Journal articles: 'Adipokin'

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ÇELİK, Menşure Nur, and Mehtap ÜNLÜ SÖĞÜT. "GÜNCEL BİR ADİPOKİN: CHEMERİN." Kocatepe Tıp Dergisi 20, no. 2 (April 29, 2019): 98–104. http://dx.doi.org/10.18229/kocatepetip.557987.

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Legiran, Legiran. "Obesitas dan pengeroposan tulang, Bagaimana hubungannya?" Jurnal Kedokteran dan Kesehatan : Publikasi Ilmiah Fakultas Kedokteran Universitas Sriwijaya 5, no. 2 (April 22, 2018): 66–71. http://dx.doi.org/10.32539/jkk.v5i2.6127.

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Latar Belakang: Penelitian tentang hubungan obesitas dan pengeroposan tulang telah banyak dilakukan dan secara epidemiologik menunjukkan obesitas berhubungan dengan peningkatan massa tulang. Penelitian lainnya menemukan bahwa obesitas menjadi faktor risiko terjadinya osteoporosis. Berat badan lebih dianggap sebagai faktor protektif bagi terjadinya proses pengeroposan tulang terutama pada wanita pascamenopause akibat dipertahankannya kadar estrogen selama masa menopause. Bagaimana hubungan obesitas dalam menghambat terjadinya proses pengeroposan tulang?Tujuan: Mendiskusikan hubungan obesitas sebagai faktor protektif proses pengeroposan tulang.Isi: Tulang sebagai bagian dari rangka tubuh manusia memiliki fungsi utama sebagai kerangka yang keras untuk mendukung, melindungi, dan memudahkan fungsi jaringan lunak. Jika ukuran rangka semua orang sama berapapun berat badannya, pasti beberapa tulang akan kesulitan memenuhi tugasnya dan akan tidak menguntungkan jika rangka yang ada secara signifikan lebih berat dari kebutuhannya. Pada individu yang gemuk maka dibutuhkan rangka yang lebih kuat dibanding kurus. Ini secara sederhana ingin menyebutkan bahwa gemuk memiliki hubungan dengan rangka. Penelitian membuktikan bahwa obesitas berhubungan dengan peningkatan kadar adipokin-adipokin seperti leptin, adinopektin, visfatin, resistin, apelin, dan lainnya yang dapat berpengaruh terhadap makronutrien metabolisme dan selanjutnya adipokin-adipokin tersebut mungkin saja berinteraksi dengan modulator energy jangka panjang seperti insulin. Hal ini masih belum bisa diungkap hubungan erat antara obesitas, hormon-hormon yang dipengaruhinya, dan efek fisiologi yang ditimbulkan. Obesitas dapat menguntungkan bagi kesehatan tulang karena efek mekanik dari berat badan pada pembentukan tulang karena obesitas berkaitan dengan inflamasi kronik dimana terjadi peningkatan sitokin proinflamasi di jaringan dan sirkulasi yang dapat meningkatkan aktivitas osteoklas dan resorpsi tulang melalui modifikasi receptor activator nuclear kappa B, RANK Ligand, dan Osteoprotegerin (RANK/RANKL/OPG) pathway. Obesitas juga dapat menjadi sebuah mekanisme patofisiologi berupa efek metabolic toksik asam lemak bebas dan adipokin yang berpengaruh pada metabolisme tulang.Kesimpulan: Obesitas mungkin berhubungan dengan penghambatan proses pengeroposan tulang dan sebaliknya obesitas mungkin juga menjadi faktor yang menyebabkan pengeroposan tulang. Nyatanya proses pengeroposan tulang sangat dipengaruhi baik oleh faktor genetik dan faktor lingkungan.

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Pasierb, Anna, Radosław Pietrzak, Paweł Rykowski, Zbigniew Bartoszewicz, Małgorzata Stakun, Lidia Rudnicka, and Joanna Czuwara. "Serum concentrations of adipokines in psoriasis and cardiometabolic risk." Dermatology Review 106, no. 1 (2019): 16–24. http://dx.doi.org/10.5114/dr.2019.83441.

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Dorofeeva, N. P., A. O. Ter-Akopyan, Yu N. Оrekhova, D. N. Ivanchenko, S. V. Shlyk, O. G. Mashtalova, I. E. Kulikova, S. A. Chibineva, F. V. Sklyarov, and А. S. Pleskachev. "Adipokine status in patients with stable ischemic heart disease associated with affective disorders." Journal of Clinical Practice 9, no. 3 (December 10, 2018): 54–59. http://dx.doi.org/10.17816/clinpract09354-59.

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One of the factors negatively affecting the cardiac prognosis of coronary heart disease (CHD) is affective disorders of the depressive spectrum. Symptoms of depression may increase the level of systemic inflammation and promote disorders of carbohydrate metabolism by altering the synthesis and secretion of adipokines: leptin, resistin, adiponectin. The aim of this study was to assess the adipokin status in patients with stable coronary artery disease in the conditions of conservative therapy and during percutaneous coronary interventions (PCI) with stenting, including patients with depressive symptoms. The presence of depressive symptoms was accompanied by an increase in the level of resistin in the blood plasma in patients with stable ischemic heart disease. PCI with coronary artery stenting resulted in an increase in the concentration of all the adipokines: adiponectin, leptin, resistin. Stenting of coronary arteries in people with depressive symptoms led to an increase in the level of resistin, adiponectin with a decrease in the concentration of leptin in the blood plasma on the third day after the operative intervention.

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Wargasetia, Teresa Liliana. "MEMAHAMI KAITAN OBESITAS DAN KANKER: PELUANG UNTUK PENCEGAHAN KANKER." Berkala Ilmiah Kedokteran Duta Wacana 1, no. 3 (September 20, 2016): 219. http://dx.doi.org/10.21460/bikdw.v1i3.20.

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Jumlah kasus kanker yang disebabkan oleh obesitas diperkirakan sebesar 20%. The International Agency for Research into Cancer dan the World Cancer Research Fund melaporkan bahwa kanker yang sering dialami oleh penderita obesitas adalah kanker endometrium, adenokarsinoma esofagus, kolorektal, payudara postmenopause, prostat, dan ginjal. Risiko keganasan yang meningkat dipengaruhi distribusi lemak tubuh dan peningkatan berat badan yang menyebabkan transfer lipid dari adiposit ke tumor. Sejumlah studi melaporkan bahwa kelebihan berat badan dan obesitas berkorelasi dengan tingkat kematian akibat kanker hepar, pankreas, kolon, endometrium, ginjal, payudara postmenopause, mieloma, dan Hodgkin’s lymphoma. Empat sistem yang teridentifikasi sebagai penyebab kanker pada obesitas adalah peningkatan lipid, respons inflamasi, resistensi insulin, dan adipokin. Konsumsi sejumlah makanan yang bersifat antikanker dan antiobesitas bersama dengan restriksi kalori dan aktivitas fisik membantu dalam pencegahan kanker yang berkaitan dengan obesitas.

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Molnár, Ágnes, Ferenc Sztanek, Anita Szentpéteri, György Paragh, Mariann Harangi, and Zoltán Balogh. "Mozgásterápia hatása diabeteses polyneuropathiás betegek adipokin- és miokinszintjére és életminőségére." Diabetologia Hungarica 28, Suppl.1 (2020): 82–83. http://dx.doi.org/10.24121/dh.2020.s1.55.

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Chulkov, Vl S., V. A. Sumerkina, V. S. Chulkov, S. P. Sinitsin, and N. K. Vereina. "Hemostasis state, adipokine levels and markers of endothelial dysfunction in young patients with components of the metabolic syndrome." Kazan medical journal 96, no. 5 (October 15, 2015): 787–91. http://dx.doi.org/10.17750/kmj2015-787.

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Aim. To carry out a comparative assessment of hemostasis, adipokines levels and markers of endothelial dysfunction in young patients with a variety of components of the metabolic syndrome. Methods. The study included 154 patients aged 18-44 years who were divided into four groups matched for age and sex: the first group - 35 patients with metabolic syndrome, the second group - 25 patients with hypertension without abdominal obesity, the third group - 22 patients with abdominal obesity without hypertension, the fourth group - 72 healthy subjects (control group). We studied the vascular-platelet, coagulation and anticoagulation units of the hemostasis system, the fibrinolytic system, the levels of adipokines and markers of endothelial dysfunction. Results. Patients with metabolic syndrome showed signs of activation of coagulation together with a slowdown functions of the fibrinolytic system and activation of the anticoagulation system. In young patients with hypertension without abdominal obesity increased were the levels of endothelin, plasminogen activator inhibitor type 1, angiotensin II inhibitor and extrinsic pathway of coagulation. Patients with abdominal obesity without arterial hypertension had no significant change in adipokin levels and markers of endothelial dysfunction compared to control group. Conclusion. In young patients with a variety of components of the metabolic syndrome revealed were signs of intravascular activation of blood coagulation in conjunction with the imbalance of adipokines levels and endothelial dysfunction.

