Satellite cells are skeletal muscle progenitor/stem cells that reside between the basal lamina and plasma membranes of skeletal fibers in vivo. These cells can give rise to both myogenic and adipogenic cells. Given the possible role for differentiation of satellite cells into adipocytes in marbling and in some pathological disorders like sarcopenia, knowledge of the proteins involved in such process remains obscure. Using two-dimensional polyacrylamide gel electrophoresis coupled with mass spectrometry, we investigated the proteins that are differentially expressed during adipogenic differentiation of satellite cells from bovine longissimus muscle. Our proteome mapping strategy to identify the differentially expressed intracellular proteins during adipogenic differentiation revealed a total of 25 different proteins. The proteins up-regulated during adipogenic differentiation of satellite cells like Cathepsin H precursor, Retinal dehydrogenase 1, Enoyl-CoA hydratase, Ubiquinol-cytochrome-c reductase, T-complex protein 1 subunit beta and ATP synthase D chain were found to be associated with lipid metabolism. The down-regulated proteins like LIM protein, annexin proteins, cofilin-1, Rho GDP-dissociation inhibitor 1 and septin-2, identified in the present study were found to be associated with myogenesis. These results clearly demonstrate that the adipogenic conversion of muscle satellite cells is associated with the up-regulated and down-regulated proteins involved in adipogenesis and myogenesis respectively.
Journal of the Korean Society of Food Science and Nutrition
/
v.43
no.7
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pp.963-971
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2014
This study investigated the effects of exercise intensity on PGC-$1{\alpha}$, PPAR-${\gamma}$, and insulin resistance in skeletal muscle of high fat diet-fed Sprague-Dawley rats. Forty rats were randomly divided into five groups: sedentary control group (SED), high fat diet group (HF), high fat diet+low-intensity exercise group (HFLE, 22 m/min, 60 min, 6 days/week), high fat diet+moderate-intensity exercise group (HFME, 26 m/min, 51 min), and high fat diet+high-intensity exercise group (HFHE, 30 m/min, 46 min). After 4 weeks of high fat diet and endurance exercise training, the lipid profiles, insulin, and glucose concentrations were determined in plasma. PGC-$1{\alpha}$, PPAR-${\gamma}$, and GLUT-4 contents were measured in plantaris muscle. The rate of glucose transport in soleus muscle was determined under submaximal insulin concentration ($1,000{\mu}IU/mL$ insulin, 20 min) during muscle incubation. Plasma glucose during oral glucose tolerance test in HF was significantly greater than that in SED, and plasma glucose levels in the three exercise (EX) groups were significantly lower that those in SED and HF at 30 and 60 min, respectively (P<0.05). Plasma insulin levels in the EX groups were significantly reduced by 60 min compared to that in HF (P<0.05). The protein expression level of PGC-$1{\alpha}$ as well as muscle glucose uptake were significantly higher in SED and HF than those in the three EX groups (P<0.05), and HFHE showed significantly higher levels than HFLE and HFME. Expression levels of GLUT-4 and PPAR-${\gamma}$ were significantly higher in the HFLE, HFME, and HFHE groups compared to the SED and HF (P<0.05). Therefore, the results of this study indicate that 4 weeks of high fat diet significantly developed whole body insulin resistance but did not affect PGC-$1{\alpha}$, PPAR-${\gamma}$, or the glucose transport rate in skeletal muscle, and exercise training was able to attenuate deteriorated whole body insulin resistance due to high fat diet. In addition, high intensity training significantly affected PGC-$1{\alpha}$ expression and the glucose transport rate of skeletal muscle in comparison with low and middle training intensities.
In native-polyacrylamide gel electrophoresis of Pangasius polyuranodon, the lactate dehydrogenase (EC 1.1.1.27, LDH) $A_4$, $A_3$B, $A_2$$B_2$,$AB_3$ and $B_4$ isozymes were expressed in various tissues. The LDH $A_4$ and liver-specific $C_4$ isozymes were expressed in the tissues of Hypostomus Plecostomus. The bands of LDH in skeletal muscle, heart and eye tissues were not detected while one band was detected in kidney and liver, and four bands were detected in brain. The detected one band in liver was identified as alcohol dehydrogenase and an anodal band of skeletal muscle was identified as nothing dehydrogenase. The LDH in skeletal muscle, heart and eye might function as pyruvate reductase. The degree of inhibitions of LDH in skeletal muscle and heart of P. polyuranodon by 10 mM pyruvate were measured 57.6% and 73.8%, respectively. However, those of LDH in tissues of H. plecostomus were measured 52.7-61.8% so tissue specificity did not appear. Therefore, H. ple-costomus might be more acclimated to hypoxic environment by anaerobic metabolism of LDH iso-zymes than P. polyuranodon.
