scholarly journals Comment on: Sitnick et al. Skeletal Muscle Triacylglycerol Hydrolysis Does Not Influence Metabolic Complications of Obesity. Diabetes 2013;62:3350-3361

Diabetes ◽  
2013 ◽  
Vol 62 (12) ◽  
pp. e29-e29 ◽  
Author(s):  
C. Moro ◽  
D. Langin
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Complications ◽  
Triacylglycerol Hydrolysis

scholarly journals Skeletal Muscle Triacylglycerol Hydrolysis Does Not Influence Metabolic Complications of Obesity

Diabetes ◽  
2013 ◽  
Vol 62 (10) ◽  
pp. 3350-3361 ◽  
Author(s):  
M. T. Sitnick ◽  
M. K. Basantani ◽  
L. Cai ◽  
G. Schoiswohl ◽  
C. F. Yazbeck ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Complications ◽  
Triacylglycerol Hydrolysis

scholarly journals Effects of epinephrine on lipid metabolism in resting skeletal muscle

1998 ◽  
Vol 275 (2) ◽  
pp. E300-E309 ◽  
Author(s):  
Sandra J. Peters ◽  
David J. Dyck ◽  
Arend Bonen ◽  
Lawrence L. Spriet
Keyword(s):  
Skeletal Muscle ◽  
Lipid Metabolism ◽  
Lipid Synthesis ◽  
Hormone Sensitive Lipase ◽  
Simultaneous Estimation ◽  
Lipid Hydrolysis ◽  
Muscle Lipid ◽  
Triacylglycerol Hydrolysis ◽  
Skeletal Muscle Lipid ◽  
Glycogen Breakdown

The effects of physiological (0, 0.1, 2.5, and 10 nM) and pharmacological (200 nM) epinephrine concentrations on resting skeletal muscle lipid metabolism were investigated with the use of incubated rat epitrochlearis (EPT), flexor digitorum brevis (FDB), and soleus (SOL) muscles. Muscles were chosen to reflect a range of oxidative capacities: SOL > EPT > FDB. The muscles were pulsed with [1-14C]palmitate and chased with [9,10-3H]palmitate. Incorporation and loss of the labeled palmitate from the triacylglycerol pool (as well as mono- and diacylglycerol, phospholipid, and fatty acid pools) permitted the simultaneous estimation of lipid hydrolysis and synthesis. Endogenous and exogenous fat oxidation was quantified by14CO2and3H2O production, respectively. Triacylglycerol breakdown was elevated above control at all epinephrine concentrations in the oxidative SOL muscle, at 2.5 and 200 nM (at 10 nM, P= 0.066) in the FDB, and only at 200 nM epinephrine in the EPT. Epinephrine stimulated glycogen breakdown in the EPT at all concentrations but only at 10 and 200 nM in the FDB and had no effect in the SOL. We further characterized muscle lipid hydrolysis potential and measured total hormone-sensitive lipase content by Western blotting (SOL > FDB > EPT). This study demonstrated that physiological levels of epinephrine cause measurable increases in triacylglycerol hydrolysis at rest in oxidative but not in glycolytic muscle, with no change in the rate of lipid synthesis or oxidation. Furthermore, epinephrine caused differential stimulation of carbohydrate and fat metabolism in glycolytic vs. oxidative muscle. Epinephrine preferentially stimulated glycogen breakdown over triacylglycerol hydrolysis in the glycolytic EPT muscle. Conversely, in the oxidative SOL muscle, epinephrine caused an increase in endogenous lipid hydrolysis over glycogen breakdown.