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Kozak-Nurczyk, Patrycja, Kamil Nurczyk, Andrzej Prystupa, Grzegorz Szcześniak, and Lech Panasiuk. "The influence of adipose tissue and selected adipokines on insulin resistance and development of diabetes mellitus type 2." Medycyna Ogólna i Nauki o Zdrowiu 24, no. 4 (December 21, 2018): 210–13. http://dx.doi.org/10.26444/monz/99047.

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Farag, Azza G. A., Mostafa A. Hammam, Hesham N. Khaled, ShimaE Soliman, Nermin Reda Tayel, Amira A. EL‐Shamendy, and Wafaa A. Shehata. "Resistin adipokin in atopic dermatitis patients: A clinical, biochemical, and genetic study." Journal of Cosmetic Dermatology 19, no. 11 (February 28, 2020): 2929–35. http://dx.doi.org/10.1111/jocd.13338.

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Mohammadi, Amin, and Ali khajehlandi. "Hs-CRP and Adipokin (Lcn2): Response to Exercise Training in Obese Men." Biomedical & Pharmacology Journal 7, no. 1 (June 30, 2014): 17–22. http://dx.doi.org/10.13005/bpj/447.

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Tan, Bee K., Krzysztof C. Lewandowski, Joseph Paul O'Hare, and Harpal S. Randeva. "Insulin regulates the novel adipokine adipolin/CTRP12: in vivo and ex vivo effects." Journal of Endocrinology 221, no. 1 (February 3, 2014): 111–19. http://dx.doi.org/10.1530/joe-13-0537.

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There has been intense interest in the adipokines of the C1q complement/TNF-related protein (CTRP) superfamily. Adipolin (CTRP12) has been described as a novel adipokine, abundantly expressed in adipose tissue with insulin-sensitising and anti-inflammatory effects. We wanted to investigate the effects of acute and chronic hyperinsulinaemia on circulating adipolin concentrations (ELISA) via a prolonged insulin–glucose infusion in humans. We also examined the effects of insulin and the insulin sensitiser, rosiglitazone, on adipolin concentrations (western blotting) in human adipose tissue explants. We found that hyperinsulinaemic induction in healthy lean human subjects significantly increased circulating levels of adipolin (P<0.05 and P<0.01). Furthermore, in subcutaneous adipose tissue explants, insulin significantly increased adipolin protein expression and secretion (P<0.05 and P<0.01). This effect was attenuated by the phosphatidylinositol 3-kinase inhibitor, LY294002 (P<0.05). Moreover, the insulin-sensitising peroxisome proliferator-activated receptor γ (PPARγ) agonist, rosiglitazone, significantly increased adipolin protein expression and secretion in subcutaneous adipose tissue explants (P<0.05 and P<0.01). This effect was inhibited by the PPARγ antagonist, GW9662 (P<0.05). Our data provide novel insights into adipolin physiology in human subjects.

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Buczkowska, Marta, Krzysztof Buczkowski, Anna Głogowska-Gruszka, Sylwia Duda, Michał Dyaczyński, and Przemysław Nowak. "Adipose tissue – the structure and its functions, with particular emphasis on the characteristics of selected adipokines and their effects on the organism." Medycyna Ogólna i Nauki o Zdrowiu 25, no. 3 (September 20, 2019): 162–69. http://dx.doi.org/10.26444/monz/110429.

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Kuznetsova, L. A. "Metabolic Syndrome: the Influence of Adipokines on the L-Arginine-NO Synthase-Nitric Oxide Signaling Pathway." Acta Biomedica Scientifica 6, no. 2 (June 24, 2021): 22–40. http://dx.doi.org/10.29413/abs.2021-6.2.3.

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Metabolic syndrome includes the following symptoms: obesity, hyperlipidemia, hypertension, insulin resistance, and cardiovascular disease. The purpose of this review is to elucidate the role of adipokines in the regulation of the L-arginine-NO-synthas-NO signaling pathway in the pathogenesis of metabolic syndrome. The main questions raised in the review are: how adipokine secretion changes, how the level of their receptors is regulated, and which signaling pathways are involved in the transmission of adipokine signals when coupled to the L-arginine-NO-synthase-NO signaling cascade. Adipokines are peptide hormones that transmit a signal from adipose tissue to targets in the brain, blood vessels, liver, pancreas, muscles, and other tissues. Some adipokines have anti-inflammatory and insulin-sensitive effects: adiponectin, omentin, adipolin, chemerin, progranulin. Others have the negative inflammatory effect in the development ofmetabolic syndrome: visfatin, vaspin, apelin. Adipokines primarily regulate the expression and activity of endothelial NO-synthase. They either activate an enzyme involving 5-AMP protein kinase or Akt kinase, increasing its activity and synthesis of NO in the tissues of healthy patients: adiponectin, adipolin, omentin, or inhibit the activity of eNOS, which leads to a decrease in NO-synthase and suppression of mRNA bioavailability: vaspin, visfatin, apelin in metabolic syndrome, and a decrease in its activity leads to dissociation and endothelial dysfunction. It should be noted that the bioavailability of NO formed by NO-synthase is affected at many levels, including: the expression ofNO-synthase mRNA and its protein; the concentration of L-arginine; the level of cofactors of the reaction; and to detect the maximum activity of endothelial NO-synthase, dimerization of the enzyme is required, posttranslational modifications are important, in particular, phosphorylation of endothelial NO-synthase by serine 1177 with the participation of 5-AMP protein kinase, Akt kinase and other kinases. It should be noted that the participation of adiponectin, omentin, and kemerin in the regulation of the L-arginine-NO-synthase-NO cascade in metabolic syndrom opens up certain opportunities for the development of new approaches for the correction of disorders observed in this disease. The review analyzes the results of research searching in PubMed databases, starting from 2001 and up to 2020 using keywords and adipokine names, more than half of the references of the last 5 years.

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Arhire, L. "Changes in Bone Mineral Parameters after Sleeve Gastrectomy Relationship with Ghrelin and Plasma Adipokin Levels." Acta Endocrinologica (Bucharest) 14, no. 4 (2018): 498–504. http://dx.doi.org/10.4183/aeb.2018.498.

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Krysiak, Robert, Witold Żmuda, Bogdan Marek, and Bogusław Okopień. "Wpływ krótkotrwałego leczenia skojarzonego simwastatyną i ezetimibem na stężenie adipokin w osoczu pacjentów na izolowaną hipercholesterolemię." Endokrynologia Polska 65, no. 4 (August 29, 2014): 275–80. http://dx.doi.org/10.5603/ep.2014.0037.

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Krysiak, Robert, Witold Żmuda, Bogdan Marek, and Bogusław Okopień. "Porównanie wpływu krótkotrwałego leczenia hipolipemicznego na stężenie adipokin w osoczu kobiet i mężczyzn z izolowaną hipercholesterolemią." Endokrynologia Polska 66, no. 2 (May 1, 2015): 114–20. http://dx.doi.org/10.5603/ep.2015.0017.

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Schipper, Henk S., Wilco de Jager, Mariska EA van Dijk, Jenny Meerding, Pierre MJ Zelissen, Roger A. Adan, Berent J. Prakken, and Eric Kalkhoven. "A Multiplex Immunoassay for Human Adipokine Profiling." Clinical Chemistry 56, no. 8 (August 1, 2010): 1320–28. http://dx.doi.org/10.1373/clinchem.2010.146118.

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BACKGROUNDAdipose tissue secretory proteins, called adipokines, play pivotal roles in the pathophysiology of obesity and its associated disorders such as metabolic syndrome, type 2 diabetes, and cardiovascular disease. Because methods for comprehensive adipokine profiling in patient plasma and other biological samples are currently limited, we developed a multiplex immunoassay for rapid and high-throughput measurement of 25 adipokines in only 50 μL of sample.METHODS(Pre)adipocyte and ex vivo cultured adipose tissue supernatants were generated and together with plasma from 5 morbidly obese patients and 5 healthy and normal weight controls used to develop the adipokine multiplex immunoassay and test its usefulness in biological samples. We assessed adipokine dynamic ranges, lower limits of detection and quantification, cross-reactivity, intra- and interassay variation, and correlation with adipokine ELISAs.RESULTSThe limits of quantification and broad dynamic ranges enabled measurement of all 25 adipokines in supernatants and patient plasmas, with the exception of TNF-α in plasma samples. Intraassay variation was <10% for all adipokines; interassay variation was <15%. The multiplex immunoassay results correlated significantly with ELISA measurements. Plasma adipokine profiling showed significantly higher concentrations of the novel adipokines cathepsin S (5.1 × 104 vs 4.3 × 104 ng/L, P = 0.003) and chemerin (4.1 × 105 vs 2.7 × 105 ng/L, P = 0.0008) in morbidly obese patients than normal weight controls, besides the established differences in adiponectin and leptin concentrations.CONCLUSIONSOur findings underscore the relevance of the novel adipokines cathepsin S and chemerin, but foremost the potential of this novel method for both comprehensive adipokine profiling in large patient cohorts and for biological discovery.