Objective: It is commonly accepted that adiponectin binds to its two receptors to regulate fatty acid metabolism in adipocytes. To better understand their functions in the regulation of intramuscular adipogenesis in goats, we cloned the three genes (adiponectin [AdipoQ], adiponectin receptor 1 [AdipoR1], and AdipoR2) encoding these proteins and detected their mRNA distribution in different tissues. We also determined the role of AdipoQ in the adipogenic differentiation of goat skeletal muscle satellite cells (SMSCs). Methods: SMSCs were isolated using 1 mg/mL Pronase E from the longissimus dorsi muscles of 3-day-old female Nanjiang brown goats. Adipogenic differentiation was induced in satellite cells by transferring the cells to Dulbecco's modified Eagle's medium supplemented with an isobutylmethylxanthine, dexamethasone and insulin cocktail. The pEGFP-N1-AD plasmid was transfected into SMSCs using Lipofectamine 2000. Expression of adiponectin in tissues and SMSCs was detected by quantitative polymerase chain reaction and immunocytochemical staining. Results: The three genes were predominantly expressed in adipose and skeletal muscle tissues. According to fluorescence and immunocytochemical analyses, adiponectin protein expression was only observed in the cytoplasm, suggesting that adiponectin is localized to the cytoplasm of goat SMSCs. In SMSCs overexpressing the AdipoQ gene, adiponectin promoted SMSC differentiation into adipocytes and significantly (p<0.05) up-regulated expression of AdipoR2, acetyl-CoA carboxylase, fatty-acid synthase, and sterol regulatory element-binding protein-1, though expression of CCAAT/enhancer-binding $protein-{\alpha}$, peroxisome proliferator-activated receptor ${\gamma}$, and AdipoR1 did not change significantly. Conclusion: Adiponectin induced SMSC differentiation into adipocytes, indicating that adiponectin may promote intramuscular adipogenesis in goat SMSC.
The aim of this study was to examine the metabolic adjustment of lactate dehydrogenase (EC 1.1.1.27, LDH) isozymes to the environmental temperature in bluegill (Lepomis macrochirus). This study included three groups of bluegill collected in April (group Ⅰ), May (group Ⅱ), and September (group Ⅲ). The LDH activities of skeletal muscle, heart, and brain tissues were higher in group Ⅲ than in groups Ⅰ and Ⅱ. The citrate synthase (EC 4.1.3.7, CS) activity was higher in skeletal muscle but lower in heart and brain tissues of group Ⅱ as compared to group Ⅰ. In contrast, the CS activity was lower in skeletal muscle and higher in heart and brain tissues in group Ⅲ than in group Ⅱ. Furthermore, the LDH/CS activity ratio was higher in the skeletal muscle and brain in group Ⅲ than in groups Ⅰ and Ⅱ. Accordingly, anaerobic metabolism was increased in group Ⅲ. LDH A4, A2B2, and B4 isozymes were expressed in skeletal muscle, heart, liver, and brain tissues. The LDH C hybrid was detected in brain tissue. The LDH A4 isozyme was successfully purified by affinity chromatography. The molecular weight of the purified LDH A4 isozyme was 136 kDa and its optimal pH for enzymatic activity was 8.0. The KmPYR values of LDH in skeletal muscle were 0.161-0.227 mM using pyruvate as a substrate. These kinetic properties of LDH in skeletal muscle are consistent with the fact that bluegill is a cold-adapted species. These results may be useful for predicting the habitat use of this fish.
