Articles de revues : « Preadipociti »

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Shao, Jiahao, Ting Pan, Jie Wang, Tao Tang, Yanhong Li, Xianbo Jia et Songjia Lai. « MiR-208b Regulates Rabbit Preadipocyte Proliferation and Differentiation ». Genes 12, n^o 6 (9 juin 2021) : 890. http://dx.doi.org/10.3390/genes12060890.

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microRNAs (miRNAs) play an important role in gene regulation in animals by pairing with target gene mRNA. Many miRNAs are differentially expressed in the adipose tissue, often with conserved expression. In our study, we found that miR-208b expression was observed differently in the preadipocyte differentiation model. When miR-208b was overexpressed in the preadipocyte differentiation model, the overexpressed group displayed higher expression of PPARγ and FABP4—the markers of preadipocyte differentiation. Oil Red O staining revealed that the count of lipid droplets was increased in the overexpressed group. When the expression of miR-208b was inhibited, the above indicators showed an opposite trend. Moreover, results from both 5-ethynyl-2′-deoxyuridine (EDU) and cell counting kit (CCK) analysis showed that miR-208b promoted the proliferation of preadipocyte. Expression of gene CSNK2A2, a direct miR-208b target, was downregulated in the overexpressed group, providing a possible link to multiple signal pathways. Overall, our data indicate that miR-208b play a positive regulatory effect on the proliferation and differentiation of rabbit preadipocyte.

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Molgat, André S. D., AnneMarie Gagnon, Charlie Foster et Alexander Sorisky. « The activation state of macrophages alters their ability to suppress preadipocyte apoptosis ». Journal of Endocrinology 214, n^o 1 (3 mai 2012) : 21–29. http://dx.doi.org/10.1530/joe-12-0114.

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Adipose tissue contains macrophages whose state of activation is regulated as obesity develops. Macrophage-secreted factors influence critical processes involved in adipose tissue homeostasis, including preadipocyte proliferation and differentiation into adipocytes. Macrophage-conditioned medium (MacCM) from J774A.1 macrophages protects 3T3-L1 preadipocytes from apoptosis through platelet-derived growth factor (PDGF) signaling. Here, we investigated the effect of macrophage activation on MacCM-dependent preadipocyte survival. MacCM was prepared following activation of either J774A.1 macrophages with lipopolysaccharide (LPS) or human primary monocyte-derived macrophages (MD-macrophages) with LPS or interleukin 4 (IL4). 3T3-L1 and human primary preadipocytes were induced to undergo apoptosis in MacCM, and apoptosis was quantified by cell enumeration or Hoechst nuclear staining. Preadipocyte PDGF signaling was assessed by immunoblot analysis of phosphorylated PDGF receptor, Akt, and ERK1/2. Pro-inflammatory activation of J774A.1 macrophages with LPS inhibited the pro-survival activity of MacCM on 3T3-L1 preadipocytes, despite intact PDGF signaling. Upregulation of macrophage tumor necrosis factor a (TNFα) expression occurred in response to LPS, and TNFα was demonstrated to be responsible for the inability of LPS-J774A.1-MacCM to inhibit preadipocyte apoptosis. Furthermore, MacCM from human MD-macrophages (MD-MacCM) inhibited apoptosis of primary human preadipocytes. MD-MacCM from LPS-treated macrophages, but not IL4-treated anti-inflammatory macrophages, was unable to protect human preadipocytes from cell death. In both murine cell lines and human primary cells, pro-inflammatory activation of macrophages inhibits their pro-survival activity, favoring preadipocyte death. These findings may be relevant to preadipocyte fate and adipose tissue remodeling in obesity.

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Wagoner, Blair, Dorothy B. Hausman et Ruth B. S. Harris. « Direct and indirect effects of leptin on preadipocyte proliferation and differentiation ». American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, n^o 6 (juin 2006) : R1557—R1564. http://dx.doi.org/10.1152/ajpregu.00860.2005.

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Leptin has been shown to reduce body fat in vivo. Adipocytes express the leptin receptor; therefore, it is realistic to expect a direct effect of leptin on adipocyte growth and metabolism. In vitro studies examining the effect of leptin on adipocyte metabolism require supraphysiological doses of the protein to see a decrease in lipogenesis or stimulation of lipolysis, implying an indirect action of leptin. It also is possible that leptin reduces adipose mass by inhibiting preadipocyte proliferation (increase in cell number) and/or differentiation (lipid filling). Thus we determined direct and indirect effects of leptin on preadipocyte proliferation and differentiation in vitro. We tested the effect of leptin (0–500 ng/ml), serum from leptin-infused rats (0.25% by volume), and adipose tissue-conditioned medium from leptin-infused rats (0–30% by volume) on preadipocyte proliferation and differentiation in a primary culture of cells from male Sprague-Dawley rat adipose tissue. Leptin (50 ng/ml) stimulated proliferation of preadipocytes ( P < 0.05), but 250 and 500 ng leptin/ml inhibited proliferation of both preadipocyte and stromal vascular cell fractions ( P < 0.01), as measured by [3H]thymidine incorporation. Serum from leptin-infused rats inhibited proliferation of the adipose and stromal vascular fractions ( P = 0.01), but adipose tissue-conditioned medium had no effect on proliferation of either cell fraction. None of the treatments changed preadipocyte differentiation as measured by sn-glycerophosphate dehydrogenase activity. These results suggest that leptin could inhibit preadipocyte proliferation by modifying release of a factor from tissue other than adipose tissue.

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Tchkonia, Tamara, Yourka D. Tchoukalova, Nino Giorgadze, Tamar Pirtskhalava, Iordanes Karagiannides, R. Armour Forse, Ada Koo et al. « Abundance of two human preadipocyte subtypes with distinct capacities for replication, adipogenesis, and apoptosis varies among fat depots ». American Journal of Physiology-Endocrinology and Metabolism 288, n^o 1 (janvier 2005) : E267—E277. http://dx.doi.org/10.1152/ajpendo.00265.2004.

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Fat depots vary in function and size. The preadipocytes that fat cells develop from exhibit distinct regional characteristics that persist in culture. Human abdominal subcutaneous cultured preadipocytes undergo more extensive lipid accumulation, higher adipogenic transcription factor expression, and less TNF-α-induced apoptosis than omental preadipocytes. We found higher replicative potential in subcutaneous and mesenteric than in omental preadipocytes. In studies of colonies arising from single preadipocytes, two preadipocyte subtypes were found, one capable of more extensive replication, differentiation, and adipogenic transcription factor expression and less apoptosis in response to TNF-α than the other. The former was more abundant in subcutaneous and mesenteric than in omental preadipocyte populations, potentially contributing to regional variation in replication, differentiation, and apoptosis. Both subtypes were found in strains derived from single human preadipocytes stably expressing telomerase, confirming that both subtypes are of preadipocyte lineage. After subcloning of cells of either subtype, both subtypes were found, indicating that switching can occur between subtypes. Thus proportions of preadipocyte subtypes with distinct cell-dynamic properties vary among depots, potentially permitting tissue plasticity through subtype selection during development. Furthermore, mesenteric preadipocyte cell-dynamic characteristics are distinct from omental cells, indicating that visceral fat depots are not functionally uniform.

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Kwon, Hyo-Shin, et Byeong-Churl Jang. « Anti-adipogenic Effect and Mechanism in 3T3-L1 Preadipocyte Differentiation by Salvianolic Acid B ». Keimyung Medical Journal 41, n^o 2 (15 décembre 2022) : 67–75. http://dx.doi.org/10.46308/kmj.2022.00213.