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Elfassy, Yaelle, Jean-Philippe Bastard, Chloe McAvoy, Soraya Fellahi, Joëlle Dupont, and Rachel Levy. "Adipokines in Semen: Physiopathology and Effects on Spermatozoas." International Journal of Endocrinology 2018 (June 5, 2018): 1–11. http://dx.doi.org/10.1155/2018/3906490.

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Adipokines are secreted by adipose tissue and could be the link between obesity and infertility. Different studies investigated the involvement of adipokines in reproductive functions but only a few have looked into the male part. This review assesses adipokine functions on male reproductive parameters. Adiponectin seems to have a positive effect on sperm parameters, whereas other adipokines such as resistin or chemerin would have a rather deleterious effect on spermatogenesis. Semen parameters seem to be impacted when resistin and chemerin are increased: indeed, there is a decrease of sperm motility. Sperm morphology is improved when adiponectin is increased. The most studied adipokine, leptin, has a dual effect with a positive effect on sperm at physiological levels and a negative one for high seminal concentrations. Many semen parameters and fertility itself are disturbed according to semen adipokine levels, even if it is not the only interfering element. Taken together, adipokines are found in human and animal semen and most of them or their receptors are expressed in male genital tract. Although the pathophysiological role of adipokines in semen is not clearly elucidated, the adipokines could influence sperm functionality and could be potential biomarkers of male fertility.

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Blüher, M., U. Ceglarek, J. Thiery, M. Hamm, and V. Richter. "Adipositas und Omega-3-Fettsäuren." Adipositas - Ursachen, Folgeerkrankungen, Therapie 08, no. 01 (2014): 25–31. http://dx.doi.org/10.1055/s-0037-1618832.

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ZusammenfassungEine chronische subklinische Entzündung des Fettgewebes, charakterisiert durch ein proinflammatorisches Adipokin-Sekretionsmuster und durch die Infiltration von Entzündungszellen, trägt zu verschiedenen mit der Adipositas verbundenen Stoffwechselstörungen bei. Die langkettigen Omega-3-Fettsäuren Eicosapentaensäure (EPA) und Docosahexaensäure (DHA) wirken inflammatorischen Prozessen im Fettgewebe entgegen, und zwar sowohl auf Stufen der Entwicklung als auch bei der Auflösung der Entzündung. EPA und DHA stellen Substrate für kürzlich identifizierte Familien von entzündungsauflösenden Lipid-Mediatoren dar, speziell von Resolvinen, Protektinen und Maresinen, denen eine wesentliche Rolle in der Begrenzung von Entzündungen zukommt.Als eine Strategie zur Prävention systemischer, mit der Adipositas assoziierter Komplikationen ist es notwendig, die inflammatorischen Prozesse im Fettgewebe günstig zu beeinflussen. Zahlreiche Untersuchungen haben ergeben, dass langkettige Omega-3-Fettsäuren hierzu beitragen und dass die Verfügbarkeit von EPA und DHA das Risiko von Adipositas-assoziierten Stoffwechselerkrankungen verringert. Deshalb ist die Versorgung mit langkettigen Omega-3-Fettsäuren sowohl auf Bevölkerungsebene als auch speziell für adipöse Personen bedeutsam.

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Koçak, Betül, and Aysun Yüksel. "Kemik-eklem hastalıklarının obezite ile ilişkisi." Sağlık ve Yaşam Bilimleri Dergisi 3, no. 1 (April 10, 2021): 97–100. http://dx.doi.org/10.33308/2687248x.202131205.

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Obezite; kas ve iskelet sistemi üzerinde osteoartrit, osteoporoz ve sistemik enflamatuar romatizmal hastalıkları da içeren geniş bir hastalık yelpazesini etkilemektedir. Konu üzerine yapılan çalışmalar, genellikle beden kütle indeksi ile tayin edilen obezite varlığı ile diz osteoartrid prevalansı ve insidansı arasında ilişki olduğunu göstermiştir. Yürüyüş analizi, diz eklemi boyunca yükü azaltmak için kilo kaybının yararlı olduğunu göstermiştir, yaklaşık 0.5 kg ağırlık kaybı, adım başına iki ila dört kat yükte azalmaya neden olmaktadır. Öte yandan obezitenin kemik yapımını artırması ve çözülümünü azaltmasıyla toplam kemik metabolizmasının korunmasına yönelik etkisi, osteoporoz için göz ardı edilmemelidir. Beden kütle indeksiin 25 üzerinde olduğu, normal ağırlığın üzerindeki hastalarda aktif olan hipertrofik adipositlerden adipositokin veya adipokin olarak tanımlanan mediatörler salınmakta, pro-enflamatuar aktiviteleri olan bu adipokinlerin enflamatuar romatizmal hastalıklar üzerine de etkisi bulunmaktadır. Kemik-eklem hastalıklarında obezitenin etkisi göz ardı edilmemeli ve klinik yaklaşımda tedavinin önemli bir parçası olarak yer almalıdır. Bu derlemede obezitenin kas-iskelet sistemi üzerinde oluşturduğu etkilerinin, güncel veriler ışığında incelenmesi amaçlanmıştır.

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Tzanavari, Theodora, Jason Tasoulas, Chrysoula Vakaki, Chrysovalantou Mihailidou, Gerasimos Tsourouflis, and Stamatios Theocharis. "The Role of Adipokines in the Establishment and Progression of Head and Neck Neoplasms." Current Medicinal Chemistry 26, no. 25 (October 16, 2019): 4726–48. http://dx.doi.org/10.2174/0929867325666180713154505.

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Adipokines constitute a family of protein factors secreted by white adipose tissue (WAT), that regulate the functions of WAT and other sites. Leptin, adiponectin and resistin, are the main adipokines present in serum and saliva, targeting several tissues and organs, including vessels, muscles, liver and pancreas. Besides body mass regulation, adipokines affect glucose homeostasis, inflammation, angiogenesis, cell proliferation and apoptosis, and other crucial cell procedures. Their involvement in tumor formation and growth is well established and deregulation of adipokine and adipokine receptors’ expression is observed in several malignancies including those located in the head and neck region. Intracellular effects of adipokines are mediated by a plethora of receptors that activate several signaling cascades including Janus kinase/ Signal transducer and activator of transcription (JAK/ STAT pathway), Phospatidylinositol kinase (PI3/ Akt/ mTOR) and Peroxisome proliferator-activated receptor (PPAR). The present review summarizes the current knowledge on the role of adipokines family members in carcinogenesis of the head and neck region. The diagnostic and prognostic significance of adipokines and their potential role as serum and saliva biomarkers are also discussed.

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Miller, Norman E., C. Charles Michel, M. Nazeem Nanjee, Waldemar L. Olszewski, Irina P. Miller, Matthew Hazell, Gunilla Olivecrona, Pauline Sutton, Sandy M. Humphreys, and Keith N. Frayn. "Secretion of adipokines by human adipose tissue in vivo: partitioning between capillary and lymphatic transport." American Journal of Physiology-Endocrinology and Metabolism 301, no. 4 (October 2011): E659—E667. http://dx.doi.org/10.1152/ajpendo.00058.2011.

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Peptides secreted by adipose tissue (adipokines) may enter blood via capillaries or lymph. The relative importance of these pathways for a given adipokine might influence its biological effects. Because this has not been studied in any species, we measured the concentrations of seven adipokines and eight nonsecreted proteins in afferent peripheral lymph and venous plasma from 12 healthy men. Data for nonsecreted proteins were used to derive indices of microvascular permeability, which in conjunction with the molecular radii of the adipokines were used to estimate the amounts leaving the tissue via capillaries. Transport rates via lymph were estimated from the lymph adipokine concentrations and lymph flow rates and total transport (secretion) as the sum of this and capillary transport. Concentrations of nonsecreted proteins were always lower in lymph than in plasma. With the exception of adiponectin, adipokine concentrations were always higher in lymph ( P < 0.01). Leptin and MCP-1 were secreted at the highest rates (means: 43 μg/h or 2.7 nmol/h and 32 μg/h or 2.4 nmol/h, respectively). IL-6 and MCP-1 secretion rates varied greatly between subjects. The proportion of an adipokine transported via lymph was directly related to its molecular radius ( r s = +0.94, P = 0.025, n = 6), increasing from 14 to 100% as the radius increased from 1.18 (IL-8) to 3.24 nm (TNFα). We conclude that the lymph/capillary partitioning of adipokines is a function of molecular size, which may affect both their regional and systemic effects in vivo. This finding may have implications for the physiology of peptides secreted by other tissues.

