Relevant bibliographies by topics / Tissue Adipokine

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Academic literature on the topic 'Tissue Adipokine'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Tissue Adipokine"

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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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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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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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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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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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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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Ali, Mohamed M., Chandra Hassan, Mario Masrur, Francesco M. Bianco, Dina Naquiallah, Imaduddin Mirza, Patrice Frederick, et al. "Adipose Tissue Hypoxia Correlates with Adipokine Hypomethylation and Vascular Dysfunction." Biomedicines 9, no. 8 (August 18, 2021): 1034. http://dx.doi.org/10.3390/biomedicines9081034.

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Obesity is characterized by the accumulation of dysfunctional adipose tissues, which predisposes to cardiometabolic diseases. Our previous in vitro studies demonstrated a role of hypoxia in inducing adipokine hypomethylation in adipocytes. We sought to examine this mechanism in visceral adipose tissues (VATs) from obese individuals and its correlation with cardiometabolic risk factors. We propose an involvement of the hypoxia-inducible factor, HIF1α, and the DNA hydroxymethylase, TET1. Blood samples and VAT biopsies were obtained from obese and non-obese subjects (n = 60 each) having bariatric and elective surgeries, respectively. The analyses of VAT showed lower vascularity, and higher levels of HIF1α and TET1 proteins in the obese subjects than controls. Global hypomethylation and hydroxymethylation were observed in VAT from obese subjects along with promoter hypomethylation of several pro-inflammatory adipokines. TET1 protein was enriched near the promotor of the hypomethylated adipokines. The average levels of adipokine methylation correlated positively with vascularity and arteriolar vasoreactivity and negatively with protein levels of HIF1α and TET1 in corresponding VAT samples, serum and tissue inflammatory markers, and other cardiometabolic risk factors. These findings suggest a role for adipose tissue hypoxia in causing epigenetic alterations, which could explain the increased production of adipocytokines and ultimately, vascular dysfunction in obesity.
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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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Vargas, Diana, Jaime Camacho, Juan Duque, Marisol Carreño, Edward Acero, Máximo Pérez, Sergio Ramirez, et al. "Functional Characterization of Preadipocytes Derived from Human Periaortic Adipose Tissue." International Journal of Endocrinology 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/2945012.

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Adipose tissue can affect the metabolic control of the cardiovascular system, and its anatomic location can affect the vascular function differently. In this study, biochemical and phenotypical characteristics of adipose tissue from periaortic fat were evaluated. Periaortic and subcutaneous adipose tissues were obtained from areas surrounding the ascending aorta and sternotomy incision, respectively. Adipose tissues were collected from patients undergoing myocardial revascularization or mitral valve replacement surgery. Morphological studies with hematoxylin/eosin and immunohistochemical assay were performed in situ to quantify adipokine expression. To analyze adipogenic capacity, adipokine expression, and the levels of thermogenic proteins, adipocyte precursor cells were isolated from periaortic and subcutaneous adipose tissues and induced to differentiation. The precursors of adipocytes from the periaortic tissue accumulated less triglycerides than those from the subcutaneous tissue after differentiation and were smaller than those from subcutaneous adipose tissue. The levels of proteins involved in thermogenesis and energy expenditure increased significantly in periaortic adipose tissue. Additionally, the expression levels of adipokines that affect carbohydrate metabolism, such as FGF21, increased significantly in mature adipocytes induced from periaortic adipose tissue. These results demonstrate that precursors of periaortic adipose tissue in humans may affect cardiovascular events and might serve as a target for preventing vascular diseases.
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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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Dissertations / Theses on the topic "Tissue Adipokine"

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DeGroat, Ashley. "The Effect of Alcohol Consumption on Adipokine Secretion." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etd/3425.

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Alcoholic Fatty Liver Disease (AFLD) is caused by excessive alcohol consumption and is a leading cause of liver related mortalities, with currently no treatments available. The goal of this project was to establish the effect of alcohol consumption on adipose tissue-derived secreted factors, adiponectin and C1q TNF Related Proteins 1-3 (CTRP1-3). We propose that excessive alcohol consumption will reduce circulating levels of adiponectin and CTRPs 1-3. Mice were fed a Lieber-Decarli control or alcohol diet for 10-days with a gavage (NIAAA model) or 6-weeks with no gavage (chronic model). Serum and adipose tissue were collected and CTRPs 1-3 and adiponectin levels were examined by immunoblot analysis. Our results indicate that long-term alcohol consumption effects adipokine secretion in a sex specific manner. Further research will be needed to explore the physiological relevance of these findings, to determine if these changes are beneficial to combat the negative effects of excessive alcohol consumption.
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Magon, Vishakha. "Body Composition and Adipokine Levels in Growth Hormone Antagonist Mice." Ohio University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1244481356.