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Salvianolic acid B (Sal B) is one of the most active hydrophilic compounds extracted from Salvia miltiorrhiza root. Previous in vitro and in vivo studies demonstrate the ability of Sal B to modulate adipocyte differentiation. However, the lipid-modulating effect and mechanism of Sal B in adipocytes remain controversial. Here we investigated the regulatory effect and mode of action of Sal B on lipid accumulation in 3T3-L1 preadipocyte differentiation. Lipid droplet (LD) accumulation and triglyceride (TG) content during 3T3-L1 preadipocyte differentiation were measured by Oil Red O staining and AdipoRed assay. The growth inhibition during 3T3-L1 preadipocyte differentiation was measured by cell count analysis. Western blotting and real-time qPCR analysis were utilized to determine the protein and mRNA expression in the preadipocyte differentiation. Notably, in 3T3-L1 preadipocyte differentiation, treatment with Sal B at 100 M led to a marked decrease in LD accumulation and TG content without influencing cell growth. Sal B treatment (100 M) further reduced the expression and phosphorylation levels of adipogenic transcription factors, including CCAAT/enhancer-binding protein- (C/EBP-), peroxisome proliferator-activated receptor-gamma (PPAR)-, and signal transducer and activator of transcription (STAT)-3/5. Treatment with Sal B (100 M) also reduced the expression and phosphorylation levels of fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC), two lipogenic enzymes and perilipin A, an LD-binding and stabilizing protein. These results collectively demonstrate that Sal B at 100 M strongly inhibits lipid accumulation in 3T3-L1 preadipocyte differentiation, mediated through regulation of the expression and phosphorylation levels of C/EBP-, PPAR-, STAT-3/5, FAS, ACC, and perilipin.

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Charrière, Guillaume, Béatrice Cousin, Emmanuelle Arnaud, Mireille André, Francis Bacou, Luc Pénicaud et Louis Casteilla. « Preadipocyte Conversion to Macrophage ». Journal of Biological Chemistry 278, n^o 11 (7 janvier 2003) : 9850–55. http://dx.doi.org/10.1074/jbc.m210811200.

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Cho, Young-Min, Seon-Mi Lee, Young-Hwa Kim, Geon-Uk Jeon, Jee-Hy Sung, Heon-Sang Jeong et Jun-Soo Lee. « Defatted Grape Seed Extracts Suppress Adipogenesis in 3T3-L1 Preadipocytes ». Journal of the Korean Society of Food Science and Nutrition 39, n^o 6 (30 juin 2010) : 927–31. http://dx.doi.org/10.3746/jkfn.2010.39.6.927.

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McNelis, Joanne C., Konstantinos N. Manolopoulos, Laura L. Gathercole, Iwona J. Bujalska, Paul M. Stewart, Jeremy W. Tomlinson et Wiebke Arlt. « Dehydroepiandrosterone exerts antiglucocorticoid action on human preadipocyte proliferation, differentiation, and glucose uptake ». American Journal of Physiology-Endocrinology and Metabolism 305, n^o 9 (1 novembre 2013) : E1134—E1144. http://dx.doi.org/10.1152/ajpendo.00314.2012.

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Glucocorticoids increase adipocyte proliferation and differentiation, a process underpinned by the local reactivation of inactive cortisone to active cortisol within adipocytes catalyzed by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). The adrenal sex steroid precursor dehydroepiandrosterone (DHEA) has been shown to inhibit 11β-HSD1 in murine adipocytes; however, rodent adrenals do not produce DHEA physiologically. Here, we aimed to determine the effects and underlying mechanisms of the potential antiglucocorticoid action of DHEA and its sulfate ester DHEAS in human preadipocytes. Utilizing a human subcutaneous preadipocyte cell line, Chub-S7, we examined the metabolism and effects of DHEA in human adipocytes, including adipocyte proliferation, differentiation, 11β-HSD1 expression, and activity and glucose uptake. DHEA, but not DHEAS, significantly inhibited preadipocyte proliferation via cell cycle arrest in the G1 phase independent of sex steroid and glucocorticoid receptor activation. 11β-HSD1 oxoreductase activity in differentiated adipocytes was inhibited by DHEA. DHEA coincubated with cortisone significantly inhibited preadipocyte differentiation, which was assessed by the expression of markers of early ( LPL) and terminal ( G3PDH) adipocyte differentiation. Coincubation with cortisol, negating the requirement for 11β-HSD1 oxoreductase activity, diminished the inhibitory effect of DHEA. Further consistent with glucocorticoid-opposing effects of DHEA, insulin-independent glucose uptake was significantly enhanced by DHEA treatment. DHEA increases basal glucose uptake and inhibits human preadipocyte proliferation and differentiation, thereby exerting an antiglucocorticoid action. DHEA inhibition of the amplification of glucocorticoid action mediated by 11β-HSD1 contributes to the inhibitory effect of DHEA on human preadipocyte differentiation.

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Molgat, André SD, AnneMarie Gagnon et Alexander Sorisky. « Preadipocyte apoptosis is prevented by macrophage-conditioned medium in a PDGF-dependent manner ». American Journal of Physiology-Cell Physiology 296, n^o 4 (avril 2009) : C757—C765. http://dx.doi.org/10.1152/ajpcell.00617.2008.

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Obesity is associated with macrophage accumulation and inflammation in adipose tissue. Macrophage-secreted factors have been reported to inhibit the differentiation of preadipocytes into adipocytes and to modulate adipogenic extracellular matrix gene expression. To enlarge our understanding of macrophages and the scope of their interactions with preadipocytes, we investigated their effect on preadipocyte survival. Acute exposure of 3T3-L1 preadipocytes to J774A.1 macrophage-conditioned medium (MacCM) stimulated platelet-derived growth factor receptor (PDGFR) tyrosine phosphorylation by 4.1-fold. There were significant increases in the phosphocontent of downstream PDGFR targets Akt and ERK1/2 (5.3-fold and 2.4-fold, respectively) that were inhibited by PDGF immunoneutralization or by the selective PDGFR inhibitor imatinib. Serum-free J774A.1-MacCM or RAW264.7-MacCM completely prevented 3T3-L1 preadipocyte apoptosis normally induced by serum deprivation. Addition of PDGF alone to serum-free control medium was sufficient to prevent 3T3-L1 preadipocyte apoptosis. Inhibition of PDGFR activation by MacCM, either by addition of imatinib or by PDGF immunodepletion of MacCM, effectively disrupted the prosurvival effect. In summary, our data indicate that MacCM promotes preadipocyte survival in a PDGF-dependent manner.

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Kawarasaki, Satoko, Kazuki Matsuo, Hidetoshi Kuwata, Lanxi Zhou, Jungin Kwon, Zheng Ni, Haruya Takahashi et al. « Screening of flavor compounds using Ucp1-luciferase reporter beige adipocytes identified 5-methylquinoxaline as a novel UCP1-inducing compound ». Bioscience, Biotechnology, and Biochemistry 86, n^o 3 (22 décembre 2021) : 380–89. http://dx.doi.org/10.1093/bbb/zbab216.

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ABSTRACT Uncoupling protein 1 (UCP1) in brown or beige adipocytes is a mitochondrial protein that is expected to enhance whole-body energy expenditure. For the high-throughput screening of UCP1 transcriptional activity regulator, we established a murine inguinal white adipose tissue-derived Ucp1-luciferase reporter preadipocyte line. Using this reporter preadipocyte line, 654 flavor compounds were screened, and a novel Ucp1 expression-inducing compound, 5-methylquinoxaline, was identified. Adipocytes treated with 5-methylquinoxaline showed increased Ucp1 mRNA expression levels and enhanced oxygen consumption. 5-Methylquinoxaline induced Ucp1 expression through peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α), and 5-methylquinoxaline-induced PGC1α activation seemed to be partially regulated by its phosphorylation or deacetylation. Thus, our Ucp1-luciferase reporter preadipocyte line is a useful tool for screening of Ucp1 inductive compounds.

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Siao, An-Ci, Yen-Yue Lin, Li-Jane Shih, Yi-Wei Tsuei, Chih-Pin Chuu, Yow-Chii Kuo et Yung-Hsi Kao. « Endothelin-1 stimulates preadipocyte growth via the PKC, STAT3, AMPK, c-JUN, ERK, sphingosine kinase, and sphingomyelinase pathways ». American Journal of Physiology-Cell Physiology 319, n^o 5 (1 novembre 2020) : C839—C857. http://dx.doi.org/10.1152/ajpcell.00491.2019.