Kim, Kyong;Sim, Mi-Seong;Kwak, Min-Kyu;Jang, Se-Eun;Oh, Yoon Sin
Journal of Nutrition and Health
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v.55
no.4
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pp.462-475
/
2022
Purpose: Allomyrina dichotoma larvae are one of the approved edible insects with nutritional value and various functional and medicinal properties. Previously we have demonstrated that the Allomyrina dichotoma larval extract (ADLE) ameliorates hepatic insulin resistance in high-fat diet (HFD)-induced diabetic mice through the activation of adenosine monophosphate-activated protein kinase (AMPK). This study investigated the effects of ADLE on insulin resistance in the skeletal muscle and explored mechanisms for enhancing the glucose uptake in palmitate (PAL)-treated C2C12 myotubes. Methods: To induce insulin resistance, the differentiated C2C12 myotubes were treated with PAL (0.5 mM) for 24 hours, and then treated with a 0.5 mg/ml concentration of ADLE, and the resultant effects were measured. The expression levels of glucose transporter-4 (GLUT4), AMPK, and the mitochondrial metabolism-related proteins were analyzed by western blotting. The mRNA expression levels of lipogenesis- related genes were determined by quantitative reverse-transcriptase PCR. Results: The exposure of C2C12 myotubes to 0.5 mg/ml of ADLE increased cell viability significantly compared to PAL-treated cells. ADLE upregulated the protein expression of GLUT4 and enhanced glucose uptake in the PAL-treated cells. ADLE increased the phosphorylated AMPK in both the PAL-treated C2C12 myotubes and HFD-treated skeletal muscle. The reduced expression levels of peroxisome-proliferator-activated receptor gamma co-activator-1 alpha (PGC1α) and uncoupling protein 3 (UCP3) due to the PAL and HFD treatment were reversed by the ADLE treatment. The citrate synthase activity was also significantly increased with the PAL and ADLE co-treatment. Moreover, the mRNA and protein expressions of fatty acid synthesis-related factors were reduced in the PAL and HFD-treated muscle cells, and this effect was significantly attenuated by the ADLE treatment. Conclusion: ADLE activates AMPK, which in turn induces mitochondrial metabolism and reduces fatty acid synthesis in C2C12 myotubes. Therefore, ADLE could be useful for preventing or treating insulin resistance of skeletal muscles in diabetes.
Diabetes mellitus revealed a chronic disorder of lipid, carbohydrate and protein metabolism characterized by insulin deficiency, and a striking tendency toward development of atherosclerosis, microangiopathy, nephropathy, neuropathy and recently cardiomyopathy etc. The mechanism of heart failure in patients with diabetic cardiomyopathy is not clear but diabetic cardiomyopathy usually occurs in persons with long standing diabetes. After diabetes induced in made Sprague- Dawley strain rats by injection of streptozotocin(60mg/kg), cardiac tissue with hematoxylin-eosin and Masson's trichrome stain was examined at 3 days, 1, 2, 4, 6 weeks later under light microscope. The results were obtained as follows : 1. In H&E stain of control group, myocardiac cells were shorter than skeletal muscle cell, which was branched out and connected each other at terminal with striation, intercalated disk and nucleus at center of cell. 2. In MT stain of control group, a few of collagen fibrile were seen at periva scular interstium, but wasn't seen between skeletal muscle fiber, and cardiac muscle was seen in various size. 3. In MT stain of experimental group, increased collagen fiber deposition at perivascular interstiums were seen periodically. 4. In MT stain of experimental group, increased collagen fiber deposition at interstitial matrix between perimyocardiac cells were seen at 3 day, 4 weeks and 6 weeks after DM induction. 5. In H&E stain of experimental group, partial degeneration of myocardiac cells was seen after 4 weeks of DM induction. From above results, streptozotocin induced diabetes mellitus increased collagen around perivascular and between intercellular matrix in heart.