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Kim, Ji-Youn, Seon-Eun Baek, Rehna Paula Ginting, Min-Woo Lee, and Jeong-Eun Yoo. "Potential Benefits of Acupuncture and Herbs for Obesity-Related Chronic Inflammation by Adipokines." Evidence-Based Complementary and Alternative Medicine 2020 (October 9, 2020): 1–12. http://dx.doi.org/10.1155/2020/3285363.

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The adipose tissue is an organ that stores energy in the form of fats. It also has been known as an endocrine playing an integral role in metabolic homeostasis by secreting various adipokines. In obesity, the adipokine components and secretion patterns are altered toward proinflammation with weight gain, causing low chronic inflammation, which is closely linked to various metabolic diseases. Acupuncture and herbs are used for the management of obesity and its comorbidities, and it has been observed that these therapies affect the amount of expression and concentration of adipokines with improved metabolic phenotypes in both animal and human metabolic diseases. In this review, we discuss the role of adipokines and summarize beneficial effects of the treatments such as electroacupuncture, pharmacopuncture, catgut embedding acupuncture, and single and multiple medicinal herbs on obesity and its relations to adipokine composition. It will provide a new insight for applying adipokines as surrogate markers in complementary and alternative medicine practice.

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Nigro, Ersilia, Aurora Daniele, Alessia Salzillo, Angela Ragone, Silvio Naviglio, and Luigi Sapio. "AdipoRon and Other Adiponectin Receptor Agonists as Potential Candidates in Cancer Treatments." International Journal of Molecular Sciences 22, no. 11 (May 25, 2021): 5569. http://dx.doi.org/10.3390/ijms22115569.

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The high mortality rate together with an ever-growing number of annual cases have defined neoplastic disorders as “the real 21st-century disease”. Its dubious distinction also results from conventional therapy failure, which has made cancer an orphan disease. Therefore, innovative and alternative therapeutic strategies are mandatory. The ability to leverage human naturally occurring anti-tumor defenses has always represented a fascinating perspective, and the immuno blockage approval in cancer treatment represents in timeline the latest success. As a multifunctional organ, adipose tissue releases a large amount of adipokines having both carcinogenic and antitumor properties. The negative correlation between serum levels and risk for developing malignancies, as well as the huge number of existing preclinical studies, have identified adiponectin as a potential anticancer adipokine. Nevertheless, its usage in clinical has constantly clashed with the inability to reproduce a mimic synthetic compound. Between 2011 and 2013, two distinct adiponectin receptor agonists were recognized, opening new scenarios even in cancer. Here, we review the first orally active adiponectin receptor agonists AdipoRon, from the discovery to the anticancer evidence. Including our latest findings in osteosarcoma models, we summarize AdipoRon and other existing agonists state-of-art, questioning about the feasibility assessment of this strategy in cancer treatment.

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Hillenbrand, Andreas, Manfred Weiss, Uwe Knippschild, Anna Maria Wolf, and Markus Huber-Lang. "Sepsis-Induced Adipokine Change with regard to Insulin Resistance." International Journal of Inflammation 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/972368.

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Background. Assessment of white adipose tissue has changed in recent years, with WAT now being considered as an active endocrine organ, secreting a large number of bioactive mediators, so-called adipokines. Besides other functions, these adipokines are involved in inflammatory response thereby exhibiting predominantly proinflammatory or anti-inflammatory properties and contribute to insulin resistance.Methods. Comprehensive review of the literature of the role of adipokines relevant to critical care medicine using PubMed search.Results. Adiponectin—the prototype of an anti-inflammatory and insulin-sensitizing adipokine—is diminished in sepsis, while resistin—a protein with proinflammatory properties—is elevated. Plasminogen activator inhibitor-1, interleukin (IL)-1, IL-6, IL-8, and IL-10, and tumor-necrosis-factor-alpha mediate insulin resistance and are elevated in sepsis, while retinol-binding protein-4 concentrations are significantly reduced in sepsis. Chemerin displays potent anti-inflammatory and insulin-resistance properties, while monocyte chemotactic protein-1—increased in sepsis—contributes to macrophage infiltration in adipose tissue and insulin resistance.Conclusions. The expression of adipokines in humans is altered as well in obese as in septic patients with elevated levels of proinflammatory adipokines. Changes in adipokine levels in acute sepsis could contribute to insulin resistance. Consequently, in critically ill patients, these alterations underline a possible contribution of adipokines in the development of hyperglycemia.

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Pham, Duc-Vinh, and Pil-Hoon Park. "Tumor Metabolic Reprogramming by Adipokines as a Critical Driver of Obesity-Associated Cancer Progression." International Journal of Molecular Sciences 22, no. 3 (February 1, 2021): 1444. http://dx.doi.org/10.3390/ijms22031444.

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Adiposity is associated with an increased risk of various types of carcinoma. One of the plausible mechanisms underlying the tumor-promoting role of obesity is an aberrant secretion of adipokines, a group of hormones secreted from adipose tissue, which have exhibited both oncogenic and tumor-suppressing properties in an adipokine type- and context-dependent manner. Increasing evidence has indicated that these adipose tissue-derived hormones differentially modulate cancer cell-specific metabolism. Some adipokines, such as leptin, resistin, and visfatin, which are overproduced in obesity and widely implicated in different stages of cancer, promote cellular glucose and lipid metabolism. Conversely, adiponectin, an adipokine possessing potent anti-tumor activities, is linked to a more favorable metabolic phenotype. Adipokines may also play a pivotal role under the reciprocal regulation of metabolic rewiring of cancer cells in tumor microenvironment. Given the fact that metabolic reprogramming is one of the major hallmarks of cancer, understanding the modulatory effects of adipokines on alterations in cancer cell metabolism would provide insight into the crosstalk between obesity, adipokines, and tumorigenesis. In this review, we summarize recent insights into putative roles of adipokines as mediators of cellular metabolic rewiring in obesity-associated tumors, which plays a crucial role in determining the fate of tumor cells.

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Tan, Bee K., Jing Chen, Raghu Adya, Manjunath Ramanjaneya, Vanlata Patel, and Harpal S. Randeva. "Metformin increases the novel adipokine adipolin/CTRP12: role of the AMPK pathway." Journal of Endocrinology 219, no. 2 (August 14, 2013): 101–8. http://dx.doi.org/10.1530/joe-13-0277.

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Adipolin is a novel adipokine with anti-inflammatory and glucose-lowering properties. Lower levels of adipolin are found in obese and diabetic mice. Polycystic ovary syndrome (PCOS) is a pro-inflammatory state associated with obesity and diabetes. To date, there are no human studies on adipolin. Therefore, we measured serum (ELISA) and adipose tissue adipolin mRNA expression (RT-PCR) and protein concentrations (western blotting) in PCOS and control subjects. We also investigated the ex vivo effect of glucose and metformin on adipolin protein production in human subcutaneous adipose tissue explants. We report novel data that serum and subcutaneous adipose tissue adipolin mRNA expression and protein concentrations were significantly lower in women with PCOS compared with control subjects. Furthermore, Spearman's rank analysis showed that serum adipolin concentrations were significantly negatively correlated with BMI, waist-to-hip ratio, and glucose (P<0.05). However, when subjected to multiple regression analysis, none of these variables were predictive of serum adipolin concentrations (P>0.05). Also, subcutaneous adipose tissue adipolin mRNA expression and protein concentrations were only significantly negatively correlated with glucose (P<0.05). No significant correlations were found with omental adipose tissue adipolin mRNA expression and protein concentrations (P>0.05). Moreover, glucose profoundly reduced and metformin significantly increased adipolin protein production in human adipose tissue explants respectively. Importantly, metformin's effects appear to be via the AMP-activated protein kinase signaling pathway.

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Schrover, Ilse M., Yolanda van der Graaf, Wilko Spiering, and Frank LJ Visseren. "The relation between body fat distribution, plasma concentrations of adipokines and the metabolic syndrome in patients with clinically manifest vascular disease." European Journal of Preventive Cardiology 25, no. 14 (July 27, 2018): 1548–57. http://dx.doi.org/10.1177/2047487318790722.