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Ahn, Jinsoo. "Roles of Adipose Tissue-Derived Factors in Adipose Tissue Development and Lipid Metabolism." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1430496153.

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Ameen, G. I. "Investigating the impact of c-Cbl deficiency in adipose tissue : its role in insulin sensitivity and adipokine production." Thesis, University of Liverpool, 2018. http://livrepository.liverpool.ac.uk/3028221/.

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Musick, Adam, Madison Shipley, Fei Tu, Chuanfu Li, Valentin Yakubenko, and Jonathan Peterson. "Effect of Sepsis on Circulating CTRP3 Levels." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/207.

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Effect of Sepsis on Circulating CTRP3 Levels Adam Musick, Madison Shipley, Fei Tu, Chuanfu Li, Valentin Yakubenko, and Jonathan M. Peterson. Adipose tissue is an active endocrine organ which secrets several pro- and anti- inflammatory mediators, collectively called adipokines. Our previous work has identified a novel anti-inflammatory adipokine called C1q TNF Related Protein 3 (CTRP3). Others have previously demonstrated that localized overexpression of CTRP3 protects myocardial tissue from lipopolysaccharide (LPS)-induced sepsis, further supporting the potential protective role of CTRP3. However, endogenous regulation of CTRP3 in response to a sepsis event has not been explored. Further, other adipokines have been identified as diagnostic/prognostic biomarkers for critically ill patients. Therefore, the purpose of this project was to determine the effects of a sepsis event on the circulating CTRP3 levels. METHODS: Gonadal adipose tissue and serum were collected 8 hours after induction of the cecal-puncture and ligation (CLP) model of sepsis or sham control mice. The circulating levels of CTRP3 were quantified by immunoblot analysis. The transcription levels of CTRP3 in adipose tissue were measured by Real-Time PCR. In addition, to explore a potential mechanism for a protective role of CTRP3, thioglycollate-induced peritoneal macrophages were isolated and binding of recombinant CTRP3 was determined by imaging flow cytometry. RESULTS: Circulating CTRP3 levels decreased by approximately 90% compared to sham mice. However, adipose tissue transcription levels of CTRP3 was not difference between CLP and sham mice. Further, imaging flow cytometry demonstrated that CTRP3 binds directly to isolated macrophages. CONCLUSION: The overserved reduction in circulating CTRP3 protein levels and the absence of changes to the CTRP3 transcription, indicate that during sepsis CTRP3 is actively removed from the blood. As CTRP3 binds directly to macrophages and has been previously shown to attenuate LPS-induced macrophage activation these data could indicate that under normal conditions CTRP3 combines with active macrophages to help suppress cytokine overexpression. However, it appears that during sepsis the endogenous CTRP3 levels are quickly depleted. Combine these data support future research to determine if circulating CTRP3 levels are a biomarker indicative of sepsis prognosis and to determine if increasing the circulating levels of CTRP3 could reduce the cytokine storm associated to a sepsis event. Further, as we have demonstrated CTRP3 binds directly to macrophages, future studies are also needed to explore the potential anti-inflammatory mechanism of CTRP3 action on macrophages.
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Zapfe, Luise. "mRNA-Expression von Genen des Fett- und Kohlenhydratstoffwechsels unterschiedlicher Fettlokalisationen bei Kühen." Doctoral thesis, Universitätsbibliothek Leipzig, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-62426.