Although atopic dermatitis (AD) is known to be a representative skin disorder, it also affects the systemic immune response. In a recent study, myoblasts were shown to be involved in the immune regulation, but the roles of muscle cells in AD are poorly understood. We aimed to identify the relationship between mitochondria and atopy by genome-wide analysis of skeletal muscles in mice. We induced AD-like symptoms using house dust mite (HDM) extract in NC/Nga mice. The transcriptional profiles of the untreated group and HDM-induced AD-like group were analyzed and compared using microarray, differentially expressed gene and functional pathway analyses, and protein interaction network construction. Our microarray analysis demonstrated that immune response-, calcium handling-, and mitochondrial metabolism-related genes were differentially expressed. In the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology pathway analyses, immune response pathways involved in cytokine interaction, nuclear factor-kappa B, and T-cell receptor signaling, calcium handling pathways, and mitochondria metabolism pathways involved in the citrate cycle were significantly upregulated. In protein interaction network analysis, chemokine family-, muscle contraction process-, and immune response-related genes were identified as hub genes with many interactions. In addition, mitochondrial pathways involved in calcium signaling, cardiac muscle contraction, tricarboxylic acid cycle, oxidation-reduction process, and calcium-mediated signaling were significantly stimulated in KEGG and Gene Ontology analyses. Our results provide a comprehensive understanding of the genome-wide transcriptional changes of HDM-induced AD-like symptoms and the indicated genes that could be used as AD clinical biomarkers.
Shin, Donghyun;Kim, Kyoung Hwan;Lee, Ji Hyun;Cho, Byung-Wook
Journal of Life Science
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v.28
no.10
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pp.1127-1131
/
2018
Cortisol, a steroid hormone, functions within metabolism, immune response, and stress. Intense or prolonged physical exercise increases cortisol levels to enhance the gluconeogenesis pathway and stabilize blood glucose level. However, cortisol also exerts a negative impact on muscle function and creates a stressful environment in skeletal muscle cells. The present study investigated the function of cortisol as a stress hormone. To examine the effect of the exercise-induced hormone cortisol on skeletal muscles, C2C12 cells were cultured and treated with cortisol at different concentrations. As a result, we found that the morphology of C2C12 changed remarkably with 5 ug/ml cortisol treatment. Western blot analysis was conducted to learn whether ER-stress and autophagy were induced. We found that the expression ratio of LC3I/LC3II decreased and BiP expression increased after cortisol treatment. In addition, immunocytochemistry analysis with IER3 antibody clearly showed that apoptosis is induced after 12-hour cortisol treatment. These results indicate that cortisol treatment could induce apoptosis, ER-stress, and autophagy in muscle cells. This study would provide valuable information in the study of the effects of exercise on skeletal muscle cells and the development of additives to reduce cortisol stress.
Objective: We previously found that the incidence of sarcopenia increased with declining glucose metabolism of muscle in patients with treatment-naïve diffuse large B-cell lymphoma (DLBCL). This study aimed to investigate the relationship between sarcopenia and muscle glucometabolism using 18F-FDG PET/CT at baseline and end-of-treatment, analyze the changes in these parameters through treatment, and assess their prognostic values. Materials and Methods: The records of 103 patients with DLBCL (median 54 years [range, 21-76]; male:female, 50:53) were retrospectively reviewed. Skeletal muscle area at the third lumbar vertebral (L3) level was measured, and skeletal muscle index (SMI) was calculated to determine sarcopenia, defined as SMI < 44.77 cm2/m2 and < 32.50 cm2/m2 for male and female, respectively. Glucometabolic parameters of the psoas major muscle, including maximum standardized uptake value (SUVmax) and mean standardized uptake value (SUVmean), were measured at L3 as well. Their changes across treatment were also calculated as ΔSMI, ΔSUVmax, and ΔSUVmean; Δbody mass index was also calculated. Associations between SMI and the metabolic parameters were analyzed, and their associations with progression-free survival (PFS) and overall survival (OS) were identified. Results: The incidence of sarcopenia was 29.1% and 36.9% before and after treatment, respectively. SMI (P = 0.004) was lower, and sarcopenia was more frequent (P = 0.011) at end-of-treatment than at baseline. The SUVmax and SUVmean of muscle were lower (P < 0.001) in sarcopenia than in non-sarcopenia at both baseline and end-of-treatment. ΔSMI was positively correlated with ΔSUVmax of muscle (P = 0.022). Multivariable Cox regression analysis showed that sarcopenia at end-of-treatment was independently negatively associated with PFS (adjusted hazard ratio [95% confidence interval], 2.469 [1.022-5.965]), while sarcopenia at baseline was independently negatively associated with OS (5.051 [1.453-17.562]). Conclusion: Sarcopenic patients had lower muscle glucometabolism, and the muscular and metabolic changes across treatment were positively correlated. Sarcopenia at baseline and end-of-treatment was negatively associated with the prognosis of DLBCL.
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