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Introduction We evaluated the relationship between adipokine plasma concentrations and body fat distribution and the metabolic syndrome. Methods In a cohort of 1215 patients with clinically manifest vascular disease the relation between subcutaneous adipose tissue, visceral adipose tissue, waist circumference, body mass index and plasma concentrations of adipsin, chemerin, monocyte chemoattractant protein-1, migration inhibitory factor, nerve growth factor, resistin, plasma amyloid A1, adiponectin, leptin, plasminogen activator inhibitor-1 and hepatic growth factor were cross-sectionally assessed with linear regression and adjusted for age and gender. The relation between adipokines and the metabolic syndrome was cross-sectionally evaluated using logistic regression. An adipokine profile was developed to measure the effect of combined rather than single adipokines. Results Adiposity was related to higher nerve growth factor, hepatic growth factor, migration inhibitory factor, leptin and adipsin and with lower chemerin, plasminogen activator inhibitor-1, resistin, plasma amyloid A1 and adiponectin. The strongest positive relations were between body mass index and adipsin (β 0.247; 95% CI 0.137–0.356) and leptin (β 0.266; 95% CI 0.207–0.324); the strongest negative relations were between body mass index and plasma amyloid A1 (β –0.266; 95% CI –0.386 to –0.146) and visceral adipose tissue and adiponectin (β –0.168; 95% CI –0.226 to –0.111). There was no relation between subcutaneous adipose tissue and adipokines. Odds for the metabolic syndrome were higher with each 1 SD higher hepatic growth factor (OR 1.21; 95% CI 1.06–1.38) and leptin (OR 1.26; 95% CI 1.10–1.45) and lower with each 1 SD higher adiponectin (OR 0.73; 95% CI 0.64–0.83) and resistin (OR 0.85; 95% CI 0.74–0.97). The adipokine profile was related to the metabolic syndrome (OR 1.03; 95% CI 1.00–1.06). Conclusion Plasma concentrations of adipokines are related to obesity and body fat distribution. The relation between adipokine concentrations and the metabolic syndrome is independent of visceral adipose tissue.

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Chaldakov, G., I. Stankulov, M. Hristova, and P. Ghenev. "Adipobiology of Disease: Adipokines and Adipokine-Targeted Pharmacology." Current Pharmaceutical Design 9, no. 12 (May 1, 2003): 1023–31. http://dx.doi.org/10.2174/1381612033455152.

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Taylor, Erin B. "The complex role of adipokines in obesity, inflammation, and autoimmunity." Clinical Science 135, no. 6 (March 2021): 731–52. http://dx.doi.org/10.1042/cs20200895.

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Abstract The global obesity epidemic is a major contributor to chronic disease and disability in the world today. Since the discovery of leptin in 1994, a multitude of studies have characterized the pathological changes that occur within adipose tissue in the obese state. One significant change is the dysregulation of adipokine production. Adipokines are an indispensable link between metabolism and optimal immune system function; however, their dysregulation in obesity contributes to chronic low-grade inflammation and disease pathology. Herein, I will highlight current knowledge on adipokine structure and physiological function, and focus on the known roles of these factors in the modulation of the immune response. I will also discuss adipokines in rheumatic and autoimmune diseases.

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Chang, Ming-Ling, Zinger Yang, and Sien-Sing Yang. "Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression." International Journal of Molecular Sciences 21, no. 21 (November 5, 2020): 8308. http://dx.doi.org/10.3390/ijms21218308.

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Adipose tissue is a highly dynamic endocrine tissue and constitutes a central node in the interorgan crosstalk network through adipokines, which cause pleiotropic effects, including the modulation of angiogenesis, metabolism, and inflammation. Specifically, digestive cancers grow anatomically near adipose tissue. During their interaction with cancer cells, adipocytes are reprogrammed into cancer-associated adipocytes and secrete adipokines to affect tumor cells. Moreover, the liver is the central metabolic hub. Adipose tissue and the liver cooperatively regulate whole-body energy homeostasis via adipokines. Obesity, the excessive accumulation of adipose tissue due to hyperplasia and hypertrophy, is currently considered a global epidemic and is related to low-grade systemic inflammation characterized by altered adipokine regulation. Obesity-related digestive diseases, including gastroesophageal reflux disease, Barrett’s esophagus, esophageal cancer, colon polyps and cancer, non-alcoholic fatty liver disease, viral hepatitis-related diseases, cholelithiasis, gallbladder cancer, cholangiocarcinoma, pancreatic cancer, and diabetes, might cause specific alterations in adipokine profiles. These patterns and associated bases potentially contribute to the identification of prognostic biomarkers and therapeutic approaches for the associated digestive diseases. This review highlights important findings about altered adipokine profiles relevant to digestive diseases, including hepatic, pancreatic, gastrointestinal, and biliary tract diseases, with a perspective on clinical implications and mechanistic explorations.

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Ciancarelli, Irene, Giovanni Morone, Marco Iosa, Stefano Paolucci, Loris Pignolo, Paolo Tonin, Antonio Cerasa, and Maria Giuliana Tozzi Ciancarelli. "Adipokines as Potential Biomarkers in the Neurorehabilitation of Obese Stroke Patients." Current Neurovascular Research 17, no. 4 (December 14, 2020): 437–45. http://dx.doi.org/10.2174/1567202617666200603150901.

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Background: Limited studies concern the influence of obesity-induced dysregulation of adipokines in functional recovery after stroke neurorehabilitation. Objective: To investigate the relationship between serum leptin, resistin, and adiponectin and functional recovery before and after neurorehabilitation of obese stroke patients. The adipokine potential significance as prognostic markers of rehabilitation outcomes was also verified. Methods: Twenty obese post-acute stroke patients before and after neurorehabilitation and thirteen obese volunteers without-stroke, as controls, were examined. Adipokines were determined by commercially available enzyme-linked immunosorbent assay (ELISA) kits. Functional deficits were assessed before and after neurorehabilitation with the Barthel Index (BI), modified Rankin Scale (mRS), and Functional Independence Measure (FIM). Results: Compared to controls, higher leptin and resistin values and lower adiponectin values were observed in stroke patients before neurorehabilitation and no correlations were found between adipokines and clinical outcome measures. Neurorehabilitation was associated with improved scores of BI, mRS, and FIM. After neurorehabilitation, decreased values of Body Mass Index (BMI) and resistin together increased adiponectin were detected in stroke patients, while leptin decreased but not statistically. Comparing adipokine values assessed before neurorehabilitation with the outcome measures after neurorehabilitation, correlations were observed for leptin with BI-score, mRS-score, and FIM-score. No other adipokine levels nor BMI assessed before neurorehabilitation correlated with the clinical measures after neurorehabilitation. The forward stepwise regression analysis identified leptin as prognostic factor for BI, mRS, and FIM. Conclusions: Our data show the effectiveness of neurorehabilitation in modulating adipokines levels and suggest that leptin could assume the significance of biomarker of functional recovery.

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Gutaj, Paweł, Rafał Sibiak, Maurycy Jankowski, Karina Awdi, Rut Bryl, Paul Mozdziak, Bartosz Kempisty, and Ewa Wender-Ozegowska. "The Role of the Adipokines in the Most Common Gestational Complications." International Journal of Molecular Sciences 21, no. 24 (December 10, 2020): 9408. http://dx.doi.org/10.3390/ijms21249408.

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Adipocytokines are hormonally active molecules that are believed to play a key role in the regulation of crucial biological processes in the human body. Numerous experimental studies established significant alterations in the adipokine secretion patterns throughout pregnancy. The exact etiology of various gestational complications, such as gestational diabetes, preeclampsia, and fetal growth abnormalities, needs to be fully elucidated. The discovery of adipokines raised questions about their potential contribution to the molecular pathophysiology of those diseases. Multiple studies analyzed their local mRNA expression and circulating protein levels. However, most studies report conflicting results. Several adipokines such as leptin, resistin, irisin, apelin, chemerin, and omentin were proposed as potential novel early markers of heterogeneous gestational complications. The inclusion of the adipokines in the standard predictive multifactorial models could improve their prognostic values. Nonetheless, their independent diagnostic value is mostly insufficient to be implemented into standard clinical practice. Routine assessments of adipokine levels during pregnancy are not recommended in the management of both normal and complicated pregnancies. Based on the animal models (e.g., apelin and its receptors in the rodent preeclampsia models), future implementation of adipokines and their receptors as new therapeutic targets appears promising but requires further validation in humans.

