scholarly journals Oleic acid in the absence of a PPARγ agonist increases adipogenic gene expression in bovine muscle satellite cells1

2019 ◽  
Vol 97 (10) ◽  
pp. 4114-4123 ◽  
Author(s):  
Xiang Z Li ◽  
Yan Yan ◽  
Jun F Zhang ◽  
Jian F Sun ◽  
Bin Sun ◽  
...  
Keyword(s):  
Gene Expression ◽  
Oleic Acid ◽  
Myogenic Differentiation ◽  
Binding Protein ◽  
Regulatory Element ◽  
Horse Serum ◽  
Peroxisome Proliferator ◽  
Bovine Muscle ◽  
Pparγ Agonist ◽  
Adipogenic Gene

Abstract We hypothesized that oleic acid (OA) in the absence of a thiazolidinedione (i.e., a synthetic peroxisome proliferator-activated receptorγ [PPARγ] agonist) would increase adipogenic gene expression in bovine muscle satellite cells (BSC). The BSC were cultured in differentiation medium containing 10 µM ciglitazone (CI), 100 µM OA, or 100 µM OA plus 10 µM CI (CI-OA). Control (CON) BSC were cultured only in differentiation media (containing 2% horse serum). The presence of myogenin, desmin, and paired box 7 proteins was confirmed in the BSC by immunofluorescence staining, demonstrating that we had isolated myogenic cells. The OA BSC had lesser paired box 3 (Pax3) and myogenic differentiation 1 expression but greater Pax7 and mygogenin (MYOG) expression (P < 0.05), than the CON BSC. The CI BSC had greater Pax3, Pax7, and MYOG expression than CON BSC (P < 0.05), suggesting that CI would promote BSC myogenesis under pro-myogenic conditions (i.e., when cultured with horse serum). However, both the OA and CI treatments upregulated the expression of PPARγ, CCAAT/enhancer-binding protein alpha (C/EBPα) and C/EBPß, sterol regulatory element-binding protein 1, lipoprotein lipase, and glycerol-3-phosphate acyltransferase 3 gene expression, as well as media adiponectin concentration (P < 0.05). The CI, OA, and CI-OA treatments also increased triacylglycerol and lipid droplet accumulation, in spite of upregulation (relative to CON BSC) of adenosine monophosphate-activated protein kinase alpha-1, perilipin 2 (PLIN2), and PLIN3 in BSC and downregulation of G protein-coupled protein receptor 43, acyl-CoA synthetase long chain family member 3, and stearoyl-CoA desaturase (P < 0.05). These results indicate that OA in the absence of a synthetic PPARγ agonist can effectively increase adipogenic gene expression in BSC.

scholarly journals PSXIV-32 Oleic acid stimulate the formation of adipocyte-like cells from bovine satellite cells via G Protein Coupled Receptor 43 and CCAAT/Enhancer Binding Protein Beta

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 308-309
Author(s):  
Jongkyoo Kim ◽  
Ki Yong Chung ◽  
Bradley J Johnson ◽  
Stephen B Smith
Keyword(s):  
Gene Expression ◽  
Oleic Acid ◽  
Satellite Cells ◽  
Myogenic Differentiation ◽  
Adipogenic Differentiation ◽  
Horse Serum ◽  
Enhancer Binding Protein ◽  
Mrna Gene ◽  
Fetal Bovine ◽  
Mrna Gene Expression

Abstract Numerous physiological and pathological processes are controlled by free fatty acids (FFAs), which act as a signaling molecule in mammals. We hypothesized that oleic acid (Ole) may stimulate the formation of satellite cell-derived intramuscular adipose tissue. The objective of the current study was to determine the effect of Ole on GPR43 and factors related to the adipogenic differentiation of bovine satellite cells. Bovine satellite cells were isolated from the semimembranosus of two 14-month-old crossbreed steers. The isolated muscle satellite cells were incubated in Dulbecco’s Modified Eagle’s Medium (DMEM) solution with 10% Fetal Bovine Serum. Upon reaching 80 to 90% confluence, the growth medium was replaced with differentiation medium composed of DMEM and 2% horse serum, 10μg/mL insulin, 10μg/mL hydrocortisone, 10μM ciglitizone, and 1×antibiotic-antimycotic with dose of: 0, 1, 10, 100, or 500 μM of oleic acid (Ole). Addition of Ole on BSC induced transdifferentiation of myogenic lineage into adipocyte-like cells which formed lipid droplets within cells. Use of 100 μM and 500 μM Ole doses tended to result in a greater (P &lt; 0.1) amount of mRNA gene expression of C/EBPβ compared to all other doses. This might suppress myogenic differentiation. Expression of PPARγ was not altered (P &gt; 0.1) by treatment. The addition of 100 μM and 500 μM upregulated (P &lt; 0.05) mRNA gene expression of GPR43 and 100 μM of Ole increased protein level of GPR43 (P &lt; 0.05) and phosphorylated AMPKα (P &lt; 0.05).

