P5.65 The effects of Omega-3 fatty acid on skeletal muscle atrophy induced by Dexamethasone

2011 ◽  
Vol 21 (9-10) ◽  
pp. 744
Author(s):  
A. Fappi ◽  
T.S. Godoy ◽  
D.P. Venâncio ◽  
G. Chadi ◽  
E. Zanoteli
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy ◽  
Omega 3 ◽  
Omega 3 Fatty Acid

scholarly journals Omega‐3 fatty acid supplementation attenuates skeletal muscle disuse atrophy during two weeks of unilateral leg immobilization in healthy young women

2019 ◽  
Vol 33 (3) ◽  
pp. 4586-4597 ◽  
Author(s):  
Chris Mcglory ◽  
Stefan H. M. Gorissen ◽  
Michael Kamal ◽  
Ravninder Bahniwal ◽  
Amy J. Hector ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Young Women ◽  
Disuse Atrophy ◽  
Omega 3 ◽  
Fatty Acid Supplementation ◽  
Acid Supplementation ◽  
Omega 3 Fatty Acid ◽  
Muscle Disuse

scholarly journals The Effects of Omega-3 Fatty Acid Supplementation on Dexamethasone-Induced Muscle Atrophy

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Alan Fappi ◽  
Tiago S. Godoy ◽  
Jessica R. Maximino ◽  
Vanessa R. Rizzato ◽  
Juliana de C. Neves ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Muscle Atrophy ◽  
Saline Solution ◽  
Significant Loss ◽  
Omega 3 ◽  
Negative Effects ◽  
Muscle Weight ◽  
Cross Sectional ◽  
Omega 3 Fatty Acid

Corticosteroids cause muscle atrophy by acting on proteasomal and lysosomal systems and by affecting pathways related to muscular trophysm, such as the IGF-1/PI-3k/Akt/mTOR. Omega-3 fatty acid (n-3) has been used beneficially to attenuate muscle atrophy linked to sepsis and cachexia; however, its effect on dexamethasone-induced muscle atrophy has not been evaluated.Objectives. We evaluated whether n-3 supplementation could mitigate the development of dexamethasone-induced muscle atrophy.Methods. Two groups ofWistarrats were orally supplemented with n-3 or vehicle solution for 40 days. In the last 10 days, dexamethasone, or saline solution, was administrated establishing four groups: control, dexamethasone, n-3, and dexamethasone + n-3. The cross-sectional areas of muscle fibers, gene expression (MyoD, Myogenin, MuRF-1, andAtrogin-1), and protein expression (Akt, GSK3β, FOXO3a, and mTOR) were assessed.Results. Dexamethasone induced a significant loss in body and muscle weight, atrophy in type 2B fibers, and decreased expression of P-Akt, P-GSK3β, and P-FOXO3a. N-3 supplementation did not attenuate the negative effects of dexamethasone on skeletal muscle; instead, it caused atrophy in type 1, 2A, reduced the expression ofMyogenin, and increased the expression ofAtrogin-1.Conclusion. Food supplements containing n-3 are usually healthful, but they may potentiate some of the side effects of glucocorticoids.

scholarly journals Sphingosine-1-phosphate analog FTY720 reverses obesity but not age-induced anabolic resistance to muscle contraction

2019 ◽  
Vol 317 (3) ◽  
pp. C502-C512
Author(s):  
Donato A. Rivas ◽  
Nicholas P. Rice ◽  
Yassine Ezzyat ◽  
Devin J. McDonald ◽  
Brittany E. Cooper ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Muscle Contraction ◽  
Chronic Inflammation ◽  
Muscle Atrophy ◽  
Muscle Cells ◽  
Skeletal Muscle Atrophy ◽  
Anabolic Resistance ◽  
Sphingosine 1 Phosphate

Sarcopenia, the age-associated loss of skeletal muscle mass and function, is coupled with declines in physical functioning leading to subsequent higher rates of disability, frailty, morbidity, and mortality. Aging and obesity independently contribute to muscle atrophy that is assumed to be a result of the activation of mutual physiological pathways. Understanding mechanisms contributing to the induction of skeletal muscle atrophy with aging and obesity is important for determining targets that may have pivotal roles in muscle loss in these conditions. We find that aging and obesity equally induce an anabolic resistance to acute skeletal muscle contraction as observed with decreases in anabolic signaling activation after contraction. Furthermore, treatment with the sphingosine-1-phosphate analog FTY720 for 4 wk increased lean mass and strength, and the anabolic signaling response to contraction was improved in obese but not older animals. To determine the role of chronic inflammation and different fatty acids on anabolic resistance in skeletal muscle cells, we overexpressed IKKβ with and without exposure to saturated fatty acid (SFA; palmitic acid), polyunsaturated fatty acid (eicosapentaenoic acid), and monounsaturated fatty acid (oleic acid). We found that IKKβ overexpression increased inflammation markers in muscle cells, and this chronic inflammation exacerbated anabolic resistance in response to SFA. Pretreatment with FTY720 reversed the inflammatory effects of palmitic acid in the muscle cells. Taken together, these data demonstrate chronic inflammation can induce anabolic resistance, SFA aggravates these effects, and FTY720 can reverse this by decreasing ceramide accumulation in skeletal muscle.

scholarly journals An Omega-3 Fatty Acid-Enriched Diet Prevents Skeletal Muscle Lesions in a Hamster Model of Dystrophy