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Ogawa, Hayato, Koji Ohashi, Masanori Ito, Rei Shibata, Noriyoshi Kanemura, Daisuke Yuasa, Takahiro Kambara, et al. "Adipolin/CTRP12 protects against pathological vascular remodelling through suppression of smooth muscle cell growth and macrophage inflammatory response." Cardiovascular Research 116, no. 1 (March 15, 2019): 237–49. http://dx.doi.org/10.1093/cvr/cvz074.

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AbstractAimsSecreted factors produced by adipose tissue are involved in the pathogenesis of cardiovascular disease. We previously identified adipolin, also known as C1q/TNF-related protein 12, as an insulin-sensitizing adipokine. However, the role of adipolin in vascular disease remains unknown. Here, we investigated whether adipolin modulates pathological vascular remodelling.Methods and resultsAdipolin-knockout (APL-KO) and wild-type (WT) mice were subjected to wire-induced injury of the femoral artery. APL-KO mice showed increased neointimal thickening after vascular injury compared with WT mice, which was accompanied by an enhanced inflammatory response and vascular cell proliferation in injured arteries. Adipolin deficiency also led to a reduction in transforming growth factor-β (TGF-β) 1 protein levels in injured arteries. Treatment of cultured macrophages with adipolin protein led to a reduction in lipopolysaccharide-stimulated expression of inflammatory mediators, including tumour necrosis factor (TNF)-α, interleukin (IL) 6, and monocyte chemotactic protein (MCP)-1. These effects were reversed by inhibition of TGF-β receptor II (TGF-βRII)/Smad2 signalling. Adipolin also reduced platelet-derived growth factor (PDGF)-BB-stimulated proliferation of vascular smooth muscle cells (VSMCs) through a TGF-βRII/Smad2-dependent pathway. Furthermore, adipolin treatment significantly increased TGF-β1 concentration in media from cultured VSMCs and macrophages.ConclusionThese data indicate that adipolin protects against the development of pathological vascular remodelling by attenuating macrophage inflammatory responses and VSMC proliferation.

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Meiliana, Anna, and Andi Wijaya. "Perivascular Adipose Tissue and Cardiometabolic Disease." Indonesian Biomedical Journal 5, no. 1 (April 1, 2013): 13. http://dx.doi.org/10.18585/inabj.v5i1.46.

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BACKGROUND: Obesity is associated with insulin resistance, hypertension, and cardiovascular disease, but the mechanisms underlying these associations are incompletely understood. Microvascular dysfunction may play an important role in the pathogenesis of both insulin resistance and hypertension in obesity.CONTENT: Perivascular adipose tissue (PVAT) is a local deposit of adipose tissue surrounding the vasculature. PVAT is present throughout the body and has been shown to have a local effect on blood vessels. The influence of PVAT on the vasculature changes with increasing adiposity. PVAT similarly to other fat depots, is metabolically active, secreting a wide array of bioactive substances, termed ‘adipokines’. Adipokines include cytokines, chemokines and hormones that can act in a paracrine, autocrine or endocrine fashion. Many of the proinflammatory adipokines upregulated in obesity are known to influence vascular function, including endothelial function, oxidative stress, vascular stiffness and smooth muscle migration. Adipokines also stimulate immune cell migration into the vascular wall, potentially contributing to the inflammation found in atherosclerosis. Finally, adipokines modulate the effect of insulin on the vasculature, thereby decreasing insulin-mediated muscle glucose uptake. This leads to alterations in nitric oxide signaling, insulin resistance and potentially atherogenesis.SUMMARY: PVAT surrounds blood vessels. PVAT and the adventitial layer of blood vessels are in direct contact with each other. Healthy PVAT secretes adipokines and regulates vascular function. Obesity is associated with changes in adipokine secretion and the resultant inflammation of PVAT. The dysregulation of adipokines changes the effect of PVAT on the vasculature. Changes in perivascular adipokines secretion in obesity appear to contribute to the development of obesity-mediated vascular disease.KEYWORDS: obesity, perivascular adipose tissue, PVAT, cardiometabolic disease, adipokine

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Ambroszkiewicz, Jadwiga, Magdalena Chełchowska, Grażyna Rowicka, Witold Klemarczyk, Małgorzata Strucińska, and Joanna Gajewska. "Anti-Inflammatory and Pro-Inflammatory Adipokine Profiles in Children on Vegetarian and Omnivorous Diets." Nutrients 10, no. 9 (September 6, 2018): 1241. http://dx.doi.org/10.3390/nu10091241.

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Adipose tissue is a highly active endocrine organ that secrets many pro-inflammatory as well anti-inflammatory adipokines. The aim of the study was to assess serum adipokine profile in prepubertal vegetarian and omnivorous children. Sixty-two children on a vegetarian diet and fifty-five children on an omnivorous diet, aged 5 to 10 years, were studied. Dietary assessment was performed using a nutritional software program. Body composition was measured by dual-energy X-ray absorptiometry. Serum concentrations of adipokines: leptin, soluble leptin receptor (sOB-R), adiponectin (total and high molecular weight), resistin, visfatin, vaspin, and omentin were determined by immunoenzymatic assays. Both studied groups of children were comparable in terms of age, weight, height, body mass index, and body composition. Vegetarians had a lower (p = 0.017) leptin/sOB-R ratio and lower serum concentrations of resistin (p = 0.051), compared with omnivores. Average levels of other adipokines did not differ between both groups of children. However, we observed significantly higher ratios of anti-inflammatory to pro-inflammatory adipokines: adiponectin/leptin 0.70 (0.37–0.93) vs 0.39 (0.28–0.74), p = 0.005, and omentin/leptin 0.40 (0.23–0.83) vs. 0.33 (0.15–0.48), p = 0.011 in vegetarians compared with omnivores. A well-planned vegetarian diet might beneficially affect the adipokine profile and inflammatory status expressed by the ratios of anti-inflammatory to pro-inflammatory adipokines in prepubertal children.

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Rahayu, Luh Ade Dita, Jannatul Cahya Admiyanti, Yumna Iftinan Khalda, Fatikha Rudia Ahda, Nur Feby Febiana Agistany, Sastraningsih Setiawati, Nabila Indah Shofiyanti, and Cut Warnaini. "HIPERTENSI, DIABETES MELLITUS, DAN OBESITAS SEBAGAI FAKTOR KOMORBIDITAS UTAMA TERHADAP MORTALITAS PASIEN COVID-19: SEBUAH STUDI LITERATUR." JIMKI: Jurnal Ilmiah Mahasiswa Kedokteran Indonesia 9, no. 1 (July 12, 2021): 90–97. http://dx.doi.org/10.53366/jimki.v9i1.342.

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Pendahuluan: Pasien COVID-19 dengan penyakit penyerta atau komorbid memiliki tingkat kematian yang lebih tinggi dibandingkan dengan pasien tanpa penyakit bawaan. Komorbid yang paling umum dijumpai pada pasien COVID-19 adalah diabetes mellitus, hipertensi, dan obesitas. Prevalensi pasien COVID-19 dengan diabetes mellitus mencapai 41,7%, hipertensi mencapai 56,6%, dan obesitas mencapai 41,7%. Metode: Metode yang digunakan dalam penulisan ini adalah studi literatur yang relevan dari berbagai referensi dan terfokus pada hubungan komorbid dengan risiko kematian pada pasien COVID-19. Adapun mesin pencari yang digunakan dalam pencarian literatur antara lain NCBI dan Google Scholar. Secara keseluruhan digunakan sebanyak 21 sumber yang didapat dari berbagai basis meliputi PubMed, ScienceDirect, Researchgate, dan WHO. Pembahasan: Pada penderita hipertensi yang menderita COVID-19 terjadi peningkatan ekspresi ACE-2 yang menyebabkan tingginya kerentanan terhadap infeksi SARS-CoV-2. Gangguan fungsi sel-T dan peningkatan kadar interleukin-6 (IL-6) juga memainkan peran penting dalam peningkatan derajat keparahan penyakit COVID-19 pada penderita diabetes. Obesitas dapat menyebabkan abnormalitas pada sekresi sitokin, adipokin, dan inferferon yang akan menyebabkan terganggunya sistem imun pada tubuh manusia. Simpulan: Mekanisme patofisiologi komorbid hipertensi, diabetes mellitus, dan obesitas yang kompleks pada pasien COVID-19 meningkatkan derajat keparahan dan risiko kematian.

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Tarasova, L. V., V. N. Diomidova, N. V. Tolmacheva, Yu V. Tsyganova, A. L. Ivanova, J. V. Maslova, and E. V. Barsukova. "Correlation of secreted frizzled related protein-4 adipokin expression and expression of fatty liver changes under the conditions of a chronic experiment." Experimental and Clinical Gastroenterology 1, no. 5 (August 19, 2021): 44–48. http://dx.doi.org/10.31146/1682-8658-ecg-189-5-44-48.