Exercise training increases lipid metabolism gene expression in human skeletal muscle

2002 ◽  
Vol 283 (1) ◽  
pp. E66-E72 ◽  
Author(s):  
Rebecca J. Tunstall ◽  
Kate A. Mehan ◽  
Glenn D. Wadley ◽  
Gregory R. Collier ◽  
Arend Bonen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Plasma Membrane ◽  
Exercise Training ◽  
Lipid Oxidation ◽  
Binding Protein ◽  
Regulatory Element ◽  
Vastus Lateralis ◽  
Vastus Lateralis Muscle ◽  
Peroxisome Proliferator ◽  
Cpt I

The effects of a single bout of exercise and exercise training on the expression of genes necessary for the transport and β-oxidation of fatty acids (FA), together with the gene expression of transcription factors implicated in the regulation of FA homeostasis were investigated. Seven human subjects (3 male, 4 female, 28.9 ± 3.1 yr of age, range 20–42 yr, body mass index 22.6 kg/m2, range 17–26 kg/m2) underwent a 9-day exercise training program of 60 min cycling per day at 63% peak oxygen uptake (V˙o 2 peak; 104 ± 14 W). On days 1 and 9 of the program, muscle biopsies were sampled from the vastus lateralis muscle at rest, at the completion of exercise, and again 3 h postexercise. Gene expression of key components of FA transport [FA translocase (FAT/CD36), plasma membrane-associated FA-binding protein], β-oxidation [carntine palmitoyltransferase(CPT) I, β-hydroxyacyl-CoA dehydrogenase] and transcriptional control [peroxisome proliferator-activated receptor (PPAR)α, PPARγ, PPARγ coactivator 1, sterol regulatory element-binding protein-1c] were unaltered by exercise when measured at the completion and at 3 h postexercise. Training increased total lipid oxidation by 24% ( P < 0.05) for the 1-h cycling bout. This increased capacity for lipid oxidation was accompanied by an increased expression of FAT/CD36 and CPT I mRNA. Similarly, FAT/CD36 protein abundance was also upregulated by exercise training. We conclude that enhanced fat oxidation after exercise training is most closely associated with the genes involved in regulating FA uptake across the plasma membrane (FAT/CD36) and across the mitochondrial membrane (CPT I).

scholarly journals C/EBP transcription factors regulate SREBP1c gene expression during adipogenesis

2009 ◽  
Vol 425 (1) ◽  
pp. 215-224 ◽  
Author(s):  
Victoria A. Payne ◽  
Wo-Shing Au ◽  
Christopher E. Lowe ◽  
Shaikh M. Rahman ◽  
Jacob E. Friedman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Binding Protein ◽  
Regulatory Element ◽  
Dominant Negative ◽  
Peroxisome Proliferator ◽  
Small Interfering Rnas ◽  
Inhibitory Protein ◽  
Intact Cells ◽  
Peroxisome Proliferator Activated Receptor

The transcription factor SREBP1c (sterol-regulatory-element-binding protein 1c) is highly expressed in adipose tissue and plays a central role in several aspects of adipocyte development including the induction of PPARγ (peroxisome-proliferator-activated receptor γ), the generation of an endogenous PPARγ ligand and the expression of several genes critical for lipid biosynthesis. Despite its significance, the regulation of SREBP1c expression during adipogenesis is not well characterized. We have noted that in several models of adipogenesis, SREBP1c expression closely mimics that of known C/EBPβ (CCAAT/enhancer-binding protein β) targets. Inhibition of C/EBP activity during adipogenesis by expressing either the dominant-negative C/EBPβ LIP (liver-enriched inhibitory protein) isoform, the co-repressor ETO (eight-twenty one/MTG8) or using siRNAs (small interfering RNAs) targeting either C/EBPβ or C/EBPδ significantly impaired early SREBP1c induction. Furthermore, ChIP (chromatin immunoprecipitation) assays identified specific sequences in the SREBP1c promoter to which C/EBPβ and C/EBPδ bind in intact cells, demonstrating that these factors may directly regulate SREBP1c expression. Using cells in which C/EBPα expression is inhibited using shRNA (short hairpin RNA) and ChIP assays we show that C/EBPα replaces C/EBPβ and C/EBPδ as a regulator of SREBP1c expression in maturing adipocytes. These results provide novel insight into the induction of SREBP1c expression during adipogenesis. Moreover, the findings of the present study identify an important additional mechanism via which the C/EBP transcription factors may control a network of gene expression regulating adipogenesis, lipogenesis and insulin sensitivity.

