scholarly journals High-fat diet suppresses the positive effect of creatine supplementation on skeletal muscle function by reducing protein expression of IGF-PI3K-AKT-mTOR pathway

PLoS ONE ◽  
2018 ◽  
Vol 13 (10) ◽  
pp. e0199728 ◽  
Author(s):  
Renato Ferretti ◽  
Eliezer Guimarães Moura ◽  
Veridiana Carvalho dos Santos ◽  
Eduardo José Caldeira ◽  
Marcelo Conte ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
High Fat Diet ◽  
Muscle Function ◽  
Creatine Supplementation ◽  
Mtor Pathway ◽  
High Fat ◽  
Skeletal Muscle Function ◽  
Positive Effect

scholarly journals High-fat diet suppresses the positive effect of creatine supplementation on skeletal muscle function by reducing protein expression of IGF-PI3K-AKT-mTOR pathway

2018 ◽  
Author(s):  
Renato Ferretti ◽  
Eliezer Guimarães Moura ◽  
Veridiana Carvalho dos Santos ◽  
Eduardo José Caldeira ◽  
Marcelo Conte ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Muscle Mass ◽  
High Fat Diet ◽  
Muscle Function ◽  
Mtor Pathway ◽  
Muscle Performance ◽  
High Fat ◽  
Negative Effects ◽  
Obesity And Diabetes

AbstractHigh-fat (HF) diets in combination with sedentary lifestyle represent one of the major public health concerns predisposing to obesity and diabetes leading to skeletal muscle atrophy, decreased fiber diameter and muscle mass with accumulation of fat tissue resulting in loss of muscle strength. One strategy to overcome the maleficent effects of HF diet is resistance training, a strategy used to improve muscle mass, reverting the negative effects on obesity-related changes in skeletal muscle. Together with resistance training, supplementation with creatine monohydrate (CrM) in the diet has been used to improve muscle mass and strength. Creatine is a non-essential amino acid that is directly involved in the cross-bridge cycle providing a phosphate group to ADP during the initiation of muscle contraction. Besides its antioxidant and anti-inflammatory effects CrM also upregulates IGF-1 resulting in hyperthophy with an increase in muscle function. However, it is unknown whether CrM supplementation during resistance training would revert the negative effects of high-fat diet on the muscle performance. During 8 weeks we measured muscle performance to climb a 1.1m and 80° ladder with increasing load on trained rats that had received standard diet or high-fat diet, supplemented or not with CrM. We observed that the CrM supplementation up-regulated IGF-1 and phospho-AKT protein levels, suggesting an activation of the IGF1-PI3K-Akt/PKB-mTOR pathway. Moreover, despite the CrM supplementation, HF diet down-regulated several proteins of the IGF1-PI3K-Akt/PKB-mTOR pathway, suggesting that diet lipid content is crucial to maintain or improve muscle function during resistance training.

Aerobic exercise training improves skeletal muscle function and Ca2+ handling-related protein expression in sympathetic hyperactivity-induced heart failure

2010 ◽  
Vol 109 (3) ◽  
pp. 702-709 ◽  
Author(s):  
C. R. Bueno ◽  
J. C. B. Ferreira ◽  
M. G. Pereira ◽  
A. V. N. Bacurau ◽  
P. C. Brum
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Protein Expression ◽  
Aerobic Exercise ◽  
Muscle Function ◽  
Exercise Tolerance ◽  
Aerobic Exercise Training ◽  
Related Protein ◽  
Skeletal Muscle Function ◽  
Related Proteins