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The article highlights the results of a study of a new method for diagnosing non-alcoholic fatty liver disease in a living organism by determining the serum level of the marker Secreted frizzled related protein-4 (SFRP4) with histological confirmation of the results. In a chronic experiment, the parameters of two groups of experimental animals were studied: control and experimental, 15 rats each. The control (reference) group of animals was in the usual feed and drinking mode, the experimental received food with a high content of carbohydrates and fats. The results of biochemical blood tests and autopsy biomaterials on day 180 of the experiment indicated the presence of fatty changes in the liver in the experimental group of animals. The importance of circulating adipokine SFRP4 in the diagnosis of non-alcoholic fatty liver disease (NAFLD) has been confirmed. A histologically confirmed direct correlation of SFRP4 with the degree of liver fibrosis in NAFLD was revealed. The place of SFRP4 in the pathogenesis of non-alcoholic fatty liver damage is explained. It is noted that in case of successful extrapolation of the results of the study on the human body, information will become a successful solution to one of the most pressing problems of modern hepatology.

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Takikawa, Tomonobu, Koji Ohashi, Hayato Ogawa, Naoya Otaka, Hiroshi Kawanishi, Lixin Fang, Yuta Ozaki, et al. "Adipolin/C1q/Tnf-related protein 12 prevents adverse cardiac remodeling after myocardial infarction." PLOS ONE 15, no. 12 (December 4, 2020): e0243483. http://dx.doi.org/10.1371/journal.pone.0243483.

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Background Myocardial infarction (MI) is a leading cause of death worldwide. We previously identified adipolin, also known as C1q/Tnf-related protein 12, as an anti-inflammatory adipokine with protective features against metabolic and vascular disorders. Here, we investigated the effect of adipolin on myocardial remodeling in a mouse model of MI. Methods Male adipolin-knockout (APL-KO) and wild-type (WT) mice were subjected to the permanent ligation of the left anterior descending coronary artery to create MI. Results APL-KO mice exhibited increased ratios of heart weight/body weight and lung weight/body weight after MI compared with WT mice. APL-KO mice showed increased left ventricular diastolic diameter and decreased fractional shortening after MI compared with WT mice. APL-KO mice exhibited increased expression of pro-inflammatory mediators and enhanced cardiomyocyte apoptosis in the post-MI hearts compared with WT mice. Systemic administration of adenoviral vectors expressing adipolin to WT mice after MI surgery improved left ventricular contractile dysfunction and reduced cardiac expression of pro-inflammatory genes. Treatment of cultured cardiomyocytes with adipolin protein reduced lipopolysaccharide-induced expression of pro-inflammatory mediators and hypoxia-induced apoptosis. Treatment with adipolin protein increased Akt phosphorylation in cardiomyocytes. Inhibition of PI3 kinase/Akt signaling reversed the anti-inflammatory and anti-apoptotic effects of adipolin in cardiomyocytes. Conclusion Our data indicate that adipolin ameliorates pathological remodeling of myocardium after MI, at least in part, by its ability to reduce myocardial inflammatory response and apoptosis.

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Christian, Sherri L., Nikitha K. Pallegar, Robert J. Brown, and Alicia M. Viloria-Petit. "Collagen overlays can inhibit leptin and adiponectin secretion but not lipid accumulation in adipocytes." PeerJ 6 (April 27, 2018): e4641. http://dx.doi.org/10.7717/peerj.4641.

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BackgroundWhite adipose tissue (WAT) is essential for energy storage as well as being an active endocrine organ. The secretion of adipokines by adipocytes can affect whole body metabolism, appetite, and contribute to overall health. WAT is comprised of lipid-laden mature adipocytes, as well as immune cells, endothelial cells, pre-adipocytes, and adipose-derived stem cells. In addition, the presence of extracellular matrix (ECM) proteins in WAT can actively influence adipocyte differentiation, growth, and function. Type I collagen is an abundant fibrous ECM protein in WAT that is secreted by developing adipocytes. However, the extent and overall effect of Type I collagen on adipokine secretion in mature adipocytes when added exogenously has not been established.MethodsWe characterized the effects of Type I collagen overlays prepared using two different buffers on adipocyte physiology and function when added at different times during differentiation. In addition, we compared the effect of collagen overlays when adipocytes were cultured on two different tissue culture plastics that have different adherent capabilities. Triglyceride accumulation was analyzed to measure adipocyte physiology, and leptin and adiponectin secretion was determined to analyze effects on adipokine secretion.ResultsWe found that collagen overlays, particularly when added during the early differentiation stage, impaired adipokine secretion from mature adipocytes. Collagen prepared using PBS had a greater suppression of leptin than adiponectin while collagen prepared using HANKS buffer suppressed the secretion of both adipokines. The use of CellBind plates further suppressed leptin secretion. Triglyceride accumulation was not substantially impacted with any of the collagen overlays.DiscussionAdipokine secretion can be selectively altered by collagen overlays. Thus, it is feasible to selectively manipulate the secretion of adipokines by adipocytesin vitroby altering the composition or timing of collagen overlays. The use of this technique could be applied to studies of adipokine function and secretionin vitroas well as having potential therapeutic implications to specifically alter adipocyte functionalityin vivo.

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Pilz, Stefan, Winfried März, and Harald Mangge. "Adiponektin, ein Adipokin mit großem Potenzial für Diagnostik und Therapie des metabolischen Syndroms und assoziierter kardiovaskulärer Erkrankungen / Adiponectin, an adipokine as a promising target for diagnosis and therapy of the metabolic syndrome and associated cardiovascular diseases." LaboratoriumsMedizin 30, no. 4 (January 1, 2006): 187–91. http://dx.doi.org/10.1515/jlm.2006.030.

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Elfassy, Yaelle, Alice Bongrani, Pierre Levy, Frantz Foissac, Soraya Fellahi, Céline Faure, Chloé McAvoy, et al. "Relationships between metabolic status, seminal adipokines, and reproductive functions in men from infertile couples." European Journal of Endocrinology 182, no. 1 (January 2020): 67–77. http://dx.doi.org/10.1530/eje-19-0615.

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Objective Adipokines could be a link between metabolic syndrome (MS) and infertility. While the association between circulating adipokines and fertility has been extensively studied in females, this relationship in males was less investigated, although some adipokines are detectable in seminal plasma (SP). The aim of this study was to determine adipokine levels in blood and SP and to assess the relationships between adipokines, MS and semen parameters in men from infertile couples. Design Male partners of infertile couples referred to four medical French centers were enrolled in years 2013–2016. Methods Subjects (n = 160) aged 18–45 years were assessed for anthropometric, biochemical, sperm, and circulating hormonal parameters. Leptin, adiponectin, resistin, chemerin, visfatin, and IL-6 were measured in serum and SP. Results Infertility duration was higher in men with than without MS. Adipokine concentrations were higher in blood than in SP, except for IL-6 and visfatin. The most striking result was the significant correlation observed between seminal IL-6 and spermatozoid concentration, progressive motility, and sperm vitality. Moreover, while men with MS exhibited an expected lower adiponectinemia, they displayed 2.1-fold higher adiponectin levels in SP than men without MS. Finally, logistic regression analysis showed that BMI, infertility duration, and adiponectin serum/SP ratio were independently associated with MS. Conclusions These results suggest an involvement of seminal adipokines to modulate fertility in men with MS and that seminal IL-6 could play a beneficial role on sperm functionality. Further mechanistic studies are necessary to investigate the precise roles of these adipokines in male reproduction.

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Kotnik, Primoz, Pamela Fischer-Posovszky, and Martin Wabitsch. "RBP4: a controversial adipokine." European Journal of Endocrinology 165, no. 5 (November 2011): 703–11. http://dx.doi.org/10.1530/eje-11-0431.

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Adipose tissue is an endocrine organ secreting biologically active factors called adipokines that act on both local and distant tissues. Adipokines have an important role in the development of obesity-related comorbidities not only in adults but also in children and adolescents. Retinol binding protein 4 (RBP4) is a recently identified adipokine suggested to link obesity with its comorbidities, especially insulin resistance, type 2 diabetes (T2D), and certain components of the metabolic syndrome. However, data, especially resulting from the clinical studies, are conflicting. In this review, we summarize up-to-date knowledge on RBP4's role in obesity, development of insulin resistance, and T2D. Special attention is given to studies on children and adolescents. We also discuss the role of possible confounding factors that should be taken into account when critically evaluating published studies or planning new studies on this exciting adipokine.