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Endothelin (ET)-1 regulates adipogenesis and the endocrine activity of fat cells. However, relatively little is known about the ET-1 signaling pathway in preadipocyte growth. We used 3T3-L1 preadipocytes to investigate the signaling pathways involved in ET-1 modulation of preadipocyte proliferation. As indicated by an increased number of cells and greater incorporation of bromodeoxyuridine (BrdU), the stimulation of preadipocyte growth by ET-1 depends on concentration and timing. The concentration of ET-1 that increased preadipocyte number by 51–67% was ~100 nM for ~24–48 h of treatment. ET-1 signaling time dependently stimulated phosphorylation of ERK, c-JUN, STAT3, AMPK, and PKCα/βII proteins but not AKT, JNK, or p38 MAPK. Treatment with an ETAR antagonist, such as BQ610, but not ETBR antagonist BQ788, blocked the ET-1-induced increase in cell proliferation and phosphorylated levels of ERK, c-JUN, STAT3, AMPK, and PKCα/βII proteins. In addition, pretreatment with specific inhibitors of ERK1/2 (U0126), JNK (SP600125), JAK2/STAT3 (AG490), AMPK (compound C), or PKC (Ro318220) prevented the ET-1-induced increase in cell proliferation and reduced the ET-1-stimulated phosphorylation of ERK1/2, c-JUN, STAT3, AMPK, and PKCα/β. Moreover, the SphK antagonist suppressed ET-1-induced cell proliferation and ERK, c-JUN, STAT3, AMPK, and PKC phosphorylation, and the SMase2 antagonist suppressed ET-1-induced cell proliferation. However, neither the p38 MAPK antagonist nor the CerS inhibitor altered the effect of ET-1. The results indicate that ETAR, JAK2/STAT3, ERK1/2, JNK/c-JUN, AMPK, PKC, SphK, and SMase2, but not ETBR, p38 MAPK, or CerS, are necessary for the ET-1 stimulation of preadipocyte proliferation.

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McIntosh, M., D. Hausman, R. Martin et G. Hausman. « Dehydroepiandrosterone attenuates preadipocyte growth in primary cultures of stromal-vascular cells ». American Journal of Physiology-Endocrinology and Metabolism 275, n^o 2 (1 août 1998) : E285—E293. http://dx.doi.org/10.1152/ajpendo.1998.275.2.e285.

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The purpose of this study was to determine whether the antiobesity actions of dehydroepiandrosterone (DHEA) are due to an influence on preadipocyte proliferation and/or differentiation in primary cultures of pig and rat stromal-vascular (SV) cells. Pig SV cells were isolated from dorsal subcutaneous adipose tissue of 7-day-old pigs. For the proliferation assays, pig SV cells were grown for 4 days in plating medium containing DHEA at 0, 15, 50, or 150 μM. For the differentiation assays, pig SV cells were grown in plating medium for 3 days and then switched to a serum-free medium containing DHEA at 0, 15, 50, or 150 μM for the next 6 days. Rat SV cells were isolated from inguinal fat pads of 5-wk-old male rats. Rat SV cells were exposed to DHEA at 0, 5, 25, or 75 μM during proliferation. For the differentiation assays, rat SV cells were grown for 8 days in a serum-free medium containing DHEA at 0, 5, 25, or 75 μM. Preadipocyte differentiation [lipid staining, glycerol-3-phosphate dehydrogenase (GPDH) activity] and proliferation (preadipocyte-specific antigen staining) decreased with increasing levels of DHEA in cultures of pig SV cells. In cultures of rat SV cells, preadipocyte differentiation (lipid staining, GPDH activity) and proliferation ([3H]thymidine incorporation) were decreased in the 25 and 75 μM DHEA groups compared with the control and 5 μM DHEA groups. The level of expression of CCAAT enhancer binding protein-α, a master regulator of adipogenesis, in cultures of pig SV cells treated with 150 μM DHEA was 38% of control cultures. These data support the hypothesis that DHEA directly attenuates adipogenesis via attenuation of preadipocyte proliferation and differentiation.

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Yadav, Anil Kumar, et Byeong-Churl Jang. « Inhibition of Lipid Accumulation and Cyclooxygenase-2 Expression in Differentiating 3T3-L1 Preadipocytes by Pazopanib, a Multikinase Inhibitor ». International Journal of Molecular Sciences 22, n^o 9 (5 mai 2021) : 4884. http://dx.doi.org/10.3390/ijms22094884.

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Pazopanib is a multikinase inhibitor with anti-tumor activity. As of now, the anti-obesity effect and mode of action of pazopanib are unknown. In this study, we investigated the effects of pazopanib on lipid accumulation, lipolysis, and expression of inflammatory cyclooxygenase (COX)-2 in differentiating and differentiated 3T3-L1 cells, a murine preadipocyte. Of note, pazopanib at 10 µM markedly decreased lipid accumulation and triglyceride (TG) content during 3T3-L1 preadipocyte differentiation with no cytotoxicity. Furthermore, pazopanib inhibited not only expression of CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), and perilipin A but also phosphorylation of signal transducer and activator of transcription (STAT)-3 during 3T3-L1 preadipocyte differentiation. In addition, pazopanib treatment increased phosphorylation of cAMP-activated protein kinase (AMPK) and its downstream effector ACC during 3T3-L1 preadipocyte differentiation. However, in differentiated 3T3-L1 adipocytes, pazopanib treatment did not stimulate glycerol release and hormone-sensitive lipase (HSL) phosphorylation, hallmarks of lipolysis. Moreover, pazopanib could inhibit tumor necrosis factor (TNF)-α-induced expression of COX-2 in both 3T3-L1 preadipocytes and differentiated cells. In summary, this is the first report that pazopanib has strong anti-adipogenic and anti-inflammatory effects in 3T3-L1 cells, which are mediated through regulation of the expression and phosphorylation of C/EBP-α, PPAR-γ, STAT-3, ACC, perilipin A, AMPK, and COX-2.

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Zhao, Chen, Tan, Wang, Zhang, Yang, Liu, Ao, Xing et Wang. « Transcriptome Analysis of Landrace Pig Subcutaneous Preadipocytes during Adipogenic Differentiation ». Genes 10, n^o 7 (19 juillet 2019) : 552. http://dx.doi.org/10.3390/genes10070552.

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Fat deposition in pigs, which significantly contributes to meat quality, fattening efficiency, reproductive performance, and immunity, is critically affected by preadipocyte adipogenic differentiation. We elucidated adipogenesis in pigs using transcriptome analysis. Preadipocytes from subcutaneous adipose tissue (SAT) of Landrace piglets were differentiated into adipocytes in vitro. RNA sequencing (RNA-seq) used to screen differentially expressed genes (DEGs) during preadipocyte differentiation up to day 8 revealed 15,918 known and 586 novel genes. We detected 21, 144, and 394 DEGs, respectively, including 16 genes differentially expressed at days 2, 4 and 8 compared to day 0. Th number of DEGs increased time-dependently. Lipid metabolism, cell differentiation and proliferation, peroxisome proliferator-activated receptor (PPAR), wingless-type MMTV integration site (Wnt), tumor necrosis factor (TNF) signaling, and steroid biosynthesis were significant at days 2, 4, and 8 compared to day 0 (adjusted p < 0.05). Short time-series expression miner (STEM) analysis obtained 26 clusters of differential gene expression patterns, and nine were significant (p < 0.05). Functional analysis showed many significantly enriched lipid deposition- and cellular process-related biological processes and pathways in profiles 9, 21, 22, and 24. Glycerolipid and fatty-acid metabolism, PPAR signaling, fatty-acid degradation, phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), and TNF signaling were observed during preadipocyte differentiation in vitro. These findings will facilitate the comprehension of preadipocyte differentiation and fat deposition in pigs.

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Xi, Feng-xue, Chang-sheng Wei, Yan-ting Xu, Lu Ma, Yu-lin He, Xin-e. Shi, Gong-she Yang et Tai-yong Yu. « MicroRNA-214-3p Targeting Ctnnb1 Promotes 3T3-L1 Preadipocyte Differentiation by Interfering with the Wnt/β-Catenin Signaling Pathway ». International Journal of Molecular Sciences 20, n^o 8 (12 avril 2019) : 1816. http://dx.doi.org/10.3390/ijms20081816.