Irradiation impairs mitochondrial function and skeletal muscle oxidative capacity: significance for metabolic complications in cancer survivors

Metabolism ◽  
2020 ◽  
Vol 103 ◽  
pp. 154025 ◽  
Author(s):  
Nadia M.L. Amorim ◽  
Anthony Kee ◽  
Adelle C.F. Coster ◽  
Christine Lucas ◽  
Sarah Bould ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cancer Survivors ◽  
Mitochondrial Function ◽  
Oxidative Capacity ◽  
Metabolic Complications ◽  
Muscle Oxidative Capacity

A critical evaluation of body composition modalities used to assess adipose and skeletal muscle tissue in cancer

2012 ◽  
Vol 37 (5) ◽  
pp. 811-821 ◽  
Author(s):  
Katie M. Di Sebastiano ◽  
Marina Mourtzakis
Keyword(s):  
Skeletal Muscle ◽  
Body Composition ◽  
Adipose Tissue ◽  
Cancer Patients ◽  
Tissue Loss ◽  
Metabolic Complications ◽  
Increased Risk ◽  
Body Composition Change ◽  
Patients Experience ◽  
Risk Of Cancer

The majority of cancer patients experience some form of body composition change during the disease trajectory. For example, breast cancer patients undergoing chemotherapy and prostate cancer patients undergoing androgen deprivation therapy gain fat and lose skeletal muscle, which are associated with increased risk of cancer recurrence and clinical comorbidities. In contrast, advanced cancer patients, such as lung and colorectal cancer patients, experience symptoms of cancer cachexia (accelerated loss of skeletal muscle with or without adipose tissue loss), which are associated with decreased treatment response and poorer survival rates in advanced cancers. The heterogeneity of body composition features and their diverse implications across different cancer populations supports the need for accurate quantification of muscle and adipose tissue. Use of appropriate body composition modalities will facilitate an understanding of the complex relationship between body composition characteristics and clinical outcomes. This will ultimately support the development and evaluation of future therapeutic interventions that aim to counter muscle loss and fat gain in cancer populations. Despite the various metabolic complications that may confound the accurate body composition measurement in cancer patients (i.e., dehydration may confound lean tissue measurement), there are no guidelines for selecting the most appropriate modalities to make these measurements. In this review we outline specific considerations for choosing the most optimal approaches of lean and adipose tissue measurements among different cancer populations. Anthropometric measures, bioelectrical impedance analysis, air displacement plethysmography, dual-energy X-ray absorptiometry, computed tomography, and magnetic resonance imaging will be discussed.

scholarly journals Skeletal Muscle Lipogenic Protein Expression Is Not Different between Lean and Obese Individuals: A Potential Factor in Ceramide Accumulation

2009 ◽  
Vol 94 (12) ◽  
pp. 5053-5061 ◽  
Author(s):  
A. Brianne Thrush ◽  
David N. Brindley ◽  
Adrian Chabowski ◽  
George J. Heigenhauser ◽  
David J. Dyck
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
Retinol Binding Protein ◽  
Metabolic Complications ◽  
Muscle Lipid ◽  
Lipid Species ◽  
Skeletal Muscle Lipid ◽  
Phosphatase 2A ◽  
Potential Factor ◽  
Ceramide Accumulation

Context: Skeletal muscle lipid content is increased in obesity. Recent evidence suggests that fatty acid (FA) storage as triacylglycerol (TAG) represents a metabolically safe pool compared to the more bioactive diacylglycerol (DAG) and ceramide. Objective/Design: The purpose of this study was to compare the expression of lipogenic proteins and ceramide and DAG content in skeletal muscle of lean and obese humans. We hypothesized that lipogenic protein expression would be increased in obese to facilitate the storage of excess FA as TAG. Participants: Eighteen lean (BMI ≤26 kg/m2) and 15 obese (BMI >29 kg/m2) women participated in this study. Results: There was no difference in the expression of any lipogenic (stearoyl-CoA desaturase-1, stearoyl retinol binding protein-1c, mitochondrial glycerol-3-phosphate acyltransferase, diacylglycerol acyltransferase-1) or sphingolipid proteins measured between lean and obese humans. Total ceramide was increased in muscle from obese humans (lean vs. obese, 529.4 ± 54.8 vs. 672.4 ± 57.4 nmol/g; P < 0.05), but there was no difference in total DAG content (lean vs. obese, 2244.1 ± 278.2 vs. 1941.4 ± 165.0 nmol/g). Content of protein phosphatase 2A, a ceramide target, was increased in muscle of obese humans (P < 0.05). Conclusions: We propose that in muscle of obese humans there is an insufficient lipogenic response to the lipid oversupply, allowing more FA to be stored as reactive lipid species, particularly ceramide, potentially contributing to subsequent metabolic complications.

