Climbing exercise enhances osteoblast differentiation and inhibits adipogenic differentiation with high expression of PTH/PTHrP receptor in bone marrow cells
Kunitaka MenukiToshiharu MoriAkinori SakaiMiyuki SakumaNobukazu OkimotoYuki ShimizuNaoki KunugitaToshitaka Nakamura
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To clarify the function of miR-103 in the differentiation of porcine preadipocyte, we carried out real-time PCR to detect the expression pattern of miR-103 during adipogenesis, and clarified its expression tendency through cell differentiation. Then we used adenovirus that overexpressed miR-103 to infect porcine preadipocyte. Subsequently, mRNA and protein expression of adipogenesis marker--PPARgamma and aP2 was analyzed by real-time PCR and Western blotting. At last, Oil-Red O staining was used to detect lipids accumulation in the 8th day after adipogenic inducement. The expression of miR-103 increased during adipocyte differentiation; compared with the control, the preadipocyte infected by pAd-miR-103 had an elevated expression level of adipocyte marker gene PPARgamma, aP2, and obvious lipid droplet was seen in the 8th day after adipogenic inducement. These results showed that miR-103 can enhance adipogenesis in primary cultured porcine adipocytes.
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Sestrin-3, together with the other two members Sestrin-1 and Sestrin-2, belongs to the Sestrin family. The Sestrin protein family has been demonstrated to be involved in antioxidative, metabolic homeostasis, and even the development of nonalcoholic steatohepatitis (NASH). However, the adipogenic regulatory role of SESN3 in adipogenesis still needs to be further explored. In this study, we demonstrated SESN3 inhibited porcine pre-adipocyte proliferation, thus suppressing its adipogenesis. Meanwhile, SESN3 has been demonstrated to inhibit Smad3 thus protecting against NASH. Further, for our previous study, we found mmu-miR-124 involved in 3T3-L1 cell adipogenesis regulation. In this study, we also identified that ssc-miR-124 inhibited porcine pre-adipocyte proliferation, thus suppressing its adipogenesis, and the SMAD3 was an inhibitor of ssc-miR-124 by binding to its promoter. Furthermore, the ssc-miR-124 targeted porcine C/EBPα and GR and thus inhibited pre-adipocyte adipogenesis. In conclusion, SESN3 inhibited SMAD3, thus improving ssc-miR124, and then suppressed C/EBPα and GR to regulate pre-adipocytes adipogenesis.
Nonalcoholic steatohepatitis
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Over the last several years, the increasing prevalence of obesity has favored an intense study of adipose tissue biology and the precise mechanisms involved in adipocyte differentiation and adipogenesis. Adipocyte commitment and differentiation are complex processes, which can be investigated thanks to the development of diverse in vitro cell models and molecular biology techniques that allow for a better understanding of adipogenesis and adipocyte dysfunction associated with obesity. The aim of the present work was to update the different animal and human cell culture models available for studying the in vitro adipogenic differentiation process related to obesity and its co-morbidities. The main characteristics, new protocols, and applications of the cell models used to study the adipogenesis in the last five years have been extensively revised. Moreover, we depict co-cultures and three-dimensional cultures, given their utility to understand the connections between adipocytes and their surrounding cells in adipose tissue.