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Problemstellung: Die Tiergesundheit hat sich bei Milchkühen in den letzten Jahren weltweit negativ entwickelt. Wichtigster Ausdruck dafür ist die auf ca. 2,4 Jahre verkürzte Nutzungsdauer. Dabei spielt das Fettmobilisationssyndrom eine dominante Rolle. Das Fettgewebe ist nicht nur als reiner Energiespeicher, sondern als endokrines stoffwechselaktives Organ anzusehen. Untersuchungen an Menschen und Mäusen haben gezeigt, dass das Fettgewebe in Abhängigkeit von seiner Lokalisation im Körper unterschiedlich auf metabolische und hormonelle Stimuli reagiert. Es gibt Hinweise, dass auch für das Rind ähnliche Differenzen angenommen werden können. Zielstellung: Um die Eigenschaften des bovinen Fettgewebes und seine Rolle im Energiestoffwechsel besser charakterisieren zu können, war das Ziel der vorliegenden Untersuchung, die mRNA-Expressionen ausgewählter für den Fettstoffwechsel relevante Gene im bovinen Fettgewebe an verschiedenen Lokalisationen grundlegend in gesunden Rindern zu untersuchen. Material und Methoden: Die Probenentnahme erfolgte an 12 gesunden Schlachtkühen direkt nach der Tötung, die aufgrund Schwermelkbarkeit oder Unfruchtbarkeit geschlachtet wurden. Das Fettgewebe wurde aus dem Omentum majus, dem Depotfett der Niere, im kaudalen Beckendrittel (retroperitoneales Fett), dem Hüftbereich (subkutanes Fett) und dem Fett an der Herzbasis entnommen. Die Proben wurden in Flüssigstickstoff tiefgefroren, auf Trockeneis transportiert und bis zur Untersuchung bei -70°C gelagert. Die mRNA-Expression für die verschiedenen Gene (Hormonsensitive Lipase (HSL), Lipoproteinlipase (LPL), Fettsäuresynthase (FASN), Leptin, Adiponektin, Retinolbindungsprotein 4 (RBP4), Tumornekrosefaktor  (TNF) und Interleukin 6 (IL-6), Fettsäurebindungsproteine (FABP3, 4 und 5) und Glukosetransporter 4 (GLUT4)) , wurden mit einer quantitativen real time (RT)-PCR gemessen. Ergebnisse: Die mRNA-Expressionen der verschiedenen oben genannten Gene, ausgenommen IL-6 und FABP3, sind im bovinen Fettgewebe nachweisbar. Die mRNA-Expressionen unterschieden sich in den einzelnen Fettdepots nicht signifikant. Ausnahme hierbei bildete RBP4, dessen mRNA im pericardialen Fett signifikant höher exprimiert war als im subkutanen und omentalen Depot. Die mRNA-Expression des subkutanen, omentalen, perirenalen und pericardialen Fettdepots korrelierten signifikant positive untereinander. Schlussfolgerung: Die mRNA-Expressionen der in den Fettstoffwechsel involvierten und untersuchten Gene gesunder Rinder waren nachweisbar, unterschieden sich jedoch nicht signifikant von einander mit Ausnahme der RBP4 mRNA. Die positiven signifikanten Korrelationen zwischen dem subkutanen, omentalen, perirenalen und pericardialen Fettlokalisationen und gleichmäßigen Expressionen innerhalb der Gewebe deuten auf eine einheitliche Fettmetabolismus des gesamten Körpers. Verglichen mit Ergebnissen der Humanmedizin sind nur wenige Übereinstimmungen (HSL, LPL, GLUT4,TNF) zu eruieren. Weitere Studien mit gesunden Tieren im Vergleich zu erkrankten Rindern müssen klären, ob eine mögliche Verschiebung der mRNA-Konzentrationen auf das Fettmobilisationssyndrom hinweisen
Purpose: Over the last years, the situation of animal health concerning dairy cows has developed worldwide in an adverse way. Most important indicator is the shortened useful life of approx. 2.4 years. The fat mobilization syndrome plays a dominant role in this process. Apparently, fatty tissue does not only serve as a mere energy reservoir, but also as an endocrin organ with metabolic activity. Researches on humans and mice have shown fatty tissue to react on metabolic and hormonal stimuli in different ways, depending on its body localization. There are dues to anticipate, similar differences in cattle. Objectives: In order to better characterize the attributes of bovine fatty tissue and its purpose in metabolism, the present study aims examine basically the expression of mRNA in selected genes which are important for lipid metabolism in bovine fatty tissue of different localizations in healthy cattle. Methods and material: Samples where taken from twelve carcasses of healthy dairy cows slaughtered for reason of difficult milking or infertility directly after killing. Fatty tissue was taken from omentum major, kidney capsula, caudal pelvis area (retroperiteonal fat), hip area (subcutaneous fat), and cardiac base. It was instantly quick-freezed in liquid nitrogen, put on dry ice while transporting, and stored at -70°C until analysis. The expression of mRNA of different genes (hormone-sensitive lipase (HSL), lipoproteine lipase (LPL), fatty acid synthase (FASN), fatty acid binding proteine (FABP3,4 and 5), retinol binding proteine 4 (RBP4), adiponectine, glucose transporter 4 (GLUT4), leptin, interleukin-6 (IL-6), and tumor necrosis factor a (TNFα) was measured by means of a quantitative real-time (RT)-PCR. Results: The mRNA-expressions of all these different genes except IL-6 and FABP3 were detected in bovine fatty tissue. The differences of mRNA-expression between sample localization were not statistically significant. RBP4 was excepted, which mRNA showed a significantly higher expression in pericardial fat than in subcutaneous and omental fat, respectively. The correlation between mRNA-expressions of subcutaneous, omental, pericardial and perirenal fat was significant. Conclusions: The mRNA-expression of examined genes being involved in fatty tissue metabolism, were detected in healthy cattle, but were not significantly different, except RBP4. Significantly positive correlations between subcutaneous, omental, perirenal and pericardial localization and consistent expression indicate an integrative metabolism of the whole body. Compared to results of the human medicine only few analogies (HSL, LPL, GLUT4, TNF) were found. Further studies comparing healthy and diseased cattle will have to prove, if possible displacements of the mRNA-level can indicate the fat mobilization syndrome being present
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Neves, Karla Bianca. "Efeito da adipocina chemerin sobre a reatividade vascular: análise em aortas de rato." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/60/60138/tde-27092012-094715/.