scholarly journals The Potential Role of Polyphenols in Modulating Mitochondrial Bioenergetics within the Skeletal Muscle: A Systematic Review of Preclinical Models

Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2791
Author(s):  
Sinenhlanhla X. H. Mthembu ◽  
Phiwayinkosi V. Dludla ◽  
Khanyisani Ziqubu ◽  
Tawanda M. Nyambuya ◽  
Abidemi P. Kappo ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Antioxidant Properties ◽  
General Interest ◽  
Mitochondrial Bioenergetics ◽  
Metabolic Function ◽  
Preclinical Models ◽  
Metabolic Complications ◽  
The Impact

Polyphenols are naturally derived compounds that are increasingly being explored for their various health benefits. In fact, foods that are rich in polyphenols have become an attractive source of nutrition and a potential therapeutic strategy to alleviate the untoward effects of metabolic disorders. The last decade has seen a rapid increase in studies reporting on the bioactive properties of polyphenols against metabolic complications, especially in preclinical models. Various experimental models involving cell cultures exposed to lipid overload and rodents on high fat diet have been used to investigate the ameliorative effects of various polyphenols against metabolic anomalies. Here, we systematically searched and included literature reporting on the impact of polyphenols against metabolic function, particularly through the modulation of mitochondrial bioenergetics within the skeletal muscle. This is of interest since the skeletal muscle is rich in mitochondria and remains one of the main sites of energy homeostasis. Notably, increased substrate availability is consistent with impaired mitochondrial function and enhanced oxidative stress in preclinical models of metabolic disease. This explains the general interest in exploring the antioxidant properties of polyphenols and their ability to improve mitochondrial function. The current review aimed at understanding how these compounds modulate mitochondrial bioenergetics to improve metabolic function in preclinical models on metabolic disease.

scholarly journals Tissue-specific activity of lipoprotein lipase in skeletal muscle regulates the expression of uncoupling protein 3 in transgenic mouse models

2001 ◽  
Vol 355 (3) ◽  
pp. 647-652 ◽  
Author(s):  
Dagmar KRATKY ◽  
Juliane G. STRAUSS ◽  
Rudolf ZECHNER
Keyword(s):  
Skeletal Muscle ◽  
Lipoprotein Lipase ◽  
Specific Activity ◽  
Uncoupling Protein ◽  
Large Body ◽  
Mrna Levels ◽  
Expression Levels ◽  
Uncoupling Protein 3 ◽  
Triacylglycerol Hydrolysis ◽  
Brown Adipose