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Differentiation from preadipocytes into mature adipocytes is a complex biological process in which miRNAs play an important role. Previous studies showed that miR-214-3p facilitates adipocyte differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) in vitro. The detailed function and molecular mechanism of miR-214-3p in adipocyte development is unclear. In this study, the 3T3-L1 cell line was used to analyze the function of miR-214-3p in vitro. Using 5-Ethynyl-2′-deoxyuridine (EdU) staining and the CCK-8 assay, we observed that transfection with the miR-214-3p agomir visibly promoted proliferation of 3T3-L1 preadipocytes by up-regulating the expression of cell cycle-related genes. Interestingly, overexpression of miR-214-3p promoted 3T3-L1 preadipocyte differentiation and up-regulated the expression of key genes for lipogenesis: PPARγ, FABP4, and Adiponectin. Conversely, inhibition of miR-214-3p repressed 3T3-L1 preadipocyte proliferation and differentiation, and down-regulated the expression of cell cycle-related genes and adipogenic markers. Furthermore, we proved that miR-214-3p regulates 3T3-L1 preadipocyte differentiation by directly targeting the 3′-untranslated regions (3′UTR) of Ctnnb1, which is an important transcriptional regulatory factor of the Wnt/β-Catenin pathway. Taken together, the data indicate that miR-214-3p may positively regulate preadipocyte proliferation and enhance differentiation through the Wnt/β-Catenin signaling pathway.

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Perumal, Nivethasri Lakshmana, Amila Mufida, Anil Kumar Yadav, Dae-Gu Son, Young-Wook Ryoo, Sung-Ae Kim et Byeong-Churl Jang. « Suppression of Lipid Accumulation in the Differentiation of 3T3-L1 Preadipocytes and Human Adipose Stem Cells into Adipocytes by TAK-715, a Specific Inhibitor of p38 MAPK ». Life 13, n^o 2 (1 février 2023) : 412. http://dx.doi.org/10.3390/life13020412.

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Excessive preadipocyte differentiation is linked with obesity. Although previous studies have shown that p38 MAPK is associated with adipogenesis, the regulation of preadipocyte differentiation by TAK-715, an inhibitor of p38 mitogen-activated protein kinase (MAPK), remains unclear. Interestingly, TAK-715 at 10 μM vastly suppressed the accumulation of lipid and intracellular triglyceride (TG) content with no cytotoxicity during 3T3-L1 preadipocyte differentiation. On mechanistic levels, TAK-715 significantly decreased the expressions of the CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor gamma (PPAR-γ), fatty acid synthase (FAS), and perilipin A. Similarly, the phosphorylation of the signal transducer and activator of transcription-3 (STAT-3) in differentiating 3T3-L1 cells was also reduced with TAK-715 treatment. Moreover, TAK-715 significantly blocked the phosphorylation of activating transcription factor-2 (ATF-2), a p38 MAPK downstream molecule, during 3T3-L1 preadipocyte differentiation. Of importance, TAK-715 also markedly impeded the phosphorylation of p38 MAPK and suppressed lipid accumulation during the adipocyte differentiation of human adipose stem cells (hASCs). Concisely, this is the first report that TAK-715 (10 μM) has potent anti-adipogenic effects on the adipogenesis process of 3T3-L1 cells and hASCs through the regulation of the expression and phosphorylation of p38 MAPK, C/EBP-α, PPAR-γ, STAT-3, FAS, and perilipin A.

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Kim, Ji Hye, Mi Jeong Jo, Hye Jin Go, Nam Gyu Park et Gun Do Kim. « Anti-adipogenic effect of mastoparan B analogue peptide on 3T3-L1 preadipocytes ». Bangladesh Journal of Pharmacology 13, n^o 4 (13 novembre 2018) : 333–39. http://dx.doi.org/10.3329/bjp.v13i4.37351.

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Mastoparan B (MP-B), a cationic tetradecapeptide isolated from the venom of the Vespa basalis, exhibits cardiovascular effects, local edema and antibacterial activity. In this study, the anti-adipogenic effect of an MP-B analogue and its mechanism of action in 3T3-L1 preadipocytes were studied. The MP-B analogue (MP-B12) inhibited preadipocyte differentiation and decreased the expression of adipogenic transcription factors, including CCAAT/enhancer binding protein-alpha (C/EBPα), nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) and sterol regulatory element-binding protein-1 (SREBP-1). Moreover, MP-B12 regulated the phosphorylation of Akt and glycogen synthase kinase-3 beta (GSK-3β), both of which play a role in preadipocyte differentiation, in which insulin and certain growth factors stimulated adipogenesis. This study demonstrates that MP-B12 inhibits preadipocyte differentiation and the accumulation of lipid droplets in 3T3-L1 preadipocytes and could potentially be used to treat obesity.Video Clip of Methodology:4 min 11 sec Full Screen Alternate

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Chen, Dingshuang, Yaqiu Lin, Nan Zhao, Yong Wang et Yanyan Li. « Hoxa5 Inhibits the Proliferation and Induces Adipogenic Differentiation of Subcutaneous Preadipocytes in Goats ». Animals 12, n^o 14 (21 juillet 2022) : 1859. http://dx.doi.org/10.3390/ani12141859.

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The homeobox a5 (Hoxa5) plays considerable roles in the differentiation and lipid metabolism of adipocytes. However, the current knowledge about the mechanistic roles and functions of Hoxa5 in goat subcutaneous preadipocyte remains unclear. Therefore, Hoxa5 loss-of-function and gain-of-function was performed to reveal its functions in adipogenesis. For differentiation, overexpression of Hoxa5 notably increased the expression of adipogenic genes (PPARγ, CEBP/α, CEBP/β, AP2, and SREBP1), as well as promoted goat subcutaneous preadipocyte lipid accumulation. Knockdown of Hoxa5 mediated by siRNA technique significantly inhibited its differentiation and suppressed the accumulation of lipid droplets. Regarding proliferation, overexpression of Hoxa5 reduced the number of cells stained with crystal violet, and inhibited mRNA expression of the marker genes including CCNE1, PCNA, CCND1, and CDK2, and also significantly reduced EdU-positive rates. Consistently, knockdown of Hoxa5 demonstrated the opposite tendency. In conclusion, these data demonstrated that Hoxa5 promotes adipogenic differentiation of goat subcutaneous preadipocyte and inhibits its proliferation in vitro.

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Zhai, Guiying, Yongjia Pang, Yichong Zou, Xinyu Wang, Jie Liu, Qi Zhang, Zhiping Cao, Ning Wang, Hui Li et Yuxiang Wang. « Effects of PLIN1 Gene Knockout on the Proliferation, Apoptosis, Differentiation and Lipolysis of Chicken Preadipocytes ». Animals 13, n^o 1 (26 décembre 2022) : 92. http://dx.doi.org/10.3390/ani13010092.

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Perilipin 1 (PLIN1) is one of the most abundant lipid droplet-related proteins on the surface of adipocytes. Our previous results showed that PLIN1 plays an important role in chicken lipid metabolism. To further reveal the role of PLIN1 in the growth and development of adipocytes, a chicken preadipocyte line with a PLIN1 gene knockout was established by the CRISPR/Cas9 gene editing technique, and the effects of the PLIN1 gene on the proliferation, apoptosis, differentiation and lipolysis of chicken preadipocytes were detected. The results showed that the CRISPR/Cas9 system effectively mediated knockout of the PLIN1 gene. After the deletion of PLIN1, the differentiation ability and early apoptotic activity of chicken preadipocytes decreased, and their proliferation ability increased. Moreover, knockout of PLIN1 promoted chicken preadipocyte lipolysis under basal conditions and inhibited chicken preadipocyte lipolysis under hormone stimulation. Taken together, our results inferred that PLIN1 plays a regulatory role in the process of proliferation, apoptosis, differentiation and lipolysis of chicken preadipocytes.

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Taleb, Soraya, Raffaella Cancello, Karine Clément et Daniele Lacasa. « Cathepsin S Promotes Human Preadipocyte Differentiation : Possible Involvement of Fibronectin Degradation ». Endocrinology 147, n^o 10 (1 octobre 2006) : 4950–59. http://dx.doi.org/10.1210/en.2006-0386.