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Embora seja na obesidade onde se observa hipertrofia e hiperplasia dos adipócitos e aumento da síntese e liberação de adipocinas, condição associada com resistência à insulina e disfunção endotelial, é de suma importância entender os efeitos biológicos de adipocinas, mais especificamente da adipocina chemerin, em condições não patológicas. Os mecanismos pelos quais as citocinas liberadas pelo tecido adiposo podem interferir na função vascular ainda não estão totalmente esclarecidos. Além disso, praticamente não se conhecem os efeitos da citocina/adipocina chemerin sobre a função vascular. Levando-se em consideração que o receptor para chemerin está presente no músculo liso vascular e no endotélio, este trabalho avaliou a atividade biológica e celular desta adipocina sobre a vasculatura de animais não obesos. Investigou-se os efeitos produzidos por esta citocina na reatividade vascular, bem como os mecanismos pelos quais ela modifica a função vascular em animais não obesos. A hipótese deste trabalho é que chemerin aumenta a reatividade vascular a estímulos constritores de endotelina-1 (ET-1) e fenilefrina (PhE) e diminui a vasodilatação induzida pela acetilcolina (ACh) e nitroprussitao de sódio (NPS). Nossos objetivos específicos incluíram determinar: 1) se chemerin promove alterações na reatividade vascular; 2) se as alterações de reatividade vascular promovidas por chemerin são mediadas por modificações da função das células endoteliais ou células de músculo liso vascular; 3) quais vias de sinalização (foco na via das MAPKs) estão sendo modificadas por chemerin e como elas contribuem para as alterações de reatividade vascular produzidas por esta citocina. Nosso estudo demonstrou que a adipocina chemerin possui atividade biológica e celular em aortas de ratos não obesos. Chemerin aumentou respostas vasculares a estímulos contráteis (ET-1 e PhE), atuando tanto no endotélio quanto diretamente em células do músculo liso vascular. O aumento da resposta a estímulos contráteis à ET-1 e PhE foi mediado pela via MEK-ERK1/2, COX-1 e COX-2 e aumento da expressão dos receptores para ET-1, ETA e ETB. Além disso, esta adipocina diminuiu a vasodilatação induzida pela ACh, por meio do desacoplamento da eNOS e aparente envolvimento de estresse oxidativo, e pelo NPS, através de ação sobre a guanilato ciclase. Nossos estudos poderão contribuir para um melhor entendimento sobre o papel dos fatores liberados pelo tecido adiposo visceral sobre a função vascular e, consequentemente, sobre as alterações vasculares presentes na obesidade e patologias associadas.
Although hypertrophy and hyperplasia of adipocytes as well as increased synthesis and release of adipokines are commonly observed in obesity, a condition associated with insulin resistance and endothelial dysfunction, it is extremely important to understand the biological effects of adipokines, or more specifically of the adipokine chemerin, in non-pathological conditions,. The mechanisms by which cytokines released by the adipose tissue may interfere with vascular function are not yet fully understood. Furthermore, the effects of the cytokine/adipokine chemerin on vascular function are not known. Considering that the chemerin receptor is expressed by vascular smooth muscle and endothelial cells, this study investigated the effects produced by this cytokine in vascular reactivity, as well as the mechanisms by which it modifies vascular function in non-obese animals. Our working hypothesis is that chemerin enhances vascular reactivity to constrictor stimuli, such as endothelin-1(ET-1) and phenylephrine (Phe), and decreases the vasodilation induced by acetylcholine (ACh) and sodium nitroprussiate (SNP). Our specific aims were to determine: 1) whether chemerin induces changes in vascular reactivity, 2) if the alterations of vascular reactivity induced by chemerin are mediated by changes in the function of endothelial cells or vascular smooth muscle cells, 3) which signaling pathways (focus on the MAPKs pathway) are being modified by chemerin and how they contribute to changes in vascular reactivity produced by this cytokine. Our study showed that the adipokine chemerin has biological and cellular activity in aortas from non-obese rats. Chemerin increased vascular responses to contractile stimuli (ET-1 and PhE), producing effects both in the endothelial and vascular smooth muscle cells. The increased contractile responses to ET-1 and PhE were mediated via activation of MEK-ERK1/2, COX-1 and COX-2 and increased expression of the ETA and ETB receptors. Furthermore, this adipokine reduced the vasodilation induced by ACh via eNOS uncoupling and oxidative stress, and by SNP, via effects in the enzyme guanylate cyclase. Our studies may contribute to a better understanding of the role of factors released by the visceral adipose tissue on vascular function and, consequently, on the vascular lesions in obesity and obesity-associated diseases.
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Fazenda, Maria Inês Nunes. "Estudo da relação entre a obesidade e a hipertensão em cães." Master's thesis, Universidade Técnica de Lisboa. Faculdade de Medicina Veterinária, 2010. http://hdl.handle.net/10400.5/3530.

