Adipocyte最新文献

{"title":"Associations of <i>GHR, IGF-1</i> and <i>IGFBP-3</i> expression in adipose tissue cells with obesity-related alterations in corresponding circulating levels and adipose tissue function in children.","authors":"Elena Kempf,&nbsp;Kathrin Landgraf,&nbsp;Tim Vogel,&nbsp;Ulrike Spielau,&nbsp;Robert Stein,&nbsp;Matthias Raschpichler,&nbsp;Jürgen Kratzsch,&nbsp;Wieland Kiess,&nbsp;Juraj Stanik,&nbsp;Antje Körner","doi":"10.1080/21623945.2022.2148886","DOIUrl":"https://doi.org/10.1080/21623945.2022.2148886","url":null,"abstract":"<p><p>Components of the growth hormone (GH) axis, such as insulin-like growth factor-1 (IGF-1), IGF-1 binding protein-3 (IGFBP-3), GH receptor (GHR) and GH-binding protein (GHBP), regulate growth and metabolic pathways. Here, we asked if serum levels of these factors are altered with overweight/obesity and if this is related to adipose tissue (AT) expression and/or increased fat mass. Furthermore, we hypothesized that expression of <i>GHR, IGF-1</i> and <i>IGFBP-3</i> is associated with AT function. Serum GHBP levels were increased in children with overweight/obesity throughout childhood, while for IGF-1 levels and the IGF-1/IGFBP-3 molar ratio obesity-related elevations were detectable until early puberty. Circulating levels did not correlate with AT expression of these factors, which was decreased with overweight/obesity. Independent from obesity, expression of <i>GHR, IGF-1</i> and <i>IGFBP-3</i> was related to AT dysfunction,and increased insulin levels. Serum GHBP was associated with liver fat percentage and transaminase levels. We conclude that obesity-related elevations in serum GHBP and IGF-1 are unlikely to be caused by increased AT mass and elevations in GHBP are more closely related to liver status in children. The diminished AT expression of these factors with childhood obesity may contribute to early AT dysfunction and a deterioration of the metabolic state.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"11 1","pages":"630-642"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9683049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10618079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasminogen-derived peptide promotes adipogenic differentiation of preadipocytes <i>in vitro</i> and <i>in vivo</i>.","authors":"Hea Jung Yang,&nbsp;Jong-Ho Kim,&nbsp;Jung Hee Shim,&nbsp;Chan Yeong Heo","doi":"10.1080/21623945.2022.2149121","DOIUrl":"https://doi.org/10.1080/21623945.2022.2149121","url":null,"abstract":"<p><p>Soft tissue defects caused by adipose tissue loss can result in various conditions such as lipodystrophy in congenital diseases, trauma secondary to ageing, and mastectomy in breast cancer; fat grafting is commonly performed to restore these defects. Although various enrichment strategies have been studied, novel therapeutics that are cost-effective, safe, technologically easy to manufacture, and minimally invasive are required. In this study, we identified a novel peptide derived from plasminogen, named plasminogen-derived peptide-1 (PLP-1), which showed adipogenic differentiation potential and led to an increase in the expression levels of adiponectin, C1Q and collagen domain containing protein, fatty acid-binding protein 4, and CCAAT/enhancer-binding protein-alpha. <i>In vivo</i> experiments confirmed an increase in the rate of adipocyte differentiation and the expression levels of CD31 in the PLP-1-treated mice groups. These results suggested that PLP-1 plays an important role in promoting the differentiation of preadipocytes and may be useful for developing therapeutic approaches to treat adipose tissue defects.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"11 1","pages":"643-652"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0a/d2/KADI_11_2149121.PMC9718552.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10680029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial transformation occurs in cultured adipocytes, but fails to increase adipose tissue metabolic activity in mice in vivo.","authors":"Lucia Balazova,&nbsp;Natalia Palesova,&nbsp;Miroslav Balaz","doi":"10.1080/21623945.2022.2107178","DOIUrl":"https://doi.org/10.1080/21623945.2022.2107178","url":null,"abstract":"<p><p>A large number of studies in recent years have aimed to devise novel therapeutic strategies to increase adipose tissue metabolic activity and fight the global obesity epidemics. Growing evidence suggests that cells are able to accept isolated mitochondria by a simple coincubation in a process known as mitochondrial transformation. Therefore, we aimed to test whether mitochondrial transformation occurs in mature adipocytes, and whether this phenomenon could be utilized as a therapeutic approach to increase adipose tissue mitochondrial content and improve metabolic control. We provide evidence that both brown and white adipocytes are able to rapidly accept a large amount of brown adipocyte-derived mitochondria, which remain functional for several days and significantly contribute to cellular respiration <i>in vitro</i>. However, we did not find any evidence that internalization of exogenous mitochondria would trigger transcriptional changes in the recipient cells. Moreover, injection of a large amount of brown adipocyte-derived mitochondria into the inguinal fat of C57BL/6 mice failed to increase whole-body energy expenditure, and reduce body weight gain under obesogenic conditions. This might be due to activation of immune response and rapid removal of administered mitochondria. Altogether, our study adds information on the usability of mitochondrial transformation in the treatment of metabolic disease.