The cellular mechanisms of positive effects associated with aerobic exercise training on overall intrinsic skeletal muscle changes in heart failure (HF) remain unclear. We investigated potential Ca2+ abnormalities in skeletal muscles comprising different fiber compositions and investigated whether aerobic exercise training would improve muscle function in a genetic model of sympathetic hyperactivity-induced HF. A cohort of male 5-mo-old wild-type (WT) and congenic α2A/α2C adrenoceptor knockout (ARKO) mice in a C57BL/6J genetic background were randomly assigned into untrained and trained groups. Exercise training consisted of a 8-wk running session of 60 min, 5 days/wk (from 5 to 7 mo of age). After completion of the exercise training protocol, exercise tolerance was determined by graded treadmill exercise test, muscle function test by Rotarod, ambulation and resistance to inclination tests, cardiac function by echocardiography, and Ca2+ handling-related protein expression by Western blot. α2A/α2CARKO mice displayed decreased ventricular function, exercise intolerance, and muscle weakness paralleled by decreased expression of sarcoplasmic Ca2+ release-related proteins [α1-, α2-, and β1-subunits of dihydropyridine receptor (DHPR) and ryanodine receptor (RyR)] and Ca2+ reuptake-related proteins [sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)1/2 and Na+/Ca2+ exchanger (NCX)] in soleus and plantaris. Aerobic exercise training significantly improved exercise tolerance and muscle function and reestablished the expression of proteins involved in sarcoplasmic Ca2+ handling toward WT levels. We provide evidence that Ca2+ handling-related protein expression is decreased in this HF model and that exercise training improves skeletal muscle function associated with changes in the net balance of skeletal muscle Ca2+ handling proteins.

scholarly journals Cysteamine Decreases Low‐Density Lipoprotein Oxidation, Causes Regression of Atherosclerosis, and Improves Liver and Muscle Function in Low‐Density Lipoprotein Receptor–Deficient Mice

2021 ◽  
Vol 10 (18) ◽  
Author(s):  
Feroz Ahmad ◽  
Robert D. Mitchell ◽  
Tom Houben ◽  
Angela Palo ◽  
Tulasi Yadati ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Fat Diet ◽  
Muscle Function ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Low Density ◽  
High Fat ◽  
Atherosclerotic Lesions ◽  
Deficient Mice

Background We have shown previously that low‐density lipoprotein (LDL) can be oxidized in the lysosomes of macrophages, that this oxidation can be inhibited by cysteamine, an antioxidant that accumulates in lysosomes, and that this drug decreases atherosclerosis in LDL receptor–deficient mice fed a high‐fat diet. We have now performed a regression study with cysteamine, which is of more relevance to the treatment of human disease. Methods and Results LDL receptor–deficient mice were fed a high‐fat diet to induce atherosclerotic lesions. They were then reared on chow diet and drinking water containing cysteamine or plain drinking water. Aortic atherosclerosis was assessed, and samples of liver and skeletal muscle were analyzed. There was no regression of atherosclerosis in the control mice, but cysteamine caused regression of between 32% and 56% compared with the control group, depending on the site of the lesions. Cysteamine substantially increased markers of lesion stability, decreased ceroid, and greatly decreased oxidized phospholipids in the lesions. The liver lipid levels and expression of cluster of differentiation 68, acetyl–coenzyme A acetyltransferase 2, cytochromes P450 (CYP)27, and proinflammatory cytokines and chemokines were decreased by cysteamine. Skeletal muscle function and oxidative fibers were increased by cysteamine. There were no changes in the plasma total cholesterol, LDL cholesterol, high‐density lipoprotein cholesterol, or triacylglycerol concentrations attributable to cysteamine. Conclusions Inhibiting the lysosomal oxidation of LDL in atherosclerotic lesions by antioxidants targeted at lysosomes causes the regression of atherosclerosis and improves liver and muscle characteristics in mice and might be a promising novel therapy for atherosclerosis in patients.

scholarly journals Effect of Dietary Silk Peptide on Obesity, Hyperglycemia, and Skeletal Muscle Regeneration in High-Fat Diet-Fed Mice

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 377 ◽  
Author(s):  
Kippeum Lee ◽  
Heegu Jin ◽  
Sungwoo Chei ◽  
Hyun-Ji Oh ◽  
Jeong-Yong Lee ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Fat Diet ◽  
Glucose Transporter ◽  
Uncoupling Protein ◽  
Skeletal Muscle Regeneration ◽  
High Fat ◽  
Skeletal Muscle Function ◽  
Silk Peptide