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Dissertação de Mestrado Integrado em Medicina Veterinária
Nos países desenvolvidos, a prevalência do excesso de peso e da obesidade tem vindo a aumentar a uma taxa alarmante, tanto em humanos como na população canina. O termo “epidemia” é já comummente aplicado a esta realidade. Para os Médicos Veterinários, a obesidade é uma das condições patológicas mais simples de diagnosticar, a maioria fazendo-o unicamente através da inspecção visual. Contudo, a subjectividade inerente a esta práctica faz deste um método pouco útil numa perspectiva clínica. Estimar a percentagem de massa gorda é o procedimento mais exacto para um diagnóstico de obesidade. A obesidade não se resume apenas a um estado patológico de excesso de peso. A Organização Mundial da Saúde define a obesidade humana como a acumulação excessiva de gordura no organismo que induz consequências nefastas para a saúde. Tal como nos humanos, os cães são também susceptíveis às múltiplas e variadas consequências na saúde devido à obesidade, entre elas a hipertensão arterial sistémica. Os mecanismos pelos quais a obesidade induz hipertensão não estão completamente esclarecidos, mas são vários os mecanismos propostos que incluem a retenção anormal de sódio, excesso de actividade do sistema nervoso simpático, hiperactivação do sistema renina-angiotensina-aldosterona, alterações vasculares, secreção de factores de estimulação mineralocorticóide e acumulação intra-abdominal de gordura. Em 1994, a descoberta da leptina, um factor de saciedade produzido predominantemente pelo tecido adiposo e essencial no controlo do apetite e do balanço energético, levou a uma reclassificação do tecido adiposo como um órgão endócrino. O termo “adipocina” foi universalmente adoptado para descrever uma proteína que é secretada nos (e sintetizada pelos) adipócitos. Esta pode actuar localmente (efeito autócrino ou parácrino) e sistemicamente (efeito endócrino), influenciando uma variedade de sistemas biológicos. A implicação de diversas adipocinas na modulação de algumas alterações neurohormonais que conduzem ao aumento da pressão arterial sistémica na obesidade, foca a importância do tecido adiposo como órgão endócrino. Foi realizado um estudo clínico com uma amostra de 30 cães, divididos em dois grupos, de acordo com a classificação da condição corporal segundo o modelo do índice de massa corporal canino proposto por Muller et al. (2008): Grupo O – obesos; Grupo EP – excesso de peso. Da medição da pressão arterial, utilizando o método Doppler modelo 811-BL (Parks Medical Electronics), foram registados aumentos na pressão sistólica em cães com excesso de peso e obesidade, com uma frequência de hipertensão de 43,3%.
ABSTRACT - Study of the relation between obesity and systemic arterial hypertension - In developed countries, the prevalence of overweight and obesity has been increasing at an alarming rate, in both humans and canine population. The term “epidemic” is now commonly applied to this reality. For Veterinarians, obesity is one of the pathological conditions easier to be diagnosed, the majority doing so only by visual inspection; however, the subjectivity inherent in this practice makes this a useless method in a clinical perspective. Estimate the percentage of fat mass is the most accurate procedure for a diagnosis of obesity. Obesity is not just a pathological condition of excess weight. The World Health Organization defines human obesity as an excessive accumulation of fat in the body that induces adverse effects on health. As in humans, dogs are also liable to multiple and varied effects on health due to obesity, including systemic arterial hypertension. The mechanisms by which obesity induces hypertension are not completely understood, but there are several proposed mechanisms including abnormal sodium retention, overactivity of the sympathetic nervous system, hyperactivation of the renin-angiotensin-aldosterone system, vascular disorders, secretion of mineralocorticoid-releasing factors and accumulation of intra-abdominal fat mass. In 1994, the discovery of leptin, a satiety factor produced predominantly by adipose tissue and essential in controlling appetite and energy balance, led to the reclassification of adipose tissue as an endocrine organ. The term “adipokine” was universally adopted to describe a protein that is secreted from (and synthesised by) adipocytes. It can act locally (autocrine or paracrine effect) and systemically (endocrine effect), influencing multiple biological systems. The implication of several adipokines in the modulation of some neurohormonal changes that led to increased systemic blood pressure in obesity focuses the importance of adipose tissue as an endocrine organ. It was conducted a clinical study with a sample of 30 dogs, divided into two groups according to the classification of body condition in the canine body mass index model proposed by Muller et al. (2008): Group O – obese; group EP – overweight. When measuring blood pressure using the Doppler method model 811-BL (Parks Medical Electronics), it has been recorded an increase in blood pressure in overweight and obese dogs, with a hypertension frequency of 43, 3%.
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Axelsson, Jonas. "Fat tissue, adipokines and clinical complications of chronic kidney disease /." Stockholm : Department of Clinical Science, Intervention and Technology, Divisions of Renal Medicine and Baxter Novum, Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7140-653-0/.