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糖尿病和许多另外的新陈代谢症候群是仔细与肥胖有关。揭示胖免职的内在的机制，越来越多的研究在 adipocytes 开发期间正在集中于 miRNAs 的功能。以前的研究 haveproved 那出 miR-15a/b 戏在多重生理的过程的重要角色；然而，他们的功能在 adipogenesisremain 期间不清楚。揭示这，我们在猪的 pre-adipocyte 在 adipogenesis 期间检测了 miR-15a/b 的表示侧面，并且发现那他们层次在 adipocyte 区别的早阶段增加了并且在白天 4 .Moreover 以后落下的表示，在猪的 pre-adipocytes 的 miR-15a/b 的在表示上支持了 adipocyte 区别， miR-15a/b 的类脂化合物 accumulation.Target 基因被预言并且检验，它表明 Forkhead 盒子蛋白质 O1 ( FoxO1 )是目标 geneof miR-15a/b 。表示水平由 miR-15a/b 在表示上引起了的 FoxO1 的抑制在 adipogenesis.Thus 上有积极效果，我们断定 miR-15a/b 经由镇压在猪的 pre-adipocyte 支持 adipogenesis FoxO1。
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Substantial levels of lysozyme in adipose tissue in association to obesity have been recently demonstrated in mice and humans. In addition, experiments in mice suggest that lysozyme might impact on adipose tissue adipogenesis. To further investigate the relationship between lysozyme and adipogenesis, in the present study, we aimed to study lysozyme (Lyz2) during 3T3-L1 adipocyte differentiation and its possible role in adipogenesis. Time course experiment during 3T3-L1 adipocyte differentiation indicated that Lyz2 gene expression decreased at day 4, which was caused by isobutylmethylxanthine administration, and recovered at the end of the process (day 8). Importantly, the impact of isobutylmethylxanthine-induced downregulation of Lyz2 gene expression on adipogenesis was not comparable to that observed in the full cocktail, questioning whether the reduction in lysozyme at early stage of adipocyte differentiation is relevant to this process. In fact, the depletion in Lyz2 expression had a negative impact on adipogenesis, and rosiglitazone administration failed to compensate for the anti-adipogenic effect observed in Lyz2 gene knockdown cells. Otherwise, when Lyz2 gene knockdown cells were co-cultured with control cells, these cells had higher expression of adipogenic genes than those co-cultured with themselves at the end of adipocyte differentiation. In conclusion, this study suggests that lysozyme expression in 3T3-L1 cells sustains expression of adipogenic genes and adipocyte differentiation.
3T3-L1
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Obesity and associated metabolic complications, including diabetes, cardiovascular and hepatic diseases, and certain types of cancers, create a major socioeconomic burden. Obesity is characterized by excessive expansion of white adipose tissue resulting from increased adipocyte size, and enhanced adipocyte precursor cells proliferation and differentiation into mature adipocytes, a process well-defined as adipogenesis. Efforts to develop therapeutically potent strategies to circumvent obesity are impacted by our limited understanding of molecular mechanisms regulating adipogenesis. In this review, we discuss recently discovered molecular mechanisms restraining adipogenesis. In this perspective, the discoveries of white adipose tissue endogenous adipogenesis-regulatory cells (Aregs) that negatively regulate adipocyte differentiation, platelet-derived growth factor receptor isoform α (PDGFRα) activation and downstream signaling that hinder adipocyte precursors differentiation, and a group of obesity-associated non-coding RNAs (ncRNAs) that regulate adipogenesis open up promising therapeutic avenues to prevent and/or treat obesity.
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Abstract The number of adipocytes is relevant to the extent of differentiation from pluripotent stem cells into pre‐adipocytes, whereas the size of adipocytes relates to the extent of differentiation from pre‐adipocytes into mature fat cells and the accumulation of triglyceride. Investigation of the molecular regulatory mechanism of adipocyte differentiation is not only essential for understanding the physiological processes of adipogenesis, but it is also important for identifying new biomarkers and therapeutic targets for some metabolic diseases, such as obesity and diabetes. microRNAs (miRNAs) appear to play important roles in adipocyte differentiation. During adipogenesis, miRNAs can accelerate or inhibit adipocyte differentiation by acting on transcription factors, regulating signalling pathways related to adipogenesis, or blocking the mitotic clonal expansion stage, thus regulating adipocyte development. The regulatory role of some miRNAs varies in different species or different cells. In this review, the biological characteristics of miRNA and the adipocyte differentiation process are concisely discussed. Recent advances in our understanding of the role of miRNAs in adipocytes development or adipogenesis are discussed.
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