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We previously showed that the cysteine protease cathepsin S (CTSS), known to degrade several components of the extracellular matrix (ECM), is produced by human adipose cells and increased in obesity. Because ECM remodeling is a key process associated with adipogenesis, this prompted us to assess the potential role of CTSS to promote preadipocyte differentiation. Kinetic studies in primary human preadipocytes revealed a modest increase in CTSS gene expression and secretion at the end of differentiation. CTSS activity was maximal in preadipocyte culture medium but decreased thereafter, fitting with increased release of the CTSS endogenous inhibitor, cystatin C, during differentiation. Inhibition of CTSS activity by an exogenous-specific inhibitor added along the differentiation, resulted in a 2-fold reduction of lipid content and expression of adipocyte markers in differentiated cells. Conversely, the treatment of preadipocytes with human recombinant CTSS increased adipogenesis. Moreover, CTSS supplementation in preadipocyte media markedly reduced the fibronectin network, a key preadipocyte-ECM component, the decrease of which is required for adipogenesis. Using immunohistochemistry on serial sections of adipose tissue of obese subjects, we showed that adipose cells staining positive for CTSS are mainly located in the vicinity of fibrosis regions containing fibronectin. Herein we propose that CTSS may promote human adipogenesis, at least in part, by degrading fibronectin in the early steps of differentiation. Taken together, these results indicate that CTSS released locally by preadipocytes promotes adipogenesis, suggesting a possible contribution of this protease to fat mass expansion in obesity.

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Yang, Wenkai, Wenjin Yuan, Xinghua Peng, Meiling Wang, Jie Xiao, Cheng Wu et Lie Luo. « PPAR γ/Nnat/NF-κB Axis Involved in Promoting Effects of Adiponectin on Preadipocyte Differentiation ». Mediators of Inflammation 2019 (21 novembre 2019) : 1–9. http://dx.doi.org/10.1155/2019/5618023.

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A previous study has demonstrated that adiponectin (APN) could promote preadipocyte differentiation, and the present study further explored its mechanism. 3T3-L1 cells were infected with adenovirus holding human adiponectin gene apM1 and mouse neuronatin (Nnat) shRNA and initiated differentiation while coculturing with mature adipocytes stimulated with LPS. After 8 days, preadipocyte differentiation was observed by Oil Red O staining. Real-time quantitative PCR was used to evaluate mRNA expression levels of monocyte chemoattractant protein-1 (MCP-1), interleukin- (IL-) 6, IL-8, and tumor necrosis factor α (TNF-α). The levels of reactive oxygen species (ROS), total antioxidant capacity (T-AOC), malondialdehyde (MDA), and superoxide dismutase (SOD) in 3T3-L1 cells were detected. Western blotting was done to quantify the protein expression levels of Nnat, peroxisome proliferator-activated receptor (PPAR) γ, p65, and inhibitor of nuclear factor κB (IκB) α. Results demonstrated that APN overexpression markedly increased preadipocyte differentiation; inhibited gene expression of MCP-1, IL-6, IL-8, and TNF-α; reduced ROS and MDA release; increased T-AOC and SOD levels; upregulated Nnat, PPAR γ, and IκB α protein expressions; and downregulated p65 protein expression under LPS stimulation. However, the effects of APN were markedly attenuated when Nnat expression was knocked down. Taken together, the present study provided evidences that the effects of APN on promoting preadipocyte differentiation under inflammatory conditions via anti-inflammation and antioxidative stress may be regulated by the PPAR γ/Nnat/NF-κB signaling pathway.

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Karlina, Ruth, Dominik Lutter, Viktorian Miok, David Fischer, Irem Altun, Theresa Schöttl, Kenji Schorpp et al. « Identification and characterization of distinct brown adipocyte subtypes in C57BL/6J mice ». Life Science Alliance 4, n^o 1 (30 novembre 2020) : e202000924. http://dx.doi.org/10.26508/lsa.202000924.

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Brown adipose tissue (BAT) plays an important role in the regulation of body weight and glucose homeostasis. Although increasing evidence supports white adipose tissue heterogeneity, little is known about heterogeneity within murine BAT. Recently, UCP1 high and low expressing brown adipocytes were identified, but a developmental origin of these subtypes has not been studied. To obtain more insights into brown preadipocyte heterogeneity, we use single-cell RNA sequencing of the BAT stromal vascular fraction of C57/BL6 mice and characterize brown preadipocyte and adipocyte clonal cell lines. Statistical analysis of gene expression profiles from brown preadipocyte and adipocyte clones identify markers distinguishing brown adipocyte subtypes. We confirm the presence of distinct brown adipocyte populations in vivo using the markers EIF5, TCF25, and BIN1. We also demonstrate that loss of Bin1 enhances UCP1 expression and mitochondrial respiration, suggesting that BIN1 marks dormant brown adipocytes. The existence of multiple brown adipocyte subtypes suggests distinct functional properties of BAT depending on its cellular composition, with potentially distinct functions in thermogenesis and the regulation of whole body energy homeostasis.

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Takaya, Kento, Naruhito Matsuda, Toru Asou et Kazuo Kishi. « Brown preadipocyte transplantation locally ameliorates obesity ». Archives of Plastic Surgery 48, n^o 4 (15 juillet 2021) : 440–47. http://dx.doi.org/10.5999/aps.2020.02257.

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Background Brown adipose tissue (BAT) is a potential target for anti-obesity treatments. Previous studies have shown that BAT activation causes an acute metabolic boost and reduces adiposity. Furthermore, BAT and BAT-derived cell transplantation reportedly help treat obesity by regulating glucose and fatty acid metabolism. However, since BAT transplantation leads to whole-body weight loss, we speculated that earlier approaches cause a generalized and unnecessary fat tissue loss, including in breast and hip tissues.Methods We transplanted white adipose tissue-derived or BAT-derived preadipocytes prepared from C57BL/6 mice into one side of the inguinal fat pads of an obese mouse model (db/ db mice) to examine whether it would cause fat loss at the peri-transplant site (n=5 each). The same volume of phosphate-buffered saline was injected as a control on the other side. Six weeks after transplantation, the inguinal fat pad was excised and weighed. We also measured the concentrations of glucose, triglycerides, fatty acids, and total cholesterol in the peripheral blood.Results BAT-derived preadipocytes showed abundant mitochondria and high levels of mitochondrial membrane uncoupling protein 1 expression, both in vivo and in vitro, with a remarkable reduction in weight of the inguinal fat pad after transplantation (0.17±0.12 g, P=0.043). Only free fatty acid levels tended to decrease in the BAT-transplanted group, but the difference was not significant (P=0.11).Conclusions Our results suggest that brown adipocytes drive fat degradation around the transplantation site. Thus, local transplantation of BAT-derived preadipocytes may be useful for treating obesity, as well as in cosmetic treatments.

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Liu, Ping, Guoliang Li, Jine Wu, Xin Zhou, Liping Wang, Wenqi Han, Ying Lv et Chaofeng Sun. « Vaspin promotes 3T3-L1 preadipocyte differentiation ». Experimental Biology and Medicine 240, n^o 11 (13 janvier 2015) : 1520–27. http://dx.doi.org/10.1177/1535370214565081.

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Hausman, Gary J., et Dorothy B. Hausman. « Search for the preadipocyte progenitor cell ». Journal of Clinical Investigation 116, n^o 12 (1 décembre 2006) : 3103–6. http://dx.doi.org/10.1172/jci30666.

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Tews, D., P. Fischer-Posovszky et M. Wabitsch. « Regulation ofFTOandFTMExpression During Human Preadipocyte Differentiation ». Hormone and Metabolic Research 43, n^o 01 (23 septembre 2010) : 17–21. http://dx.doi.org/10.1055/s-0030-1265130.

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Roncari, Daniel A. K., et Paul E. Le Blanc. « Inhibition of rat perirenal preadipocyte differentiation ». Biochemistry and Cell Biology 68, n^o 1 (1 janvier 1990) : 238–42. http://dx.doi.org/10.1139/o90-032.