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Will, Katja, Judith Kuzinski, Marie-France Palin, Jan-Peter Hildebrandt, and Charlotte Rehfeldt. "A second look at leptin and adiponectin actions on the growth of primary porcine myoblasts under serum-free conditions." Archives Animal Breeding 57, no. 1 (October 29, 2014): 1–10. http://dx.doi.org/10.7482/0003-9438-57-029.

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Abstract. Cross-talk between adipose tissue and skeletal muscle may be mediated in part by adipokines. This study was conducted to elucidate further aspects of a possible role of recombinant adiponectin and leptin in the in vitro growth of primary porcine skeletal muscle cells cultured in energetically balanced, growth factor-supplemented, serum-free medium (GF-SFM). Therefore, the effects of these adipokines on cell number (DNA content), DNA synthesis rate, cell death and on key intracellular signalling molecules were investigated. Short-term adiponectin and leptin treatment decreased DNA synthesis, measured as [3H]-thymidine incorporation, as early as after 4-h exposure (P<0.01), without alterations in DNA content. Both adipokines attenuated the rate of cell death in terms of lactate dehydrogenase (LDH) activity in the culture medium after 48-h treatment (P<0.05). The specific activation of p44/42 MAP kinase (MAPK) was reduced (P<0.05) after 15-min incubation with either adipokine. In conclusion, the early decreases in DNA synthesis of primary porcine myoblasts cultured in GF-SFM in response to adiponectin or leptin are related to p44/42 MAPK signalling and adipokine treatment does not impair cell viability.

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Para, Ioana, Adriana Albu, and Mihai D. Porojan. "Adipokines and Arterial Stiffness in Obesity." Medicina 57, no. 7 (June 25, 2021): 653. http://dx.doi.org/10.3390/medicina57070653.

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Adipokines are active molecules with pleiotropic effects produced by adipose tissue and involved in obesity-related metabolic and cardiovascular diseases. Arterial stiffness, which is a consequence of arteriosclerosis, has been shown to be an independent predictor of cardiovascular morbidity and mortality. The pathogenesis of arterial stiffness is complex but incompletely understood. Adipokines dysregulation may induce, by various mechanisms, vascular inflammation, endothelial dysfunction, and vascular remodeling, leading to increased arterial stiffness. This article summarizes literature data regarding adipokine-related pathogenetic mechanisms involved in the development of arterial stiffness, particularly in obesity, as well as the results of clinical and epidemiological studies which investigated the relationship between adipokines and arterial stiffness.

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Enomoto, Takashi, Koji Ohashi, Rei Shibata, Akiko Higuchi, Sonomi Maruyama, Yasuhiro Izumiya, Kenneth Walsh, Toyoaki Murohara, and Noriyuki Ouchi. "Adipolin/C1qdc2/CTRP12 Protein Functions as an Adipokine That Improves Glucose Metabolism." Journal of Biological Chemistry 286, no. 40 (August 17, 2011): 34552–58. http://dx.doi.org/10.1074/jbc.m111.277319.

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Alanteet, Alaa A., Hala A. Attia, Sameerah Shaheen, Musaed Alfayez, and Bisher Alshanawani. "Anti-Proliferative Activity of Glucagon-Like Peptide-1 Receptor Agonist on Obesity-Associated Breast Cancer: The Impact on Modulating Adipokines’ Expression in Adipocytes and Cancer Cells." Dose-Response 19, no. 1 (January 1, 2021): 155932582199565. http://dx.doi.org/10.1177/1559325821995651.

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Obesity is associated with high risk and poor prognosis of breast cancer (BC). Obesity promotes BC cells proliferation via modulating the production of adipokines, including adiponectin (anti-neoplastic adipokine), leptin (carcinogenic adipokine) and inflammatory mediators. In the present study we investigated the anti-proliferative effects of liraglutide (LG; anti-diabetic and weight reducing drug) on MCF-7 human BC cells cultured in obese adipose tissue-derived stem cells-conditioned medium (ADSCs-CM) and whether this effect is mediated via modulating the adipokines in ADSCs and cancer cells. Proliferation was investigated using AlamarBlue viability test, colony forming assay and cell cycle analysis. Levels and expression of adipokines and their receptors were assayed using ELISA and RT-PCR. LG caused 48% inhibition of MCF-7 proliferation in obese ADSCs-CM, reduced the colony formation and induced G0/G1 phase arrest. LG also decreased the levels of inflammatory mediators, suppressed the expression of leptin, while increased mRNA levels of adiponectin and their receptors in obese ADSCs and cancer cells cultured in obese ADCSs-CM. In conclusion, LG could mitigate BC cell growth in obese subjects; therefore it could be used for clinical prevention and/or treatment of BC in obese subjects. It may assist to improve treatment outcomes and, reduce the mortality rate in obese patients with BC.

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Kovács, Dóra, Fruzsina Fazekas, Attila Oláh, and Dániel Törőcsik. "Adipokines in the Skin and in Dermatological Diseases." International Journal of Molecular Sciences 21, no. 23 (November 28, 2020): 9048. http://dx.doi.org/10.3390/ijms21239048.

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Adipokines are the primary mediators of adipose tissue-induced and regulated systemic inflammatory diseases; however, recent findings revealed that serum levels of various adipokines correlate also with the onset and the severity of dermatological diseases. Importantly, further data confirmed that the skin serves not only as a target for adipokine signaling, but may serve as a source too. In this review, we aim to provide a complex overview on how adipokines may integrate into the (patho) physiological conditions of the skin by introducing the cell types, such as keratinocytes, fibroblasts, and sebocytes, which are known to produce adipokines as well as the signals that target them. Moreover, we discuss data from in vivo and in vitro murine and human studies as well as genetic data on how adipokines may contribute to various aspects of the homeostasis of the skin, e.g., melanogenesis, hair growth, or wound healing, just as to the pathogenesis of dermatological diseases such as psoriasis, atopic dermatitis, acne, rosacea, and melanoma.

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Briffa, Jessica F., Andrew J. McAinch, Philip Poronnik, and Deanne H. Hryciw. "Adipokines as a link between obesity and chronic kidney disease." American Journal of Physiology-Renal Physiology 305, no. 12 (December 15, 2013): F1629—F1636. http://dx.doi.org/10.1152/ajprenal.00263.2013.

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Adipocytes secrete a number of bioactive adipokines that activate a variety of cell signaling pathways in central and peripheral tissues. Obesity is associated with the altered production of many adipokines and is linked to a number of pathologies. As an increase in body weight is directly associated with an increased risk for developing chronic kidney disease (CKD), there is significant interest in the link between obesity and renal dysfunction. Altered levels of the adipokines leptin, adiponectin, resistin, and visfatin can decrease the glomerular filtration rate and increase albuminuria, which are pathophysiological changes typical of CKD. Specifically, exposure of the glomerulus to altered adipokine levels can increase its permeability, fuse the podocytes, and cause mesangial cell hypertrophy, all of which alter the glomerular filtration rate. In addition, the adipokines leptin and adiponectin can act on tubular networks. Thus, adipokines can act on multiple cell types in the development of renal pathophysiology. Importantly, most studies have been performed using in vitro models, with future studies in vivo required to further elucidate the specific roles that adipokines play in the development and progression of CKD.

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Northcott, Josette M., Azadeh Yeganeh, Carla G. Taylor, Peter Zahradka, and Jeffrey T. Wigle. "Adipokines and the cardiovascular system: mechanisms mediating health and disease." Canadian Journal of Physiology and Pharmacology 90, no. 8 (August 2012): 1029–59. http://dx.doi.org/10.1139/y2012-053.

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This review focuses on the role of adipokines in the maintenance of a healthy cardiovascular system, and the mechanisms by which these factors mediate the development of cardiovascular disease in obesity. Adipocytes are the major cell type comprising the adipose tissue. These cells secrete numerous factors, termed adipokines, into the blood, including adiponectin, leptin, resistin, chemerin, omentin, vaspin, and visfatin. Adipose tissue is a highly vascularised endocrine organ, and different adipose depots have distinct adipokine secretion profiles, which are altered with obesity. The ability of many adipokines to stimulate angiogenesis is crucial for adipose tissue expansion; however, excessive blood vessel growth is deleterious. As well, some adipokines induce inflammation, which promotes cardiovascular disease progression. We discuss how these 7 aforementioned adipokines act upon the various cardiovascular cell types (endothelial progenitor cells, endothelial cells, vascular smooth muscle cells, pericytes, cardiomyocytes, and cardiac fibroblasts), the direct effects of these actions, and their overall impact on the cardiovascular system. These were chosen, as these adipokines are secreted predominantly from adipocytes and have known effects on cardiovascular cells.

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Journal articles on the topic 'Adipokin'

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