apolexis processes within muscle fibers rupture are inhibited, interstitial edema becomes restricted by the injured area, vessel growth into the area of damaged capillaries is stimulated, macrophages migrate and the area and duration of posttraumatic inflammation decrease. Additionally, peloid medication intake shortens the length of skeletal muscle tissue reparative histogenesis stages: myosatellitocytes are activated earlier than in the control group, myoblasts and myosymplasts are detected, the separation of nuclear sarcoplasmatic areas from partly injured muscle fibers is stimulated, myotubules appear 3 – 5 days earlier than in control group. Overall, muscle tissue regeneration efficiency increases by 21%. Obtained results allow us to conclude that peloid medication based on humic acids modified by Zinc ions positively influence the stimulation of the regeneration process. This will lead to further investigation of humic substances: fulvic, hymatomelanic, humin and humic acids of peloids as medications and their implementation in clinical practice.

scholarly journals Insulin Sensitivity in Adipose and Skeletal Muscle Tissue of Dairy Cows in Response to Dietary Energy Level and 2,4-Thiazolidinedione (TZD)

PLoS ONE ◽  
2015 ◽  
Vol 10 (11) ◽  
pp. e0142633 ◽  
Author(s):  
Afshin Hosseini ◽  
Muhammad Rizwan Tariq ◽  
Fernanda Trindade da Rosa ◽  
Julia Kesser ◽  
Zeeshan Iqbal ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Energy Level ◽  
Dairy Cows ◽  
Muscle Tissue ◽  
Skeletal Muscle Tissue ◽  
Dietary Energy

Selective activation of PPARγ in skeletal muscle induces endogenous production of adiponectin and protects mice from diet-induced insulin resistance

2010 ◽  
Vol 298 (1) ◽  
pp. E28-E37 ◽  
Author(s):  
Rajesh H. Amin ◽  
Suresh T. Mathews ◽  
Heidi S. Camp ◽  
Liyun Ding ◽  
Todd Leff
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Transgenic Mice ◽  
Muscle Tissue ◽  
Glucose Homeostasis ◽  
Muscle Cells ◽  
Whole Body ◽  
Fiber Types ◽  
Dependent Manner

The nuclear receptor peroxisome proliferator-activated receptor (PPAR)γ plays a key role in regulating whole body glucose homeostasis and insulin sensitivity. Although it is expressed most highly in adipose, it is also present at lower levels in many tissues, including skeletal muscle. The role muscle PPARγ plays in metabolic regulation and in mediating the antidiabetic effects of the thiazolidinediones is not understood. The goal of this work was to examine the molecular and physiological effects of PPARγ activation in muscle cells. We found that pharmacological activation of PPARγ in primary cultured myocytes, and genetic activation of muscle PPARγ in muscle tissue of transgenic mice, induced the production of adiponectin directly from muscle cells. This muscle-produced adiponectin was functional and capable of stimulating adiponectin signaling in myocytes. In addition, elevated skeletal muscle PPARγ activity in transgenic mice provided a significant protection from high-fat diet-induced insulin resistance and associated changes in muscle phenotype, including reduced myocyte lipid content and an increase in the proportion of oxidative muscle fiber types. Our findings demonstrate that PPARγ activation in skeletal muscle can have a significant protective effect on whole body glucose homeostasis and insulin resistance and that myocytes can produce and secrete functional adiponectin in a PPARγ-dependent manner. We propose that activation of PPARγ in myocytes induces a local production of adiponectin that acts on muscle tissue to improve insulin sensitivity.

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