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The process of adipose differentiation uniquely endows fat cells to accrue triacylglycerols under conditions of nutrient energy surfeit and to release fatty acids during energy deprivation. The object of this investigation was to study influences on this process in perirenal preadipocytes, grown in primary culture or first subculture and derived from male Sprague–Dawley rats, 180–200 g. Supplementation of the culture medium with 1-methyl-3-isobutylxanthine, corticosterone, and insulin induced differentiation in practically all perirenal preadipocytes, as indicated morphologically and by rising glycerophosphate dehydrogenase activity. Appreciable differentiation was induced even in the absence of methylisobutylxanthine. Transforming growth factor β (1–1000 pM), cachectin (tumour necrosis factor α) (1–1000 pM), and basic fibroblast growth factor (0.063–63 nM) inhibited adipose differentiation significantly, almost completely at the higher concentrations. Direct inhibition, rather than a persisting mitogenic effect of fibroblast growth factor, was confirmed using demecolcine (Colcemid). The fact that transforming growth factor β and cachectin inhibit differentiation in preadipocytes from postpuberal rats suggests that this effect probably also occurs in vivo, thus diverting energy from adipose depots in certain neoplastic and inflammatory states. We propose that the anterior pituitary, through fibroblast growth factor(s), modulates the pool of preadipocytes and other mesenchymal cells. The mitogenic effect would be complemented by a concerted function, inhibition of adipose differentiation, resulting in the retention of a greater number of potentially replicative cells. Then, depending on the subject's nutritional and endocrine status, extrapituitary factors would regulate the specific process of differentiation.Key words: preadipocyte differentiation, inhibition, pituitary, cachectin.

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Coskun, Huseyin, Taryn L. S. Summerfield, Douglas A. Kniss et Avner Friedman. « Mathematical modeling of preadipocyte fate determination ». Journal of Theoretical Biology 265, n^o 1 (juillet 2010) : 87–94. http://dx.doi.org/10.1016/j.jtbi.2010.03.047.

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Gu, Nan, Shi Liu, Xirong Guo, Li Fei, Xiaoqin Pan, Mei Guo et Ronghua Chen. « Verapamil inhibits 3T3-L1 preadipocyte differentiation ». Journal of Nanjing Medical University 23, n^o 6 (novembre 2009) : 403–9. http://dx.doi.org/10.1016/s1007-4376(09)60090-3.

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Fukuwatari, T., T. Kawada, N. Aoki, Y. Kamei, T. Fushiki et E. Sugimoto. « Characterization of preadipocyte growth factor, PAGF ». Pathophysiology 1 (novembre 1994) : 196. http://dx.doi.org/10.1016/0928-4680(94)90409-x.

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Hirai, Shizuka, Haruka Matsumoto, Naoko Hino, Hiroyuki Kawachi, Tohru Matsui et Hideo Yano. « Myostatin inhibits differentiation of bovine preadipocyte ». Domestic Animal Endocrinology 32, n^o 1 (janvier 2007) : 1–14. http://dx.doi.org/10.1016/j.domaniend.2005.12.001.

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Vangipuram, Sharada D., Jonathan Sheele, Richard L. Atkinson, Thomas C. Holland et Nikhil V. Dhurandhar. « A Human Adenovirus Enhances Preadipocyte Differentiation ». Obesity Research 12, n^o 5 (mai 2004) : 770–77. http://dx.doi.org/10.1038/oby.2004.93.

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Wei, Yao, Ya Feng Cui, Hui Li Tong, Wei Wei Zhang et Yun Qin Yan. « MicroRNA-2400 promotes bovine preadipocyte proliferation ». Biochemical and Biophysical Research Communications 478, n^o 3 (septembre 2016) : 1054–59. http://dx.doi.org/10.1016/j.bbrc.2016.08.038.

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Huang, Qiong, Menglan Liu, Xinli Du, Rihua Zhang, Yi Xue, Yuanyuan Zhang, Weidong Zhu, Dong Li, Allan Zhao et Yun Liu. « Role of p53 in preadipocyte differentiation ». Cell Biology International 38, n^o 12 (1 septembre 2014) : 1384–93. http://dx.doi.org/10.1002/cbin.10334.

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Fan, Yuan, Mailin Gan, Ya Tan, Lei Chen, Linyuan Shen, Lili Niu, Yihui Liu et al. « Mir-152 Regulates 3T3-L1 Preadipocyte Proliferation and Differentiation ». Molecules 24, n^o 18 (17 septembre 2019) : 3379. http://dx.doi.org/10.3390/molecules24183379.

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Adipogenesis is a complex biological process and the main cause of obesity. Recently, microRNAs (miRNAs), a class of small endogenous non-coding RNAs, have been proven to play an important role in adipogenesis by the post-transcriptional regulation of target genes. In this current study, we observed an increment of miR-152 expression during the process of 3T3-L1 cell audiogenic differentiation. A functional analysis indicated that the overexpression of miR-152 inhibited pre-adipocyte proliferation and suppressed the expression of some cell cycle-related genes. Moreover, the overexpression of miR-152 promoted lipid accumulation in 3T3-L1 preadipocytes accompanied by increase of the expression of some pro-audiogenic genes. Additionally, a dual-luciferase reporter assay demonstrated lipoprotein lipase (LPL) was a direct target gene of miR-152 during preadipocyte differentiation. Further analysis showed that miR-152 was positively correlated with adipogenesis and intramuscular fat formation in vivo. Taken together, our findings suggest that miR-152 could suppress 3T3-L1 preadipocyte proliferation, whereas it could promote 3T3-L1 preadipocyte differentiation by negatively regulating LPL. The findings indicate that miR-152 might have a therapeutic significance for obesity and obesity-related metabolic syndrome.

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Considine, R. V., M. R. Nyce, L. M. Morales, S. A. Magosin, M. K. Sinha, T. L. Bauer, E. L. Rosato, J. Colberg et J. F. Caro. « Paracrine stimulation of preadipocyte-enriched cell cultures by mature adipocytes ». American Journal of Physiology-Endocrinology and Metabolism 270, n^o 5 (1 mai 1996) : E895—E899. http://dx.doi.org/10.1152/ajpendo.1996.270.5.e895.

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We developed a double-chamber system in which to examine the effects of mature adipocytes on the growth and differentiation of preadipocytes and other cells in the adipose tissue. In the present study we found that mature adipocytes from both lean and obese subjects release a factor that stimulates the growth of preadipocyte-enriched and dedifferentiated adipocyte-enriched cell cultures. This growth stimulation was dependent on both time of exposure to mature cells and the number of mature cells in the coculture. Proliferation of the preadipocyte-enriched (n = 4) and dedifferentiated adipocyte-enriched cultures (n = 5) in the presence of mature adipocytes from obese subjects [body mass index (BMI) > 35] was 4.1- and 2.9-fold more (P < 0.05) than that in the presence of adipocytes from lean subjects (BMI < or = 25). There was no difference in the growth of cultures enriched in preadipocytes or dedifferentiated adipocytes from lean or obese subjects in the absence of mature adipocytes. These observations demonstrate that mature adipocytes from obese patients stimulate the growth of preadipocyte-enriched cultures to a greater extent than those from lean individuals.

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Chu, Guiyan, Xiaoge Zhou, Yamei Hu, Shengjie Shi et Gongshe Yang. « Rev-erbα Inhibits Proliferation and Promotes Apoptosis of Preadipocytes through the Agonist GSK4112 ». International Journal of Molecular Sciences 20, n^o 18 (12 septembre 2019) : 4524. http://dx.doi.org/10.3390/ijms20184524.

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Proliferation and apoptosis are important physiological processes of preadipocytes. Rev-erbα is a circadian clock gene, and its activity contributes to several physiological processes in various cells. Previous studies demonstrated that Rev-erbα promotes preadipocyte differentiation, but a role of Rev-erbα on preadipocyte proliferation and apoptosis has not been demonstrated. GSK4112 is often used as an agonist of Rev-erbα. In this study, we used GSK4112 to explore the effects of Rev-erbα on preadipocyte proliferation and apoptosis by RT-qPCR, Western blot, Cell Counting Kit-8 (CCK8) measurement, 5-Ethynyl-2′-deoxyuridine (EdU) staining, Annexin V-FITC/PI staining, and flow cytometry. These results revealed that GSK4112 inhibited the viability of 3T3-L1 preadipocytes and decreased cell numbers. There was also decreased expression of the proliferation-related gene Cyclin D and the canonical Wingless-type (Wnt) signaling effect factor β-catenin. Furthermore, palmitate (PA)-inducing cell apoptosis was promoted. Overall, these results reveal that Rev-erbα plays a role in proliferation and palmitate (PA)-inducing apoptosis of 3T3-L1 preadipocytes, and thus may be a new molecular target in efforts to prevent and treat obesity and related disease.