scholarly journals Restoration of sterol-regulatory-element-binding protein-1c gene expression in HepG2 cells by peroxisome-proliferator-activated receptor-γ co-activator-1α

2004 ◽  
Vol 381 (2) ◽  
pp. 357-363 ◽  
Author(s):  
Hannes OBERKOFLER ◽  
Elisabeth SCHRAML ◽  
Franz KREMPLER ◽  
Wolfgang PATSCH
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Hepg2 Cells ◽  
Binding Protein ◽  
Regulatory Element ◽  
Brown Adipocyte ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

The expression of SREBP-1 (sterol-regulatory-element-binding protein-1) isoforms differs between tissues and cultured cell lines in that SREBP-1a is the major isoform in established cell lines, whereas SREBP-1c predominates in liver and most other human tissues. SREBP-1c is transcriptionally less active than SREBP-1a, but is a main mediator of hepatic insulin action and is selectively up-regulated by LXR (liver X receptor) agonists. LXR-mediated transactivation is co-activated by PGC-1α (peroxisome-proliferator-activated receptor-γ co-activator-1α), which displays deficient expression in skeletal-muscle-derived cell lines. In the present paper, we show that PGC-1α expression is also deficient in HepG2 cells and in a human brown adipocyte cell line (PAZ6). In transient transfection studies, PGC-1α selectively amplified the LXR-mediated transcription from the human SREBP-1c promoter in HepG2 and PAZ6 cells via two LXR-response elements with extensive similarity to the respective murine sequence. Mutational analysis showed that the human LXR-response element-1 (hLXRE-1) was essential for co-activation of LXR-mediated SREBP-1c gene transcription by PGC-1α. Ectopic overexpression of PGC-1α in HepG2 cells enhanced basal SREBP-1c and, to a lesser extent, -1a mRNA expression, but only SREBP-1c expression was augmented further in an LXR/RXR (retinoic X receptor)-dependent fashion, thereby inducing mRNA abundance levels of SREBP-1c target genes, fatty acid synthase and acetyl-CoA carboxylase. These results indicate that PGC-1α contributes to the regulation of SREBP-1 gene expression, and can restore the SREBP-1 isoform expression pattern of HepG2 cells to that of human liver.

scholarly journals The Impact of Anthocyanins and Iridoids on Transcription Factors Crucial for Lipid and Cholesterol Homeostasis

2021 ◽  
Vol 22 (11) ◽  
pp. 6074
Author(s):  
Maciej Danielewski ◽  
Agnieszka Matuszewska ◽  
Adam Szeląg ◽  
Tomasz Sozański
Keyword(s):  
Transcription Factors ◽  
Cholesterol Metabolism ◽  
Binding Protein ◽  
Regulatory Element ◽  
Cholesterol Homeostasis ◽  
Lipid Lowering ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cell Functions ◽  
The Impact

Nutrition determines our health, both directly and indirectly. Consumed foods affect the functioning of individual organs as well as entire systems, e.g., the cardiovascular system. There are many different diets, but universal guidelines for proper nutrition are provided in the WHO healthy eating pyramid. According to the latest version, plant products should form the basis of our diet. Many groups of plant compounds with a beneficial effect on human health have been described. Such groups include anthocyanins and iridoids, for which it has been proven that their consumption may lead to, inter alia, antioxidant, cholesterol and lipid-lowering, anti-obesity and anti-diabetic effects. Transcription factors directly affect a number of parameters of cell functions and cellular metabolism. In the context of lipid and cholesterol metabolism, five particularly important transcription factors can be distinguished: liver X receptor (LXR), peroxisome proliferator-activated receptor-α (PPAR-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT/enhancer binding protein α (C/EBPα) and sterol regulatory element-binding protein 1c (SREBP-1c). Both anthocyanins and iridoids may alter the expression of these transcription factors. The aim of this review is to collect and systematize knowledge about the impact of anthocyanins and iridoids on transcription factors crucial for lipid and cholesterol homeostasis.

scholarly journals Peroxisome Proliferator-Activated Receptor-α Control of Lipid and Glucose Metabolism in Human White Adipocytes