Uncoupling protein (UCP)-2 and UCP-3 are two recently discovered proteins similar to UCP-1, which regulates thermogenesis in brown adipose tissue (BAT). Whereas UCP-1 expression is restricted to BAT, UCP-2 is widely expressed. UCP-3 is found mainly in skeletal muscle and BAT. A large body of evidence exists that the expression of UCP-2 and UCP-3 in skeletal muscle of mice is regulated by feeding/fasting, and some studies have suggested that this effect might be caused by the changing concentration of plasma non-esterified fatty acids (NEFAs). In an attempt to determine whether the increased import of triacylglycerol-derived NEFAs can also affect UCP expression, we determined the mRNA levels of UCP-1, UCP-2 and UCP-3 in BAT and muscle of induced mutant mouse lines that overexpressed or lacked lipoprotein lipase (LPL) in these tissues. The expression levels of UCP-1 and UCP-2 in BAT and in skeletal and cardiac muscle respectively were not affected by variations in tissue LPL activities. In contrast, UCP-3 mRNA levels were induced 3.4-fold in mice with high levels of LPL in skeletal muscle, and down-regulated in mice that lacked LPL in skeletal muscle. The presence or absence of LPL in BAT had no effect on UCP-3 expression levels. The response of UCP-3 mRNA expression to variations in LPL activity in skeletal muscle was independent of the feeding status or of plasma NEFA concentrations. These findings indicated that NEFAs as lipolytic products of LPL-mediated triacylglycerol hydrolysis markedly affect UCP-3 expression and that increased LPL activities occurring during fasting in skeletal muscle contribute to the induction of UCP-3 expression by promoting the increased uptake of NEFAs. In addition, our results demonstrate that UCP-2 and UCP-3 are differentially regulated in response to LPL-mediated NEFA uptake in skeletal muscle of mice.

scholarly journals Adipose triglyceride lipase deletion from adipocytes, but not skeletal myocytes, impairs acute exercise performance in mice

2015 ◽  
Vol 308 (10) ◽  
pp. E879-E890 ◽  
Author(s):  
John J. Dubé ◽  
Mitch T. Sitnick ◽  
Gabriele Schoiswohl ◽  
Rachel C. Wills ◽  
Mahesh K. Basantani ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Performance ◽  
Acute Exercise ◽  
Submaximal Exercise ◽  
Adipose Triglyceride Lipase ◽  
Substrate Availability ◽  
Energy Substrate ◽  
Triglyceride Lipase ◽  
Skeletal Myocytes ◽  
Triacylglycerol Hydrolysis

Adipose triglyceride lipase (ATGL) is the rate-limiting enzyme mediating triacylglycerol hydrolysis in virtually all cells, including adipocytes and skeletal myocytes, and hence, plays a critical role in mobilizing fatty acids. Global ATGL deficiency promotes skeletal myopathy and exercise intolerance in mice and humans, and yet the tissue-specific contributions to these phenotypes remain unknown. The goal of this study was to determine the relative contribution of ATGL-mediated triacylglycerol hydrolysis in adipocytes vs. skeletal myocytes to acute exercise performance. To achieve this goal, we generated murine models with adipocyte- and skeletal myocyte-specific targeted deletion of ATGL. We then subjected untrained mice to acute peak and submaximal exercise interventions and assessed exercise performance and energy substrate metabolism. Impaired ATGL-mediated lipolysis within adipocytes reduced peak and submaximal exercise performance, reduced peripheral energy substrate availability, shifted energy substrate preference toward carbohydrate oxidation, and decreased HSL Ser660 phosphorylation and mitochondrial respiration within skeletal muscle. In contrast, impaired ATGL-mediated lipolysis within skeletal myocytes was not sufficient to reduce peak and submaximal exercise performance or peripheral energy substrate availability and instead tended to enhance metabolic flexibility during peak exercise. Furthermore, the expanded intramyocellular triacylglycerol pool in these mice was reduced following exercise in association with preserved HSL phosphorylation, suggesting that HSL may compensate for impaired ATGL action in skeletal muscle during exercise. These data suggest that adipocyte rather than skeletal myocyte ATGL-mediated lipolysis plays a greater role during acute exercise in part because of compensatory mechanisms that maintain lipolysis in muscle, but not adipose tissue, when ATGL is absent.

Endotoxin Alteration of the Mucopolysaccharide Blood Vessel Coating in Rats

1974 ◽  
Vol 32 ◽  
pp. 148-149
Author(s):  
D. E. Philpott ◽  
A. Takahashi
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Salivary Gland ◽  
Carotid Artery ◽  
Basement Membrane ◽  
Coronary Vessels ◽  
Ruthenium Red ◽  
E Coli ◽  
Old Rats ◽  
The Brain

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.

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