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Riesco, Acevedo David Gerardo. "New adipokines vaspin and omentin, circulating levels, gene expression in adipose tissue and relationship of circulating levels with nonalcoholic fatty liver disease." Doctoral thesis, Universitat Rovira i Virgili, 2016. http://hdl.handle.net/10803/379550.

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L'obesitat és una situació d'excés de massa de greix corporal que pot conduir a la síndrome metabòlica (SM). Omentin es produeix i és secretada pel TAV i pot tenir un paper antiinflamatori important en estats pro-inflamatoris. La disminució dels nivells circulants i de l'expressió génica de vaspina s'associa a empitjorament de la diabetis i la pèrdua de pes corporal. Simultàniament a l'augment de la incidència de l'obesitat i la diabetis, augmenta la prevalença de l'hepatopatia grassa no alcohòlica (HGNA). La prova gold standard per al diagnòstic histològic és la biòpsia hepàtica. Atès que és una tècnica invasiva, hi ha un interès en el desenvolupament de biomarcadors no invasius per a la identificació d'esteatohepatitis. Els objectius van ser analitzar els nivells circulants d’omentin i vaspina, la seva expressió gènica en teixit adipós en dones amb obesitat mórbida (OM) enfront de dones amb normopès. Es va examinar la seva associació amb les diferents variables bioquímiques, així com l'ús clínic dels nivells circulants d’omentin i vaspina com a potencials biomarcadors de la presència de HGNA. Primer, es van analitzar els nivells circulants i expressió génica de vaspina i omentina en individus amb pes normal i OM. Després, es van analitzar 40 mostres de fetge de les dones amb OM. Els resultats mostraren disminució dels nivells circulants d’omentin a l'OM, presentant correlació inversa amb els paràmetres glucèmics i amb el SM. L'expressió d’Omentin estava disminuïda en OM. En contrast, els nivells de vaspina en els OM no van ser diferents dels controls, amb una correlació inversa amb els nivells de lipocalina-2 i IL6. L'expressió de vaspina va ser significativament més gran en els OM. Quant a l’HGNA, els resultats van objectivar augment dels nivells circulants d’omentin en els pacients amb EHNA respecte l’esteatosi simple. D'altra banda, el rendiment dels nivells d’omentin per al diagnòstic d’EHNA va mostrar una excel•lent AUROC. Les principals conclusions són que omentin sembla exercir un efecte protector front l'obesitat, mentre que els seus nivells circulants augmenten paradoxalment en els pacients amb EHNA.
La obesidad es una situación de exceso de masa grasa corporal que puede conducir al síndrome metabólico (SM). Omentin se produce y es secretada por el TAV y puede tener un papel antiinflamatorio importante en estados pro-inflamatorios. La disminución de los niveles circulantes y de la expresión génica de vaspina se asocia a empeoramiento de la diabetes y la pérdida de peso corporal. Simultaneamente al aumento de la incidencia de la obesidad y la diabetes, aumenta la prevalencia de la hepatopatía grasa no alcohólica (HGNA). Dado que la biopsia hepática es una técnica invasiva, existe un interés en el desarrollo de biomarcadores no invasivos para la identificación de esteatohepatitis. Los objetivos fueron analizar los niveles circulantes de omentin y vaspina, su expresión génica en el tejido adiposo en mujeres con obesidad mórbida frente a mujeres con peso normal. Se examinó su asociación con las variables bioquímicas así como el uso clínico de los niveles circulantes de omentin y vaspina como potenciales biomarcadores de la presencia de la HGNA. Primero, se analizaron los niveles circulantes y la expresión génica de vaspina y omentin en sujetos con normopeso y obesidad mórbida (OM). Después, se analizaron 40 muestras de hígado de las mujeres con OM. Los resultados mostraron disminución de los niveles de omentin en la OM, presentando correlación inversa con los parámetros glucémicos y el SM. La expresión de Omentin estaba disminuida en la OM. En contraste, los niveles séricos de vaspina en los OM no fueron diferentes de los controles, con una correlación inversa con los niveles de lipocalina-2 e IL6. La expresión de vaspina fue mayor en los OM. En cuanto a la HGNA, demostramos un aumento de los niveles circulantes de omentin en los pacientes con EHNA respecto a aquellos con ES. El rendimiento de los niveles de omentin para el diagnóstico de EHNA mostró una excelente AUROC. Las conclusiones son que omentin parece ejercer un efecto protector frente la obesidad, mientras que sus niveles circulantes aumentan paradójicamente en los pacientes con EHNA.
Obesity is a situacion with excess of body fat mass that can lead to metabolic syndrome. Omentin is produced and secreted by VAT and may have an important anti-inflammatory role in pro-inflammatory states. Decreases in vaspin expression and plasma levels accompany worsening of diabetes and body weight loss. In parallel with increased incidence of obesity and type 2 diabetes, the prevalence of non-alcoholic fatty liver disease (NAFLD) is growing worldwide. Because liver biopsy is an invasive procedure there is strong interest in developing non-invasive biomarkers for identifying steatohepatitis in NAFLD. The main objectives of this doctoral thesis were to analyze omentin and vaspin gene expression in VAT and SAT as well as circulating levels in a group of morbidly obese women versus normal-weight control women and its associations with the clinical-biochemical variables as well as the clinical use of circulating omentin and vaspin levels as biomarkers for the presence of NAFLD. First, we analyzed the circulating levels and gene expression of vaspin and omentin in normal-weight and morbidly obese (MO) subjects. Then, we analyzed 40 liver samples from MO women. We showed lower circulating omentin levels in the MO, correlating inversely with glucidic metabolism parameters and also with MetS. Omentin mRNA expression in VAT was reduced in MO. In contrast, serum vaspin levels in the MO were not significantly different from those in the controls, correlating inversely with lipocalin-2 and interleukin-6 levels. Vaspin mRNA expression was significantly higher in the MO. Regarding NAFLD, we revealed increased circulating omentin levels in NASH patients in comparison with SS. The performance of omentin in diagnosing NASH showed an excellent AUROC. In conclusion, the main findings of this doctoral thesis are that omentin appears to exert a protective effect against obesity, whereas circulating omentin levels are paradoxically increased in patients with NASH.
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Books on the topic "Tissue Adipokine"