Obesity is associated with excess body fat accumulation that can cause hyperglycemia and reduce skeletal muscle function and strength, which characterize the development of sarcopenic obesity. In this study, we aimed to determine the mechanism whereby acid-hydrolyzed silk peptide (SP) prevents high-fat diet (HFD)-induced obesity and whether it regulates glucose uptake and muscle differentiation using in vivo and in vitro approaches. Our findings demonstrate that SP inhibits body mass gain and the expression of adipogenic transcription factors in visceral adipose tissue (VAT). SP also had an anti-diabetic effect in VAT and skeletal muscle because it upregulated glucose transporter type 4 (GLUT4) and uncoupling protein 3 (UCP3) expression. Furthermore, SP reduced ubiquitin proteasome and promoted myoblast determination protein 1 (MyoD)/myogenic factor 4 (myogenin) expression, implying that it may have potential for the treatment of obesity-induced hyperglycemia and obesity-associated sarcopenia.

Mitochondrial Function and Protein Expression in C5L2KO Mouse Skeletal Muscle after 10 Weeks of High-Fat Diet Intake

2011 ◽  
pp. P3-441-P3-441
Author(s):  
Christian Roy ◽  
Sabina Paglialunga ◽  
Joris Hoeks ◽  
Katherine Cianflone ◽  
Patrick Schrauwen
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
Mitochondrial Function ◽  
High Fat Diet ◽  
High Fat ◽  
Mouse Skeletal Muscle ◽  
Diet Intake

scholarly journals Pioglitazone Upregulates Angiotensin Converting Enzyme 2 Expression in Insulin-Sensitive Tissues in Rats with High-Fat Diet-Induced Nonalcoholic Steatohepatitis

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Wei Zhang ◽  
Yi-Zhi Xu ◽  
Bo Liu ◽  
Rong Wu ◽  
Ying-Ying Yang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Angiotensin Converting Enzyme ◽  
Protein Expression ◽  
Hepatic Steatosis ◽  
Nonalcoholic Steatohepatitis ◽  
High Fat Diet ◽  
Ang Ii ◽  
Converting Enzyme ◽  
High Fat

Background and Aim.Thiazolidinediones (TZDs) can improve hepatic steatosis in nonalcoholic steatohepatitis (NASH). Angiotensin (Ang) II, the primary effector of renin-angiotensin system (RAS), plays vital roles in the development and progression of NASH. And some AngII-mediated effects can be regulated by TZDs. Angiotensin-converting enzyme (ACE) 2, a new component of RAS, can degrade Ang II to attenuate its subsequent physiological actions. We aimed to evaluate the effects of TZDs on ACE2 expression in insulin-sensitive tissues in NASH rats.Methods. Forty rats were divided into the normal control, high-fat diet (HFD), pioglitazone control, and HFD plus pioglitazone groups. After 24 weeks of treatment, we evaluated changes in liver histology and tissue-specific ACE2 expression.Results. ACE2 gene and protein expression was significantly greater in liver and adipose tissue in the HFD group compared with normal control group, while was significantly reduced in skeletal muscle. Pioglitazone significantly reduced the degree of hepatic steatosis compared with the HFD group. Pioglitazone significantly increased ACE2 protein expression in liver, adipose tissue, and skeletal muscle compared with the HFD group.Conclusions. Pioglitazone improves hepatic steatosis in the rats with HFD-induced NASH and upregulates ACE2 expression in insulin-sensitive tissues.

Maternal postnatal high-fat diet, rather than gestational diet, affects morphology and mTOR pathway in skeletal muscle of weaning rat

2013 ◽  
Vol 24 (7) ◽  
pp. 1340-1348 ◽  
Author(s):  
Lucas C. Pantaleão ◽  
Gabriela F.R. Teodoro ◽  
Francisco L. Torres-Leal ◽  
Daiana Vianna ◽  
Tatyana D. de Paula ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Fat Diet ◽  
Mtor Pathway ◽  
High Fat

scholarly journals Effects of Combine Exercise on HSP70 and SOD1 Expression of Aorta, Skeletal Muscle and Myocardium in High Fat Diet induced Obese Aging Rats