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":" ","pages":"463-476"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9367671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40593708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insulin prevents fatty acid induced increase of adipocyte size.","authors":"Emmanuelle Berger,&nbsp;Alain Géloën","doi":"10.1080/21623945.2022.2107784","DOIUrl":"https://doi.org/10.1080/21623945.2022.2107784","url":null,"abstract":"<p><p>Metabolic disorders related to obesity are largely dependent on adipose tissue hypertrophy, which involves adipocyte hypertrophy and increased adipogenesis. Adiposize is regulated by lipid accumulation as a result of increased lipogenesis (mainly lipid uptake in mature adipocytes) and reduced lipolysis. Using realtime 2D cell culture analyses of lipid uptake, we show (1) that high glucose concentration (4.5 g/L) was required to accumulate oleic acid increasing lipid droplet size until unilocularization similar to mature adipocytes in few days, (2) oleic acid reduced <i>Peroxisome-Proliferator Activated Receptor Gamma</i> (<i>PPARG)</i> gene transcription and (3) insulin counteracted oleic acid-induced increase of lipid droplet size. Although the lipolytic activity observed in high <i>versus</i> low glucose (1 g/L) conditions was not altered, insulin was found to inhibit oleic acid induced gene transcription required for lipid storage such as Cell Death Inducing DFFA Like Effectors (CIDEC) and <i>G0S2 (</i>G0 switch gene S2), possibly through PPARA activity. Although this signalling pathway requires more detailed investigation, the results point out the differential mechanisms involved in the pro-adipogenic effect of insulin in absence <i>versus</i> its protective effect on adiposity in presence of oleic acid uptake.<b>Abbreviations</b>: AICAR, 5-Aminoimidazole-4-carboxamide-1-D-ribofuranoside; AMPK, AMP-Activated protein kinase, ASCs, adipose stem cell; ATGL, adipose triglyceride lipase; BSA, Bovine serum albumin; CEBPA, CCAAT enhancer binding protein alpha; CIDEs, Cell Death Inducing DFFA Like Effectors; dA, differentiated adipocyte; DMEM, Dulbecco's Modified Eagle's Medium; FABPs, Fatty Acid Binding Proteins; FAT/CD36, Fatty acid translocase; FCS, Foetal calf serum; FN1, fibronectin 1; FFA, free fatty acid; G0S2, G0 switch gene S2; GLUTs, Glucose transporters; GPR120, G protein-coupled receptor 120; HG, high glucose; HSL, hormone sensitive lipase; INSR, insulin receptor; LG, low glucose; OA, oleic acid; PBS, Phosphate buffer saline; PPARs, Peroxisome-Proliferator Activated Receptors; PKA, Protein kinase cyclic AMP-dependent; PKG, Protein kinase cyclic GMP dependent; PTGS2, cytochrome oxidase 2; RTCA, realtime cell analysis; TG, triglyceride.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":" ","pages":"510-528"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9450899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40682252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SPRY4 promotes adipogenic differentiation of human mesenchymal stem cells through the MEK-ERK1/2 signaling pathway.","authors":"Na Li,&nbsp;Yunfei Chen,&nbsp;Haiyan Wang,&nbsp;Jing Li,&nbsp;Robert Chunhua Zhao","doi":"10.1080/21623945.2022.2123097","DOIUrl":"https://doi.org/10.1080/21623945.2022.2123097","url":null,"abstract":"<p><p>Obesity is a chronic metabolic disorder characterized by the accumulation of excess fat in the body. Preventing and controlling obesity by inhibiting the adipogenic differentiation of mesenchymal stem cells (MSCs) and thereby avoiding the increase of white adipose tissue is safe and effective. Recent studies have demonstrated that Sprouty proteins (SPRYs) are involved in cell differentiation and related diseases. However, the role and mechanism of SPRY4 in MSC adipogenic differentiation remain to be explored. Here, we found that SPRY4 positively correlates with the adipogenic differentiation of human adipose-derived MSCs (hAMSCs). Via gain- and loss-of-function experiments, we demonstrated that SPRY4 promotes hAMSC adipogenesis both in vitro and in vivo. Mechanistically, SPRY4 functioned by activating the MEK-ERK1/2 pathway. Our findings provide new insights into a critical role for SPRY4 as a regulator of adipogenic differentiation, which may illuminate the underlying mechanisms of obesity and suggest the potential of SPRY4 as a novel treatment option.