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Preedy, Victor R., and Ross J. Hunter. Adipokines. Boca Raton, FL: CRC Press, 2011.

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Fantuzzi, Giamila, and Carol Braunschweig, eds. Adipose Tissue and Adipokines in Health and Disease. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-770-9.

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Fantuzzi, Giamila, and Theodore Mazzone, eds. Adipose Tissue and Adipokines in Health and Disease. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-370-7.

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Preedy, Victor R., and Ross J. Hunter. Adipokines. Taylor & Francis Group, 2016.

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Preedy, Victor R., and Ross J. Hunter. Adipokines. Taylor & Francis Group, 2016.

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Adipokines. Taylor & Francis Group, 2017.

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Neumann, Elena, Klaus Frommer, and Ulf Müller-Ladner. Acute-phase responses and adipocytokines. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0058.

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Adipokines, also called adipocytokines, are highly bioactive substances mainly expressed by adipose tissue. In addition to adipocytes, different cell types resident in various tissues produce adipokines under pathophysiological conditions. Adipokines include a growing number of pluripotent molecules such as adiponectin, resistin, leptin, and visfatin. Since distinct effects of adipokines on inflammation have been described, their influence on the (innate) immune system has been investigated in rheumatology, gastroenterology, and endocrinology. This review gives an overview on the current knowledge about the influence which adipokines have on the immune system and chronic inflammation in rheumatic diseases.
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Fantuzzi, Giamila, and Carol Braunschweig. Adipose Tissue and Adipokines in Health and Disease. Humana, 2016.

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Fantuzzi, Giamila, Theodore Mazzone, A. P. Goldberg, and S. K. Fried. Adipose Tissue and Adipokines in Health and Disease. Humana, 2011.

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Fantuzzi, Giamila, and Carol Braunschweig. Adipose Tissue and Adipokines in Health and Disease. Humana, 2014.

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Book chapters on the topic "Tissue Adipokine"

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Bastard, Jean-Philippe, Camille Vatier, and Bruno Fève. "Adiponectin: An Adipokine with Multiple Faces." In Physiology and Physiopathology of Adipose Tissue, 187–200. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-8178-0343-2_13.