2010 ◽  
Vol 177 (5) ◽  
pp. 2176-2184 ◽  
Author(s):  
Roberta Fiaccavento ◽  
Felicia Carotenuto ◽  
Alba Vecchini ◽  
Luciano Binaglia ◽  
Giancarlo Forte ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Omega 3 ◽  
Hamster Model ◽  
Omega 3 Fatty Acid ◽  
Muscle Lesions

Ethyl icosapentate (omega-3 fatty acid) causes accumulation of lipids in skeletal muscle but suppresses insulin resistance in OLETF rats

Metabolism ◽  
2003 ◽  
Vol 52 (1) ◽  
pp. 30-34 ◽  
Author(s):  
Masataka Kusunoki ◽  
Kazuhiko Tsutsumi ◽  
Tsutomu Hara ◽  
Hitoshi Ogawa ◽  
Takao Nakamura ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Omega 3 ◽  
Omega 3 Fatty Acid ◽  
Oletf Rats ◽  
Accumulation Of Lipids

scholarly journals Docosahexaenoic Acid Protects Muscle Cells from Palmitate-Induced Atrophy

ISRN Obesity ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Randall W. Bryner ◽  
Myra E. Woodworth-Hobbs ◽  
David L. Williamson ◽  
Stephen E. Alway
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Docosahexaenoic Acid ◽  
Muscle Atrophy ◽  
Muscle Growth ◽  
Muscle Cells ◽  
Skeletal Muscle Atrophy ◽  
Omega 3 ◽  
Myotube Hypertrophy

Background. Accumulation of free fatty acids leads to lipid-toxicity-associated skeletal muscle atrophy. Palmitate treatment reduces myoblast and myotube growth and causes apoptosis in vitro. It is not known if omega-3 fatty acids will protect muscle cells against palmitate toxicity. Therefore, we examined the effects of docosahexaenoic acid (DHA) on skeletal muscle growth. Methods. Mouse myoblasts (C2C12) were differentiated to myotubes, and then treated with 0 or 0.5 mM palmitic acid or 0 or 0.1 mM DHA. Results. Intramyocellular lipid was increased in palmitate-treated cells but was prevented by DHA-palmitate cotreatment. Total AMPK increased in DHA+ palmitate-treated compared to palmitate only cells. RpS6 phosphorylation decreased after palmitate (−55%) and this was blunted by DHA+ palmitate (−35%) treatment. Palmitate treatment decreased PGC1 protein expression by 69%, but was increased 165% with DHA+ palmitate () versus palmitate alone. While palmitate induced 25% and 90% atrophy in myotubes (after 48 hours and 96 hours, resp.), DHA+ palmitate treatment caused myotube hypertrophy of ~50% and 100% after 48 and 96 hours, respectively. Conclusion. These data show that DHA is protective against palmitate-induced atrophy. Although DHA did not activate the AMPK pathway, DHA treatment restored growth-signaling (i.e., rpS6) and rescued palmitate-induced muscle atrophy.

Myriocin prevents muscle ceramide accumulation but not muscle fiber atrophy during short-term mechanical unloading

2016 ◽  
Vol 120 (2) ◽  
pp. 178-187 ◽  
Author(s):  
Erwann Salaun ◽  
Luz Lefeuvre-Orfila ◽  
Thibault Cavey ◽  
Brice Martin ◽  
Bruno Turlin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Muscle Weakness ◽  
Muscle Atrophy ◽  
De Novo ◽  
Fiber Diameter ◽  
Sphingolipid Metabolism ◽  
Skeletal Muscle Atrophy ◽  
De Novo Synthesis ◽  
Skeletal Muscle Weakness

Bedridden patients in intensive care unit or after surgery intervention commonly develop skeletal muscle weakness. The latter is promoted by a variety of prolonged hospitalization-associated conditions. Muscle disuse is the most ubiquitous and contributes to rapid skeletal muscle atrophy and progressive functional strength reduction. Disuse causes a reduction in fatty acid oxidation, leading to its accumulation in skeletal muscle. We hypothesized that muscle fatty acid accumulation could stimulate ceramide synthesis and promote skeletal muscle weakness. Therefore, the present study was designed to determine the effects of sphingolipid metabolism on skeletal muscle atrophy induced by 7 days of disuse. For this purpose, male Wistar rats were treated with myriocin, an inhibitor of de novo synthesis of ceramides, and subjected to hindlimb unloading (HU) for 7 days. Soleus muscles were assayed for fiber diameter, ceramide levels, protein degradation, and apoptosis signaling. Serum and liver were removed to evaluate the potential hepatoxicity of myriocin treatment. We found that HU increases content of saturated C16:0 and C18:0 ceramides and decreases soleus muscle weight and fiber diameter. HU increased the level of polyubiquitinated proteins and induced apoptosis in skeletal muscle. Despite a prevention of C16:0 and C18:0 muscle accumulation, myriocin treatment did not prevent skeletal muscle atrophy and concomitant induction of apoptosis and proteolysis. Moreover, myriocin treatment increased serum transaminases and induced hepatocyte necrosis. These data highlight that inhibition of de novo synthesis of ceramides during immobilization is not an efficient strategy to prevent skeletal muscle atrophy and exerts adverse effects like hepatotoxicity.

Sign in / Sign up

Export Citation Format

Share Document