scholarly journals Effect of Temperature and Selection for Growth on Intracellular Lipid Accumulation and Adipogenic Gene Expression in Turkey Pectoralis Major Muscle Satellite Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Jiahui Xu ◽  
Gale M. Strasburg ◽  
Kent M. Reed ◽  
Sandra G. Velleman

As multipotential stem cells, satellite cells (SCs) have the potential to express adipogenic genes resulting in lipid synthesis with thermal stress. The present study determined the effect of temperature on intracellular lipid synthesis and adipogenic gene expression in SCs isolated from the pectoralis major (p. major) muscle of 7-day-old fast-growing modern commercial (NC) turkeys compared to SCs from unselected slower-growing turkeys [Randombred Control Line 2 (RBC2)]. Since proliferating and differentiating SCs have different responses to thermal stress, three incubation strategies were used: (1) SCs proliferated at the control temperature of 38°C and differentiated at 43° or 33°C; (2) SCs proliferated at 43° or 33°C and differentiated at 38°C; or (3) SCs both proliferated and differentiated at 43°, 38°, or 33°C. During proliferation, lipid accumulation increased at 43°C and decreased at 33°C with the NC line showing greater variation than the RBC2 line. During proliferation at 43°C, peroxisome proliferator-activated receptor-γ (PPARγ) and neuropeptide-Y (NPY) expression was reduced to a greater extent in the NC line than the RBC2 line. At 33°C, expression of PPARγ, NPY, and CCAAT/enhancer-binding protein-β (C/EBPβ) was upregulated, but only in the RBC2 line. During differentiation, both lines showed greater changes in lipid accumulation and in C/EBPβ and NPY expression if the thermal challenge was initiated during proliferation. These data suggest that adipogenic gene expression is more responsive to thermal challenge in proliferating SCs than in differentiating SCs, and that growth-selection has increased temperature sensitivity of SCs, which may significantly affect breast muscle structure and composition.

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0262576
Author(s):  
Jiahui Xu ◽  
Gale M. Strasburg ◽  
Kent M. Reed ◽  
Sandra G. Velleman

Satellite cells (SCs) are stem cells responsible for post-hatch muscle growth through hypertrophy and in birds are sensitive to thermal stress during the first week after hatch. The mechanistic target of rapamycin (mTOR) signaling pathway, which is highly responsive to thermal stress in differentiating turkey pectoralis major (p. major) muscle SCs, regulates protein synthesis and the activities of SCs through a downstream effector, S6 kinase (S6K). The objectives of this study were: 1) to determine the effect of heat (43°C) and cold (33°C) stress on activity of the mTOR/S6K pathway in SCs isolated from the p. major muscle of one-week-old faster-growing modern commercial (NC) turkeys compared to those from slower-growing Randombred Control Line 2 (RBC2) turkeys, and 2) to assess the effect of mTOR knockdown on the proliferation, differentiation, and expression of myogenic regulatory factors of the SCs. Heat stress increased phosphorylation of both mTOR and S6K in both turkey lines, with greater increases observed in the RBC2 line. With cold stress, greater reductions in mTOR and S6K phosphorylation were observed in the NC line. Early knockdown of mTOR decreased proliferation, differentiation, and expression of myoblast determination protein 1 and myogenin in both lines independent of temperature, with the RBC2 line showing greater reductions in proliferation and differentiation than the NC line at 38° and 43°C. Proliferating SCs are more dependent on mTOR/S6K-mediated regulation than differentiating SCs. Thus, thermal stress can affect breast muscle hypertrophic potential by changing satellite cell proliferation and differentiation, in part, through the mTOR/S6K pathway in a growth-dependent manner. These changes may result in irreversible effects on the development and growth of the turkey p. major muscle.


Author(s):  
Ke Fang ◽  
Fan Wu ◽  
Guang Chen ◽  
Hui Dong ◽  
Jingbin Li ◽  
...  

Abstract Background Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and is characterized by excessive hepatic lipid accumulation. Many studies have suggested that lipid overload is the key initial factor that contributes to hepatic steatosis. Our previous study indicated that diosgenin (DSG) has a beneficial effect on energy metabolism, but the underlying mechanism remains unclear. Methods Human normal hepatocytes (LO2 cells) were incubated with palmitic acid to establish the cell model of nonalcoholic fatty liver. The effects of DSG on lipid metabolism, glucose uptake and mitochondrial function were evaluated. Furthermore, the mechanism of DSG on oxidative stress, lipid consumption and lipid synthesis in LO2 cells was investigated. Results The results indicated that palmitic acid induced obvious lipid accumulation in LO2 cells and that DSG treatment significantly reduced the intracellular lipid content. DSG treatment upregulated expression of lipolysis proteins, including phospho-AMP activated protein kinase (p-AMPK), phospho-acetyl-coA carboxylase (p-ACC) and carnitine acyl transferase 1A (CPT-1A), and inhibited expression of lipid synthesis-related proteins, including sterol regulatory element-binding protein 1c (SREBP-1c) and fatty acid synthase (FAS). Additionally, DSG-treated cells displayed a marked improvement in mitochondrial function, with less production of reactive oxygen species and a higher mitochondrial membrane potential compared with the model group. Conclusion This study suggests that DSG can reduce intracellular lipid accumulation in LO2 cells and that the underlying mechanism may be related to the improving oxidative stress, increasing fatty acid β-oxidation and decreasing lipid synthesis. The above changes might be mediated by the activation of the AMPK/ACC/CPT-1A pathway and inhibition of the SREBP-1c/FAS pathway.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Heeok Hong ◽  
Joseph F. dela Cruz ◽  
Won Seob Kim ◽  
Kiyeol Yoo ◽  
Seong Gu Hwang