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DeClercq, Vanessa, Danielle Stringer, Ryan Hunt, Carla G. Taylor, and Peter Zahradka. "Adipokine Production by Adipose Tissue: A Novel Target for Treating Metabolic Syndrome and its Sequelae." In Metabolic Syndrome, 73–131. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470910016.ch4.

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Villarroya, Francesc, Aleix Gavaldà-Navarro, Marion Peyrou, Joan Villarroya, and Marta Giralt. "Brown Adipokines." In Brown Adipose Tissue, 239–56. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_119.

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Clément, Karine. "Adipokines, Inflammation, and Obesity." In Adipose Tissue in Health and Disease, 265–81. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2010. http://dx.doi.org/10.1002/9783527629527.ch14.

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Bastard, J. P., C. Vatier, and B. Fève. "L’adiponectine : une adipokine aux multiples visages." In Physiologie et physiopathologie du tissu adipeux, 189–203. Paris: Springer Paris, 2013. http://dx.doi.org/10.1007/978-2-8178-0332-6_13.

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Wieser, Verena, Alexander R. Moschen, and Herbert Tilg. "Adipose Tissue Inflammation." In Adipose Tissue and Adipokines in Health and Disease, 93–103. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-770-9_7.

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Paz-Filho, Gilberto, Ameet Kumar Mishra, and Julio Licinio. "Adipokines: Soluble Factors from Adipose Tissue Implicated in Cancer." In Adipose Tissue and Cancer, 71–97. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7660-3_5.

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Isler, Karin. "Adipose Tissue in Evolution." In Adipose Tissue and Adipokines in Health and Disease, 3–13. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-770-9_1.

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Baranova, Ancha, Aybike Birerdinc, and Zobair M. Younossi. "Adipokines in Nonalcoholic Fatty Liver Disease." In Adipose Tissue and Adipokines in Health and Disease, 249–83. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-770-9_17.

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Beylot, Michel. "Metabolism of White Adipose Tissue." In Adipose Tissue and Adipokines in Health and Disease, 33–52. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-770-9_3.

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Conference papers on the topic "Tissue Adipokine"

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Hayes, Amanda L., Michael J. Rosen, Jeffrey A. Kern, and Sanjay Patel. "Obstructive Sleep Apnea And Tissue Adipokine Levels." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2540.

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Llanos, Adana A., Ramona G. Dumitrescu, Catalin Marian, Hyunuk Seung, Kepher Makambi, Scott L. Spear, Bhaskar V. S. Kallakury, Jo Freudenheim, and Peter G. Shields. "Abstract A88: Differences in plasma and breast tissue adipokine levels by race and obesity status." In Abstracts: AACR International Conference on the Science of Cancer Health Disparities‐‐ Sep 30-Oct 3, 2010; Miami, FL. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1055-9965.disp-10-a88.

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Llanos, Adana A., Theodore M. Brasky, Kepher H. Makambi, Jo L. Freudenheim, and Peter G. Shields. "Abstract 116: Association between variation in LEP A19G and adipokine concentrations in plasma and breast tissues." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-116.

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Bulumbaeva, D. M., V. V. Klimontov, N. P. Bgatova, Yu S. Taskaeva, O. N. Fazullina, N. B. Orlov, V. I. Konenkov, M. Yu Soluyanov, and S. V. Savchenko. "Serum Levels of Adipokines in Type 2 Diabetic Subjects: the Relationships with Adipose Tissue Distribution and Microvasculature." In 2018 11th International Multiconference Bioinformatics of Genome Regulation and Structure\Systems Biology (BGRS\SB). IEEE, 2018. http://dx.doi.org/10.1109/csgb.2018.8544862.

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Frille, Armin, Hartmut Kuhn, Thomas Ebert, Hans-Juergen Seyfarth, and Hubert Wirtz. "The influence of non-small cell lung cancer cells on the expression of adipokines in brown adipose tissue." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2845.

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Frille, A., H. Kuhn, T. Ebert, HJ Seyfarth, and H. Wirtz. "Non-small cell lung cancer cells induce the expression of adipokines in brown adipose tissue in the context of cancer cachexia." In 60. Kongress der Deutschen Gesellschaft für Pneumologie und Beatmungsmedizin e. V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678077.

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Akawi, Nadia, Antonio Checa, Christos Kotanidis, Ioannis Akoumianakis, Evangelia Daskalakis, Craig Wheelock, and Charalambos Antoniades. "BS32 Untargeted metabolomics interrogation of adipose tissue secretome from participants of the oxford cohort for heart, vessels & fat highlighted ceramides as potential adipokines modulating vascular redox signalling in cardiovascular disease." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.195.

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