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Moreno Castellanos, Natalia R. « Cambios en el peril proteómico de preadipocitos con diferentes condiciones metabólicas ». Revista de la Universidad Industrial de Santander. Salud 51, n^o 4 (1 octobre 2019) : 279–87. http://dx.doi.org/10.18273/revsal.v51n4-2019001.

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Introducción y objetivos: El tejido adiposo subcutáneo se considera un depósito con un papel protector desde un punto de vista metabólico. El exceso de tejido adiposo desencadena en obesidad, la cual, está acompañada típicamente por resistencia a insulina, dislipidemia, e hipertensión arterial. No obstante, se conoce que existe un subgrupo de obesos que parecen estar protegidos de dichas complicaciones. Estos individuos son definidos como obesos sanos metabólicamente. A pesar de los avances en el conocimiento de las alteraciones que suceden en el tejido adiposo en obesidad, aún se desconocen los mecanismos que subyacen en el desarrollo de resistencia a insulina. Por lo tanto, en este trabajo, se estudió la asociación entre obesidad y desarrollo de enfermedad metabólica identificando factores y procesos que determinan la transición desde el fenotipo obeso sano y no sano, empleando preadipocitos provenientes de tejido adiposo subcutáneo. Metodología:Se emplearon datos de un estudio de proteómica comparada de preadipocitos de tejido subcutáneo obtenidos de pacientes obesos normoglucémicos no resistentes a insulina y de pacientes obesos con diabetes mellitus de tipo 2. El estudio proteómico, se llevó a cabo utilizando la técnica de iTRAQ combinada con LC-MSMS. Resultados y conclusiones: Las diferencias entre preadipocitos de tejido adiposo subcutáneo en sujetos normoglucémicos y con diabetes, afectan sobre todo a proteínas citosólicas y, en particular, a proteínas relacionadas con procesos metabólicos mientras que, las membranales no cambian entre fenotipos obesos. En el estudio se identificaron importantes diferencias en el perfil proteómico de los preadipocitos de tejido adiposo subcutáneo en obesidad, tanto en sujetos normoglucémicos como diabéticos, apoyando la importancia de estas células en el mantenimiento de la identidad del depósito graso. También se encontró que, la transición desde el fenotipo obeso sano hacia el no sano conlleva un mayor desarrollo de estrés oxidativo e inflamación en las células precursoras adipocitarias

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Fukai, Nozomi, Takanobu Yoshimoto, Toru Sugiyama, Naoko Ozawa, Ryuji Sato, Masayoshi Shichiri et Yukio Hirata. « Concomitant expression of adrenomedullin and its receptor components in rat adipose tissues ». American Journal of Physiology-Endocrinology and Metabolism 288, n^o 1 (janvier 2005) : E56—E62. http://dx.doi.org/10.1152/ajpendo.00586.2003.

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Adrenomedullin (AM) expressed by and secreted from a variety of cells plays pluripotent roles in an autocrine/paracrine fashion. The present study was undertaken to explore the expression of AM and its receptor genes in adipose tissues, their changes during the development of obesity, and the process of preadipocyte differentiation. Both mature adipocytes and stromal vascular cells constituting adipose tissue expressed AM transcript. AM and its receptor component [calcitonin receptor-like receptor and receptor activity-modifying protein-2 (CRLR/RAMP2)] mRNAs were expressed in a variety of rat adipose tissues, including epididymal, mesenteric, retroperitoneal, and subcutaneous adipose tissue. AM mRNA levels in rat and human epididymal adipose tissue were about one-tenth of those in the kidney. Steady-state mRNA levels of AM and CRLR/RAMP2 in epididymal, mesenteric, and retroperitoneal adipose tissues in rats fed a high-fat diet for 4 wk were far greater than those in rats with normal diet accompanied by increased plasma AM levels, whereas steady-state AM mRNA levels conversely decreased in other organs, such as kidney and liver. AM mRNA expressed in a mouse preadipocyte cell line (3T3-L1) transiently decreased by day 3, returned to basal level by day 6, and then increased by day 9 during preadipocyte differentiation, which paralleled AM secretion from the cells. However, the addition of either exogenous AM or AM receptor antagonist calcitonin gene-related peptide-(8–37), to block endogenous AM did not affect lipid droplet accumulation during preadipocyte differentiation. The present study demonstrates for the first time that AM and its receptor component (CRLR/RAMP2) mRNAs were concomitantly expressed in various adipose tissues, whose tissue-specific upregulation was induced during the development of obesity. These data suggest that AM may act as a new member of adipokines, although its functional role, as well as its pathophysiological significance in obesity, remains to be determined.

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You, Wenjing, Ziye Xu et Tizhong Shan. « Regulatory Roles of GADD45α in Skeletal Muscle and Adipocyte ». Current Protein & ; Peptide Science 20, n^o 9 (17 septembre 2019) : 918–25. http://dx.doi.org/10.2174/1389203720666190624143503.

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GADD45α, a member of the GADD45 family proteins, is involved in various cellular processes including the maintenance of genomic integrity, growth arrest, apoptosis, senescence, and signal transduction. In skeletal muscle, GADD45α plays an important role in regulating mitochondrial biogenesis and muscle atrophy. In adipocytes, GADD45α regulates preadipocyte differentiation, lipid accumulation, and thermogenesis metabolism. Moreover, it has been recently demonstrated that GADD45α promotes gene activation by inducing DNA demethylation. The epigenetic function of GADD45α is important for preadipocyte differentiation and transcriptional regulation during development. This article mainly reviews and discusses the regulatory roles of GADD45α in skeletal muscle development, adipocyte progenitor differentiation, and DNA demethylation.

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Zhang, Zhe, Yu Meng, Fei Gao, Yue Xiao, Yi Zheng, Hao-Qi Wang, Yan Gao, Hao Jiang, Bao Yuan et Jia-Bao Zhang. « TGF-β1-Mediated FDNCR1 Regulates Porcine Preadipocyte Differentiation via the TGF-β Signaling Pathway ». Animals 10, n^o 8 (11 août 2020) : 1399. http://dx.doi.org/10.3390/ani10081399.

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Adipocyte differentiation and lipid metabolism have important regulatory effects on the quality of meat from livestock. A variety of transcription factors regulate preadipocyte differentiation. Several studies have revealed that transforming growth factor-beta (TGF-β1) may play a key role in epithelial–mesenchymal transition (EMT); however, little is known about the effects of TGF-β1 treatment on porcine preadipocytes. To explore the role of TGF-β1 in porcine adipocyte differentiation, porcine preadipocytes were treated with 10 ng/mL TGF-β1, and two libraries were constructed for RNA-seq. We chose an abundant and differentially expressed long noncoding RNA (lncRNA), which we named fat deposition-associated long noncoding RNA1 (FDNCR1), for further study. RT-qPCR was used to detect mRNA levels of genes related to adipocyte differentiation. Triglyceride assay kits were used to detect lipid droplet deposition. TGF-β1 significantly suppressed porcine preadipocyte differentiation. We identified 8158 lncRNAs in total and 39 differentially expressed lncRNAs. After transfection with FDNCR1 siRNA, the mRNA expression of aP2, C/EBPα, and PPARγ and triglyceride levels significantly increased. Transfection with FDNCR1 siRNA significantly decreased protein levels of p-Smad2/Smad2 and p-Smad3/Smad3. These results demonstrate that FDNCR1 suppresses porcine preadipocyte differentiation via the TGF-β signaling pathway.

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Liu, Ximing, Ying Bai, Ran Cui, Shuaihan He, Yao Ling, Changxin Wu et Meiying Fang. « Integrated Analysis of the ceRNA Network and M-7474 Function in Testosterone-Mediated Fat Deposition in Pigs ». Genes 13, n^o 4 (10 avril 2022) : 668. http://dx.doi.org/10.3390/genes13040668.