2020 ◽  
Vol 29 (3) ◽  
pp. 248-255
Author(s):  
Nayoung Ahn
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
Antioxidant Enzyme ◽  
High Fat Diet ◽  
Exercise Intervention ◽  
Exercise Program ◽  
Normal Diet ◽  
High Fat ◽  
Cell Repair ◽  
Repair Protein

PURPOSE: Exercise improve myocardial cell protection and vascular function through cell repair and suppression of oxidative stress in cardiovascular diseases caused by aging. This study aimed to investigate the effect of combine exercise on HSP70 and SOD1 protein expression of aorta, skeletal muscle and myocardium in high fat diet induced obese aging rats.METHODS: Male 50-week-old Sprague Dawley rats (n=40) were divided into normal diet (ND, n=10), normal diet+exercise (NDEx, n=10), high fat diet (HFD, n=10), and high fat diet+exercise (HFDEx, n=10) groups. After six weeks on a high fat diet to induce obesity, a 12-week combine exercise program was implemented, which combine exercise (treadmill running+ladder climbing) three times a week for 45 minutes per session.RESULTS: Body weight was significantly decreased after 12 weeks combine exercise program compared to the ND group (p<.05) and HFDEx group compared to the HFD group (p<.05), respectively. After completing the 12-week exercise program, heat shock protein 70 (HSP70) and superoxide dismutase 1 (SOD1) expressions were significantly (p<.05) higher in the NDEx group compared to the ND group in the myocardium. Also, SOD1 protein expression was significantly (p<.05) higher in the NDEx group compared to the ND group and HFDEx group compared to the HFD group in the skeletal muscle.CONCLUSIONS: In conclusion, combine exercise intervention of high fat diet-induced obesity resulted in decreased cell repair protein and antioxidant enzyme protein in the myocardium. Therefore, it is thought that combine exercise intervention for obese induced rats improved the cell repair protein and antioxidant enzyme activity of the myocardium.

scholarly journals Ang-(1–7) protects skeletal muscle function in aged mice

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Ying Li ◽  
Jiao Song ◽  
Yangyang Jiang ◽  
Xue Yang ◽  
Li Cao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
Muscle Function ◽  
Molecular Mechanisms ◽  
C2c12 Cells ◽  
Skeletal Muscle Function ◽  
Protective Function ◽  
Aged Mice ◽  
Age Related ◽  
The Impact

Abstract Background The angiotensin-converting enzyme 2 (ACE2)/angiotensin 1–7 (Ang-(1–7)) axis has been shown to protect against the age-associated decline in skeletal muscle function. Here, we investigated the protective effects of ACE2 in mitigating the age-associated decline of skeletal muscle function and to identify the potential underlying molecular mechanisms. Methods We measured the expression levels of Ang-(1–7) in C57BL/6J mice of different ages and correlated these levels with measures of skeletal muscle function. We also investigated the expression of myocyte enhancer factor 2 A (MEF2A) in ACE2 knockout (ACE2KO) mice and its relationship with muscle function. We then treated aged ACE2KO mice for four weeks with Ang-(1–7) and characterized the levels of MEF2A and skeletal muscle function before and after treatment. We assessed the impact of Ang-(1–7) on the growth and differentiation of C2C12 cells in vitro and assessed changes in expression of the glucose transporter type 4 (Glut4). Results Aged mice showed reduced skeletal muscle function and levels of Ang-(1–7) expression in comparison to young and middle-aged mice. In ACE2KO mice, skeletal muscle function and MEF2A protein expression were significantly lower than in age-matched wild-type (WT) mice. After one month of Ang-(1–7) treatment, skeletal muscle function in the aged ACE2KO mice improved, while MEF2A protein expression was similar to that in the untreated group. In C2C12 cells, Ang-(1–7) was shown to promote along with the upregulated expression of Glut4. Conclusions The ACE2/ Ang-(1–7) axis has a protective function in skeletal muscle and administration of exogenous Ang-(1–7) can delay the age-related decline in the function of skeletal muscle.

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