Adipocyte最新文献

{"title":"Bioinformatics analysis of candidate genes and potential therapeutic drugs targeting adipose tissue in obesity.","authors":"Yun Yu,&nbsp;Yu-Han Zhang,&nbsp;Liang Liu,&nbsp;Ling-Ling Yu,&nbsp;Jun-Pei Li,&nbsp;Jing-An Rao,&nbsp;Feng Hu,&nbsp;Ling-Juan Zhu,&nbsp;Hui-Hui Bao,&nbsp;Xiao-Shu Cheng","doi":"10.1080/21623945.2021.2013406","DOIUrl":"https://doi.org/10.1080/21623945.2021.2013406","url":null,"abstract":"<p><p>Obesity is a complex medical condition that affects multiple organs in the body. However, the underlying <i>mechanisms</i> of obesity, as well as its treatment, <i>are largely unexplored</i>. The focus of this research was to use bioinformatics to discover possible treatment targets for obesity. To begin, the GSE133099 database was used to identify 364 differentially expressed genes (DEGs). Then, DEGs were subjected to tissue-specific analyses and enrichment analyses, followed by the creation of a protein-protein interaction (PPI) network and generation of a drug-gene interaction database to screen key genes and potential future drugs targeting obesity. Findings have illustrated that the tissue-specific expression of neurologic markers varied significantly (34.7%, 52/150). Among these genes, Lep, ApoE, Fyn, and FN1 were the key genes observed in the adipocyte samples from obese patients relative to the controls. Furthermore, nine potential therapeutic drugs (dasatinib, ocriplasmin, risperidone, gemfibrozil, ritonavir, fluvastatin, pravastatin, warfarin, atorvastatin) that target the key genes were also screened and selected. To conclude the key genes discovered (Lep, ApoE, Fyn, and FN1), as well as 9 candidate drugs, could be used as therapeutic targets in treating obesity.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":" ","pages":"1-10"},"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/c4/ea/KADI_11_2013406.PMC8726706.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39770386","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":"Cancer cell-derived exosomal miR-425-3p induces white adipocyte atrophy.","authors":"Anwen Liu,&nbsp;Wenxia Pan,&nbsp;Shutong Zhuang,&nbsp;Yuanzhi Tang,&nbsp;Haitao Zhang","doi":"10.1080/21623945.2022.2108558","DOIUrl":"https://doi.org/10.1080/21623945.2022.2108558","url":null,"abstract":"<p><p>White adipose tissue wasting plays a critical role in the development and progression of cancer cachexia. However, the mechanism behind the loss of adipose tissue remains ill-defined. In this study, we found that cancer cell-derived exosomes highly expressed miR-425-3p. Administration of cancer cell-derived exosomes significantly inhibited proliferation and differentiation of human preadipocytes-viscereal (HPA-v) cells. In mature adipocytes, cancer cell-derived exosomes activated cAMP/PKA signalling and lipophagy, leading to adipocyte lipolysis and browning of white adipocytes. These exosomes-induced alterations were almost abolished by endocytosis inhibitor cytochalasin D (CytoD) and antagomiR-425-3p, or reproduced by miR-425-3p mimics. In addition, bioinformatics analysis and luciferase reporter assay revealed that miR-425-3p directly targeted proliferation-related genes such as <i>GATA2, IGFBP4, MMP15</i>, differentiation-related gene <i>CEBPA</i>, and phosphodiesterase 4B gene (<i>PDE4B</i>). Depletion of PDE4B enhanced cAMP/PKA signalling and lipophagy, but had no effects on HPA-v proliferation and differentiation. Taken together, these results suggested that cancer cell-derived exosomal miR-425-3p inhibited preadipocyte proliferation and differentiation, increased adipocyte lipolysis, and promoted browning of white adipocytes, all of which might contribute to adipocyte atrophy and ultimately the loss of adipose tissue in cancer cachexia.<b>Abbreviations:</b> ADPN: adiponectin; aP2: adipocyte protein 2 or fatty acid binding protein 4 (FABP4); BCA: bicinchoninic acid assay; BFA: bafilomycin A1; BMI: body mass index; C/EBP: CCAAT/enhancer binding protein; CEBPA: CCAAT/enhancer-binding protein-alpha; C-Exo: cancer cell-derived exosomes; CNTL: control; CREB: cAMP-response element binding protein; CytoD: cytochalasin D; ECL: chemiluminescence; GATA2: GATA Binding Protein 2; HFD: high fat diet; HSL: hormone-sensitive lipase; IGFBP4: insulin like growth factor binding protein 4; IRS-1: insulin receptor substrate-1; ISO: isoproterenol hydrochloride; KD: knockdown; KO: knock out; LC3: microtubule-associated protein 1A/1B-light chain 3; LMF: lipid mobilizing factor; LPL: lipoprotein lipase; MMP15: matrix metallopeptidase 15; Mir-Inh-C-Exo: cancer cell-derived exosomes with miR-425-3p inhibition; mTOR: mammalian target of rapamycin; Mut: mutant; N-Exo: normal cell-derived exosomes; NSCLC: non-small cell lung cancer; PBS, phosphate buffered saline; PGC-1: peroxisome proliferator-activated receptor-gamma coactivator-1; PDEs: phosphodiesterases; PKI: PKA inhibitor; PKA: cAMP-dependent protein kinase; PLIN1: Perilipin 1; PTHRP: parathyroid hormone-related protein; PVDF: polyvinylidene difluoride; shRNA: short hairpin RNA; UCP1: uncoupling protein 1; WT: wild type.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":" ","pages":"487-500"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9367658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40611171","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":"PARP12 is required for mitochondrial function maintenance in thermogenic adipocytes.","authors":"Fan Hu,&nbsp;Chang Li,&nbsp;Yafen Ye,&nbsp;Xuhong Lu,&nbsp;Miriayi Alimujiang,&nbsp;Ningning Bai,&nbsp;Jingjing Sun,&nbsp;Xiaojing Ma,&nbsp;Xiaohua Li,&nbsp;Ying Yang","doi":"10.1080/21623945.2022.2091206","DOIUrl":"https://doi.org/10.1080/21623945.2022.2091206","url":null,"abstract":"<p><p>PARP12 is a member of poly-ADP-ribosyl polymerase (PARPs), which has been characterized for its antiviral function. Yet its physiological implication in adipocytes remains unknown. Here, we report a central function of PARP12 in thermogenic adipocytes. We show that PARP12 is highly expressed in brown adipose tissue and is mainly localized to the mitochondria. Knockdown of PARP12 in vitro reduced UCP1 expression. In parallel, the deficiency of PARP12 reduced mitochondrial respiration in adipocytes, while overexpression of PARP12 reversed these effects.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":" ","pages":"379-388"},"PeriodicalIF":3.3,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9351573/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40675288","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":"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}