Endocrinology ◽  
2010 ◽  
Vol 151 (1) ◽  
pp. 123-133 ◽  
Author(s):  
Carole Ribet ◽  
Emilie Montastier ◽  
Carine Valle ◽  
Véronic Bezaire ◽  
Anne Mazzucotelli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Biological Effects ◽  
Primary Cultures ◽  
Lactate Production ◽  
De Novo Lipogenesis ◽  
Peroxisome Proliferator ◽  
Palmitate Oxidation ◽  
White Adipocytes ◽  
Pparγ Agonist ◽  
Pparα Agonist

Abstract This work aimed at characterizing the role of peroxisome proliferator-activated receptors (PPAR)α in human white adipocyte metabolism and at comparing PPARα and PPARγ actions in these cells. Primary cultures of human fat cells were treated with the PPARα agonist GW7647 or the PPARγ agonist rosiglitazone. Changes in gene expression were determined using DNA microrrays and quantitative RT-PCR. Western blot and metabolic studies were performed to identify the biological effects elicited by PPAR agonist treatments. GW7647 induced an up-regulation of β-oxidation gene expression and increased palmitate oxidation. Unexpectedly, glycolysis was strongly reduced at transcriptional and functional levels by GW7647 leading to a decrease in pyruvate and lactate production. Glucose oxidation was decreased. Triglyceride esterification and de novo lipogenesis were inhibited by the PPARα agonist. GW7647-induced alterations were abolished by a treatment with a PPARα antagonist. Small interfering RNA-mediated extinction of PPARα gene expression in hMADS adipocytes attenuated GW7647 induction of palmitate oxidation. Rosiglitazone had no major impact on glycolysis and β-oxidation. Altogether these results show that PPARα can selectively up-regulate β-oxidation and decrease glucose utilization in human white adipocytes.

scholarly journals Sterol Regulatory Element-binding Protein-2- and Liver X Receptor-driven Dual Promoter Regulation of Hepatic ABC Transporter A1 Gene Expression

2007 ◽  
Vol 282 (29) ◽  
pp. 21090-21099 ◽  
Author(s):  
Norimasa Tamehiro ◽  
Yukari Shigemoto-Mogami ◽  
Tomoshi Kakeya ◽  
Kei-ichiro Okuhira ◽  
Kazuhiro Suzuki ◽  
...  
Keyword(s):  
Gene Expression ◽  
Abc Transporter ◽  
Binding Protein ◽  
Regulatory Element ◽  
Liver X Receptor ◽  
Promoter Regulation ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Dual Promoter

scholarly journals Diet-dependent Natriuretic Peptide Receptor C expression in adipose tissue is mediated by PPARγ via long-range distal enhancers

2021 ◽  
Author(s):  
Fubiao Shi ◽  
Zoltan Simandi ◽  
Laszlo Nagy ◽  
Sheila Collins
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Long Range ◽  
Environmental Changes ◽  
Peroxisome Proliferator ◽  
Enhancer Activity ◽  
Peroxisome Proliferator Activated Receptor ◽  
Pparγ Agonist ◽  
Mouse Adipocytes ◽  
Sirna Knockdown

AbstractIn addition to their established role to maintain blood pressure and fluid volume, the cardiac natriuretic peptides (NPs) can stimulate adipocyte lipolysis and control the brown fat gene program of nonshivering thermogenesis. The NP “clearance” receptor C (NPRC) functions to clear NPs from the circulation via peptide internalization and degradation and thus is an important regulator of NP signaling and adipocyte metabolism. It is well appreciated that the Nprc gene is highly expressed in adipose tissue and is dynamically regulated with nutrition and environmental changes. However, the molecular basis for how Nprc gene expression is regulated is still poorly understood. Here we identified Peroxisome Proliferator-Activated Receptor gamma (PPARγ) as a transcriptional regulator of Nprc expression in mouse adipocytes. During 3T3-L1 adipocyte differentiation, levels of Nprc expression increase in parallel with PPARγ induction. Rosiglitazone, a classic PPARγ agonist, increases, while siRNA knockdown of PPARγ reduces, Nprc expression in 3T3-L1 adipocytes. We demonstrate that PPARγ controls Nprc gene expression in adipocytes through its long-range distal enhancers. Furthermore, the induction of Nprc expression in adipose tissue during high-fat diet feeding is associated with increased PPARγ enhancer activity. Our findings define PPARγ as a mediator of adipocyte Nprc gene expression and establish a new connection between PPARγ and the control of adipocyte NP signaling in obesity.

Sign in / Sign up

Export Citation Format

Share Document