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Castration can significantly enhance fat deposition in pigs, and the molecular mechanism of fat deposition caused by castration and its influence on fat deposition in different parts of pigs remain unclear. RNA-seq was performed on adipose tissue from different parts of castrated and intact Yorkshire pigs. Different ceRNA networks were constructed for different fat parts. GO and KEGG pathway annotations suggested that testosterone elevates cell migration and affects differentiation and apoptosis in back fat, while it predisposes animals to glycolipid metabolism disorders and increases the expression of inflammatory cytokines in abdominal fat. The interaction between M-7474, novel_miR_243 and SGK1 was verified by dual fluorescence experiments. This ceRNA relationship has also been demonstrated in porcine preadipocytes. Overexpression of M-7474 significantly inhibited the differentiation of preadipocytes compared to the control group. When 100 nM testosterone was added during preadipocyte differentiation, the expression of M-7474 was increased, and preadipocyte differentiation was significantly inhibited. Testosterone can affect preadipocyte differentiation by upregulating the expression of M-7474, sponging novel-miR-243, and regulating the expression of genes such as SGK1. At the same time, HSD11B1 and SLC2A4 may also be regulated by the corresponding lncRNA and miRNA, which ultimately affects glucose uptake by adipocytes and leads to obesity.

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Zhang, Peiwen, Xinrong Li, Shunhua Zhang, Shuang Wu, Qian Xiao, Yang Gu, Xinyu Guo et al. « miR-370-3p Regulates Adipogenesis through Targeting Mknk1 ». Molecules 26, n^o 22 (17 novembre 2021) : 6926. http://dx.doi.org/10.3390/molecules26226926.

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Excessive fat accumulation can lead to obesity, diabetes, hyperlipidemia, atherosclerosis, and other diseases. MicroRNAs are a class of microRNAs that regulate gene expression and are highly conserved in function among species. microRNAs have been shown to act as regulatory factors to inhibit fat accumulation in the body. We found that miR-370-3p was expressed at lower levels in the fat mass of mice on a high-fat diet than in mice on a normal control diet. Furthermore, our data showed that the overexpression of miR-370-3p significantly suppressed the mRNA expression levels of adipogenic markers. Thus, miR-370-3p overexpression reduced lipid accumulation. Conversely, the inhibition of miR-370-3p suppressed 3T3-L1 preadipocyte proliferation and promoted preadipocyte differentiation. In addition, Mknk1, a target gene of miR-370-3p, plays an opposing role in preadipocyte proliferation and differentiation. Moreover, consistent results from in vitro as well as in vivo experiments suggest that the inhibition of fat accumulation by miR-370-3p may result from the inhibition of saturated fatty acids that promote the accumulation of polyunsaturated fatty acids. In conclusion, these results suggest that miR-370-3p plays an important role in adipogenesis and fatty acid metabolism through the regulation of Mknk1.

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Ambele, Melvin A., Priyanka Dhanraj, Rachel Giles et Michael S. Pepper. « Adipogenesis : A Complex Interplay of Multiple Molecular Determinants and Pathways ». International Journal of Molecular Sciences 21, n^o 12 (16 juin 2020) : 4283. http://dx.doi.org/10.3390/ijms21124283.

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The formation of adipocytes during embryogenesis has been largely understudied. However, preadipocytes appear to originate from multipotent mesenchymal stromal/stem cells which migrate from the mesoderm to their anatomical localization. Most studies on adipocyte formation (adipogenesis) have used preadipocytes derived from adult stem/stromal cells. Adipogenesis consists of two phases, namely commitment and terminal differentiation. This review discusses the role of signalling pathways, epigenetic modifiers, and transcription factors in preadipocyte commitment and differentiation into mature adipocytes, as well as limitations in our understanding of these processes. To date, a limited number of transcription factors, genes and signalling pathways have been described to regulate preadipocyte commitment. One reason could be that most studies on adipogenesis have used preadipocytes already committed to the adipogenic lineage, which are therefore not suitable for studying preadipocyte commitment. Conversely, over a dozen molecular players including transcription factors, genes, signalling pathways, epigenetic regulators, and microRNAs have been described to be involved in the differentiation of preadipocytes to adipocytes; however, only peroxisome proliferator-activated receptor gamma has proven to be clinically relevant. A detailed understanding of how the molecular players underpinning adipogenesis relate to adipose tissue function could provide new therapeutic approaches for addressing obesity without compromising adipose tissue function.

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Wang, Zhiming, Jin Chai, Yuhao Wang, Yiren Gu, Keren Long, Mingzhou Li et Long Jin. « LncPLAAT3-AS Regulates PLAAT3-Mediated Adipocyte Differentiation and Lipogenesis in Pigs through miR-503-5p ». Genes 14, n^o 1 (6 janvier 2023) : 161. http://dx.doi.org/10.3390/genes14010161.

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Animal fat deposition has a significant impact on meat flavor and texture. However, the molecular mechanisms of fat deposition are not well understood. LncPLAAT3-AS is a naturally occurring transcript that is abundant in porcine adipose tissue. Here, we focus on the regulatory role of lncPLAAT3-AS in promoting preadipocyte proliferation and adipocyte differentiation. By overexpressing or repressing lncPLAAT3 expression, we found that lncPLAAT3-AS promoted the transcription of its host gene PLAAT3, a regulator of adipocyte differentiation. In addition, we predicted the region of lncPLAAT3-AS that binds to miR-503-5p and showed by dual luciferase assay that lncPLAAT3-AS acts as a sponge to absorb miR-503-5p. Interestingly, miR-503-5p also targets and represses PLAAT3 expression and helps regulate porcine preadipocyte proliferation and differentiation. Taken together, these results show that lncPLAAT3-AS upregulates PLAAT3 expression by absorbing miR-503-5p, suggesting a potential regulatory mechanism based on competing endogenous RNAs. Finally, we explored lncPLAAT3-AS and PLAAT3 expression in adipose tissue and found that both molecules were expressed at significantly higher levels in fatty pig breeds compared to lean pig breeds. In summary, we identified the mechanism by which lncPLAAT3-AS regulates porcine preadipocyte proliferation and differentiation, contributing to our understanding of the molecular mechanisms of lipid deposition in pigs.

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Wright, J. T., et G. J. Hausman. « Flow cytometric analysis of porcine preadipocyte replication ». Journal of Animal Science 72, n^o 7 (1 juillet 1994) : 1712–18. http://dx.doi.org/10.2527/1994.7271712x.

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Cartwright, Mark J., Karen Schlauch, Marc E. Lenburg, Tamara Tchkonia, Tamar Pirtskhalava, Andrew Cartwright, Thomas Thomou et James L. Kirkland. « Aging, Depot Origin, and Preadipocyte Gene Expression ». Journals of Gerontology : Series A 65A, n^o 3 (27 janvier 2010) : 242–51. http://dx.doi.org/10.1093/gerona/glp213.

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Gupta, Rana K., Zoltan Arany, Patrick Seale, Rina J. Mepani, Li Ye, Heather M. Conroe, Yang A. Roby, Heather Kulaga, Randall R. Reed et Bruce M. Spiegelman. « Transcriptional control of preadipocyte determination by Zfp423 ». Nature 464, n^o 7288 (mars 2010) : 619–23. http://dx.doi.org/10.1038/nature08816.

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Lansdown, Andrew, Marian Ludgate et Aled Rees. « Metabolic syndrome : is the preadipocyte to blame?* ». Clinical Endocrinology 76, n^o 1 (7 décembre 2011) : 19–20. http://dx.doi.org/10.1111/j.1365-2265.2011.04176.x.

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Hasan, Arif U., Koji Ohmori, Takeshi Hashimoto, Kazuyo Kamitori, Yuko Hirata, Yasuhiro Ishihara, Naoko Okamoto et al. « Pioglitazone promotes preadipocyte proliferation by downregulating p16Ink4a ». Biochemical and Biophysical Research Communications 411, n^o 2 (juillet 2011) : 375–80. http://dx.doi.org/10.1016/j.bbrc.2011.06.152.

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