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"11 1","pages":"588-600"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9481072/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10617640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generation of functional fat organoid from rat superficial fascia.","authors":"Yanfei Zhang,&nbsp;Yuanyuan Zhang,&nbsp;Yingyue Dong,&nbsp;Tongsheng Chen,&nbsp;Guoheng Xu","doi":"10.1080/21623945.2022.2072446","DOIUrl":"https://doi.org/10.1080/21623945.2022.2072446","url":null,"abstract":"<p><p>The organoid is a 3D cell architecture formed by self-organized tissues or cells in vitro with similar cell types, histological structures, and biological functions of the native organ. Depending on the unique organ structures and cell types, producing organoids requires individualized design and is still challenging. Organoids of some tissues, including adipose tissue, remain to generate to be more faithful to their original organ in structure and function. We previously established a new model of the origin of adipose cells originating from non-adipose fascia tissue. Here, we investigated superficial fascia fragments in 3D hydrogel and found they were able to transform into relatively large adipocyte aggregates containing mature unilocular adipocytes, which were virtually \"fat organoids\". Such fascia-originated fat organoids had a typical structure of adipose tissues and possessed the principal function of adipose cells in the synthesis, storage, hydrolysis of triglycerides and adipokines secretion. Producing fat organoids from superficial fascia can provide a new approach for adipocyte research and strongly evidences that both adipose tissues and cells originate from fascia. Our findings give insights into metabolic regulation by the crosstalk between different organs and tissues and provide new knowledge for investigating novel treatments for obesity, diabetes and other metabolic diseases.<b>Abbreviations</b>: 3D: three dimensional; ASC: adipose-derived stromal cells; C/EBP: CCAAT-enhancer-binding protein; EdU: 5-ethynyl-2-deoxyuridine; FABP4: fatty acid-binding protein 4; FAS: fatty acid synthase; FSCs: fascia-derived stromal cells; Plin1: perilipin-1; Plin2: perilipin-2; PPARγ: peroxisome proliferator-activated receptor γ; WAT: white adipose tissue.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"11 1","pages":"287-300"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9116422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10347455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Straightforward Method for Adipocyte Size and Count Analysis Using Open-source Software QuPath.","authors":"Ville A Palomäki,&nbsp;Vesa Koivukangas,&nbsp;Sanna Meriläinen,&nbsp;Petri Lehenkari,&nbsp;Tuomo J Karttunen","doi":"10.1080/21623945.2022.2027610","DOIUrl":"https://doi.org/10.1080/21623945.2022.2027610","url":null,"abstract":"<p><p>Changes in adipose tissue morphology, depicted by cell morphology alterations such as enlargement of fat cells, always accompany over-weight and obesity. The variables related to cell size have been shown to associate with low-grade inflammation of adipose tissue and common obesity-related comorbidities including metabolic syndrome and type 2 diabetes. Quantifying fat cell morphology from images of histological specimens can be tedious. Here, we present a straightforward method for the task using the free open-source software QuPath with its inbuilt tools only. Measurements of human adipose tissue samples with the described protocol showed an excellent correlation with those obtained with ImageJ software with Adipocyte Tools plugin combined with manual correction of misdetections. Intraclass correlation between the two methods was at good to excellent level. The method described here can be applied to considerably large tissue areas, even whole-slide analysis.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":" ","pages":"99-107"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8803053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39748355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adipose tissue plays a major role in retinoic acid-mediated metabolic homoeostasis.","authors":"Shenglong Zhu,&nbsp;Jingwei Zhang,&nbsp;Doudou Zhu,&nbsp;Xuan Jiang,&nbsp;Lengyun Wei,&nbsp;Wei Wang,&nbsp;Yong Q Chen","doi":"10.1080/21623945.2021.2015864","DOIUrl":"https://doi.org/10.1080/21623945.2021.2015864","url":null,"abstract":"<p><p>Retinoic acid (RA), a bioactive metabolite of vitamin A, has shown therapeutic effects in liver disease, and its effect in improving non-alcoholic fatty liver disease (NAFLD) is associated with the inhibition of adipogenesis in the white adipose tissue (WAT) and fatty acid oxidation induction in the liver. However, the major target organ of RA is unknown. We performed chronic administration of RA in high-fat diet (HFD)-induced NAFLD mice. Further, hepatic and adipose cells were used to study the direct effect of RA on lipid metabolism. In addition, qRT-PCR was performed to examine differential gene expression in mouse adipose tissue. RA administration ameliorated NAFLD in HFD-induced obese mice and increased mouse energy expenditure. Although RA had therapeutic effects on liver histology and lipid accumulation, it did not directly affect lipid metabolism in HepG2 cells. In contrast, RA reduced the weight of several adipose tissues and improved lipid accumulation in OP9 cells. In addition, RA upregulated genes responsible for fatty acid oxidation and thermogenesis in three different WATs. Our work suggests that the liver may not be the main target organ of RA during NAFLD treatment. WAT browning induced by RA may be the primary contributor towards the amelioration of NAFLD in HFD-induced obese mice.