Glehnia littoralis has been reported to have several pharmacological properties but no reports describing the antiadipogenic effect of this plant have been published. This study was conducted to investigate the effects of Glehnia littoralis root hot water extract (GLE) and its underlying mechanism on 3T3-L1 cell adipogenesis and in high-fat diet- (HFD-) induced obese mice. We measured intracellular lipid accumulation using oil red O staining in vitro. For in vivo study, twenty-eight C57BL/6J male mice were randomly divided into four groups, Control, HFD, HFD + 1% GLE, and HFD + 5% GLE, which was performed for eight weeks. We determined the expression levels of the adipogenesis-related proteins by RT-PCR and western blotting in HFD-induced obese mice. The GLE dose-dependently inhibited 3T3-L1 adipocyte differentiation and intracellular lipid accumulation in differentiated adipocytes. Further, body weight gain and fat accumulation were significantly lower in the GLE-treated HFD mice than in the untreated HFD mice. GLE treatment suppressed the expression of adipogenic genes such as peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding protein (C/EBP) α, fatty acid synthase (aP2), and fatty acid synthase (FAS). These results suggest that the GLE inhibits adipocyte differentiation and intracellular lipid accumulation by downregulating the adipogenic gene expression both in vitro and in vivo.


2016 ◽  
Vol 69 (3) ◽  
pp. 485-492 ◽  
Author(s):  
Bungo Shirouchi ◽  
Kentaro Kashima ◽  
Yasutaka Horiuchi ◽  
Yuki Nakamura ◽  
Yumiko Fujimoto ◽  
...  

2020 ◽  
Author(s):  
Junfang Zhang ◽  
Yan Yan ◽  
Jianfu Sun ◽  
Ying Wang ◽  
Yan Cui ◽  
...  

Abstract Background: Ciglitazone is a member of the thiazolidinedione (TZD) family, and specifically binds to peroxisome proliferator-activated receptor-γ (PPARγ) , thereby promoting adipocyte differentiation. We hypothesized that ciglitazone as a PPARγ ligand in the absence of an adipocyte differentiation cocktail would increase adiponectin and adipogenic gene expression in bovine satellite cells (BSC).Methods: Muscle-derived bovine satellite cells were isolated from six, 18-month-old Yanbian Yellow Cattle. The BSC were cultured for 96 h in differentiation medium containing 5 µM ciglitazone (CL), 10 µM ciglitazone (CM), or 20 µM ciglitazone (CH). Control (CON) BSC were cultured only in differentiation medium (containing 2% horse serum).Results: The presence of myogenin, desmin, and paired box 7 (Pax7) proteins were confirmed in the BSC by immunofluorescence staining. The CL, CM, and CH treatments produced higher concentrations of triacylglycerol and lipid droplet accumulation in myotubes than those of the CON treatment. Ciglitazone treatments significantly increased the relative expression of PPARγ , CCAAT/enhancer-binding protein alpha (C/EBPα), C/EBPβ, fatty acid synthase stearoyl-CoA desaturase (SCD) and perilipin 2. Ciglitazone treatments increased gene expression of paired box 3 (Pax3) and Pax7 and decreased expression of myogenic differentiation-1, myogenin, myogenic regulatory factor-5 (MRF5), and MYF4 (P < 0.01). Adiponectin concentration caused by ciglitazone treatments was significantly greater than CON (P < 0.01). RNA sequencing showed that 281 differentially expressed genes (DEGs) were found in the treatments of ciglitazone. DEGs gene ontology (GO) analysis showed that the top 10 GO enrichment significantly changed the biological processes such as protein trimerization, negative regulation of cell proliferation, adipocytes differentiation, and cellular response to external stimulus. KEGG pathway analysis showed that DEGs were involved into p53 signaling pathway, PPAR signaling pathway, biosynthesis of amino acids, TNF signaling pathway, non-alcoholic fatty liver disease (NAFLD), PI3K-Akt signaling pathway, and Wnt signaling pathway.Conclusion: These results indicate that ciglitazone acts as PPARγ agonist, effectively increasing the adiponectin concentration and adipogenic gene expression, and stimulating the conversion of BSC to adipocyte-like cells in the absence of adipocyte differentiation cocktail.


2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 104-104
Author(s):  
Sandra G Velleman

Abstract Newly hatched poults and chicks have immature thermoregulatory systems and are not able to maintain a constant body temperature when exposed to hot or cold ambient temperatures. During the immediate posthatch period during handling and transport, poults and chicks are commonly exposed to acute thermal conditions. This immediate posthatch period is when satellite cells, adult myoblasts, have their highest period of mitotic activity and are sensitive to extrinsic stimuli including ambient temperature. Variable temperatures can have long-lasting positive or negative effects on skeletal muscle growth. Satellite cells are a self-renewing multipotential stem cell population located between the basement membrane and sarcolemma of muscle fibers. They are responsible for all posthatch growth of muscle through muscle fiber hypertrophy. Results have shown that satellite cells are more sensitive to thermal stress during the period of satellite cell proliferation than during differentiation into multinucleated myotubes, and that pectoralis major muscle satellite cells from growth-selected lines of chickens and turkeys are more sensitive to temperature. Recent findings have shown that the rapamycin, mTOR, signaling pathway which is involved in muscle growth through hypertrophy is differentially affected by thermal stress in a growth-dependent manner. Since satellite cells are a stem cell population, they can also transdifferentiate into other cellular lineages. Anaerobic muscles like the pectoralis major muscle are more prone to converting to an adipogenic lineage compared to aerobic muscles like the biceps femoris. Thus, variable temperatures can impact the intramuscular fat content of the breast muscle. Taken together, changes in ambient temperature alter satellite cell function causing long-term effects on growth, morphological organization, and composition of the pectoralis major, breast, muscle.


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