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":" ","pages":"47-55"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8726720/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39766953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"S1P/S1PR3 signalling axis protects against obesity-induced metabolic dysfunction.","authors":"Sagarika Chakrabarty,&nbsp;Quyen Bui,&nbsp;Leylla Badeanlou,&nbsp;Kelly Hester,&nbsp;Jerold Chun,&nbsp;Wolfram Ruf,&nbsp;Theodore P Ciaraldi,&nbsp;Fahumiya Samad","doi":"10.1080/21623945.2021.2021700","DOIUrl":"https://doi.org/10.1080/21623945.2021.2021700","url":null,"abstract":"<p><p>Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid that interacts via 5 G-protein coupled receptors, S1PR1-5, to regulate signalling pathways critical to biological processes including cell growth, immune cell trafficking, and inflammation.We demonstrate that in Type 2 diabetic (T2D) subjects, plasma S1P levels significantly increased in response to the anti-diabetic drug, rosiglitazone, and, S1P levels correlated positively with measures of improved glucose homeostasis. In HFD-induced obese C57BL/6 J mice S1PR3 gene expression was increased in adipose tissues (AT) and liver compared with low fat diet (LFD)-fed counterparts. On a HFD, weight gain was similar in both S1PR3-/- mice and WT littermates; however, HFD-fed S1PR3-/- mice exhibited a phenotype of partial lipodystrophy, exacerbated insulin resistance and glucose intolerance. This worsened metabolic phenotype of HFD-fed S1PR3-/- mice was mechanistically linked with increased adipose inflammation, adipose macrophage and T-cell accumulation, hepatic inflammation and hepatic steatosis. In 3T3-L1 preadipocytes S1P increased adipogenesis and S1P-S1PR3 signalling regulated the expression of PPARγ, suggesting a novel role for this signalling pathway in the adipogenic program. These results reveal an anti-diabetic role for S1P, and, that S1P-S1PR3 signalling in the adipose and liver defends against excessive inflammation and steatosis to maintain metabolic homeostasis at key regulatory pathways.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":" ","pages":"69-83"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8803104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39870988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulatory network of metformin on adipogenesis determined by combining high-throughput sequencing and GEO database.","authors":"Zhicong Zhao,&nbsp;Chenxi Wang,&nbsp;Jue Jia,&nbsp;Zhaoxiang Wang,&nbsp;Lian Li,&nbsp;Xia Deng,&nbsp;Zhensheng Cai,&nbsp;Ling Yang,&nbsp;Dong Wang,&nbsp;Suxian Ma,&nbsp;Li Zhao,&nbsp;Zhigang Tu,&nbsp;Guoyue Yuan","doi":"10.1080/21623945.2021.2013417","DOIUrl":"https://doi.org/10.1080/21623945.2021.2013417","url":null,"abstract":"<p><p>Adipose differentiation and excessive lipid accumulation are the important characteristics of obesity. Metformin, as a classic hypoglycaemic drug, has been proved to reduce body weight in type 2 diabetes, the specific mechanism has not been completely clear. A few studies have explored its effect on adipogenesis in vitro, but the existing experimental results are ambiguous. 3T3-L1 preadipocytes were used to explore the effects of metformin on the morphological and physiological changes of lipid droplets during adipogenesis. A high throughput sequencing was used to examine the effects of metformin on the transcriptome of adipogenesis. Considering the inevitable errors among independent experiments, we performed integrated bioinformatics analysis to identify important genes involved in adipogenesis and reveal potential molecular mechanisms. During the process of adipogenesis, metformin visibly relieved the morphological and functional changes. In addition, metformin reverses the expression pattern of genes related to adipogenesis at the transcriptome level. Combining with integrated bioinformatics analyses to further identify the potential targeted genes regulated by metformin during adipogenesis. The present study identified novel changes in the transcriptome of metformin in the process of adipogenesis that might shed light on the underlying mechanism by which metformin impedes the progression of obesity.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":" ","pages":"56-68"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8741290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39639448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}