To see the other types of publications on this topic, follow the link: Tissue Adipokine.
Journal articles on the topic 'Tissue Adipokine'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Tissue Adipokine.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
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.
Full textAbstract:
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.
2
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.
Full textAbstract:
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.
3
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.
Full textAbstract:
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.
4
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.
Full textAbstract:
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.
5
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.
Full textAbstract:
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
6
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.
Full textAbstract:
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.
7
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.
Full textAbstract:
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.
8
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.
Full textAbstract:
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.
9
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.
Full textAbstract:
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.
10
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.
Full textAbstract:
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.
11
Bremer, Andrew A., and Ishwarlal Jialal. "Adipose Tissue Dysfunction in Nascent Metabolic Syndrome." Journal of Obesity 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/393192.
Full textAbstract:
The metabolic syndrome (MetS) confers an increased risk for both type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). Moreover, studies on adipose tissue biology in nascent MetS uncomplicated by T2DM and/or CVD are scanty. Recently, we demonstrated that adipose tissue dysregulation and aberrant adipokine secretion contribute towards the syndrome’s low-grade chronic proinflammatory state and insulin resistance. Specifically, we have made the novel observation that subcutaneous adipose tissue (SAT) in subjects with nascent MetS has increased macrophage recruitment with cardinal crown-like structures. We have also shown that subjects with nascent MetS have increased the levels of SAT-secreted adipokines (IL-1, IL-6, IL-8, leptin, RBP-4, CRP, SAA, PAI-1, MCP-1, and chemerin) and plasma adipokines (IL-1, IL-6, leptin, RBP-4, CRP, SAA, and chemerin), as well as decreased levels of plasma adiponectin and both plasma and SAT omentin-1. The majority of these abnormalities persisted following correction for increased adiposity. Our data, as well as data from other investigators, thus, highlight the importance of subcutaneous adipose tissue dysfunction in subjects with MetS and its contribution to the proinflammatory state and insulin resistance. This adipokine profile may contribute to increased insulin resistance and low-grade inflammation, promoting the increased risk of T2DM and CVD.
12
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.
Full textAbstract:
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.
13
Golbidi, Saeid, and Ismail Laher. "Exercise Induced Adipokine Changes and the Metabolic Syndrome." Journal of Diabetes Research 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/726861.
Full textAbstract:
The lack of adequate physical activity and obesity created a worldwide pandemic. Obesity is characterized by the deposition of adipose tissue in various parts of the body; it is now evident that adipose tissue also acts as an endocrine organ capable of secreting many cytokines that are though to be involved in the pathophysiology of obesity, insulin resistance, and metabolic syndrome. Adipokines, or adipose tissue-derived proteins, play a pivotal role in this scenario. Increased secretion of proinflammatory adipokines leads to a chronic inflammatory state that is accompanied by insulin resistance and glucose intolerance. Lifestyle change in terms of increased physical activity and exercise is the best nonpharmacological treatment for obesity since these can reduce insulin resistance, counteract the inflammatory state, and improve the lipid profile. There is growing evidence that exercise exerts its beneficial effects partly through alterations in the adipokine profile; that is, exercise increases secretion of anti-inflammatory adipokines and reduces proinflammatory cytokines. In this paper we briefly describe the pathophysiologic role of four important adipokines (adiponectin, leptin, TNF-α, and IL-6) in the metabolic syndrome and review some of the clinical trials that monitored these adipokines as a clinical outcome before and after exercise.
14
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.
Full textAbstract:
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.
15
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.
Full textAbstract:
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.
16
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.
Full textAbstract:
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.
17
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.
Full textAbstract:
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.
18
Ziviello, Francesca, Grazia Pellegrino, Stefano Conte, Giovanni Cimmino, Alessandro Giaquinto, Francesco Pacifico, Antonio Leonardi, Paolo Golino, Bruno Trimarco, and Plinio Cirillo. "The adipokine apelin-13 induces expression of prothrombotic tissue factor." Thrombosis and Haemostasis 113, no. 02 (March 2015): 363–72. http://dx.doi.org/10.1160/th14-05-0451.
Full textAbstract:
SummaryAdipocytes are cells able to produce and secrete several active substances (adipokines) with direct effects on vascular cells. Apelin, one of the most recently identified adipokines has been studied in cardiovascular system physiology in regard to vessel vasodilation and myocardial contraction, but it has not yet completely characterised for its pathophysiological role in cardiovascular disease and especially in acute coronary syndromes (ACS). Several studies have indicated that tissue factor (TF) plays a pivotal role in the pathophysiology of ACS by triggering the formation of intracoronary thrombi following endothelial injury. This study investigates the effects of apelin 12 and apelin 13 on TF in human umbilical endothelial cells (HUVECs) and monocytes. Cells were stimulated with increasing concentrations of apelin 12 or apelin 13 and then processed to evaluate TF-mRNA levels by real-time PCR as well as TF expression/activity by FACS analysis and pro-coagulant activity. Finally, a potential molecular pathway involved in modulating this phenomenon was investigated. We demonstrate that apelin 13 but not apelin 12 induces transcription of mRNA for TF. In addition, we show that this adipokine promotes surface expression of TF that is functionally active. Apelin 13 effects on TF appear modulated by the activation of the G-protein-transcription factor nuclear factor (NF)-ΚB axis since G-protein inhibitors suppressed NF-ΚB mediated TF expression. Data of the present study, although in vitro, indicate that apelin-13, induces a procoagulant phenotype in HUVECs and monocytes by promoting TF expression. These observations support the hypothesis that this adipokine might play a relevant role as an active partaker in athero-thrombotic disease.
19
Moreno-Aliaga, María J., Silvia Lorente-Cebrián, and J. Alfredo Martínez. "Regulation of adipokine secretion byn-3 fatty acids." Proceedings of the Nutrition Society 69, no. 3 (June 14, 2010): 324–32. http://dx.doi.org/10.1017/s0029665110001801.
Full textAbstract:
Obesity leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome. White adipose tissue (WAT) metabolism and WAT-derived factors (fatty acids and adipokines) play an important role in the development of these metabolic disturbances. In fact, dysregulated adipokine secretion from the expanded WAT of obese individuals contributes to the development of systemic low-grade inflammation, insulin resistance and metabolic syndrome. Then-3 PUFA EPA and DHA have been widely reported to have protective effects in a range of chronic inflammatory conditions including obesity. In fact,n-3 PUFA have been shown to ameliorate low-grade inflammation in adipose tissue associated with obesity and up-regulate mitochondrial biogenesis and induce beta-oxidation in WAT in mice. Moreover, the ability ofn-3 PUFA to regulate adipokine gene expression and secretion has been observed bothin vitroandin vivoin rodents and human subjects. The present article reviews: (1) the physiological role of adiponectin, leptin and pre-B cell colony-enhancer factor/visfatin, three adipokines with immune-modulatory properties involved in the regulation of metabolism and insulin sensitivity and (2) the actions ofn-3 PUFA on these adipokines focusing on the underlying mechanisms and the potential relationship with the beneficial effects of these fatty acids on obesity-associated metabolic disorders. It can be concluded that the ability ofn-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of WAT metabolism and the secretion of bioactive adipokines including leptin, adiponectin and visfatin.
20
Sowka, Adrian, and Pawel Dobrzyn. "Role of Perivascular Adipose Tissue-Derived Adiponectin in Vascular Homeostasis." Cells 10, no. 6 (June 12, 2021): 1485. http://dx.doi.org/10.3390/cells10061485.
Full textAbstract:
Studies of adipose tissue biology have demonstrated that adipose tissue should be considered as both passive, energy-storing tissue and an endocrine organ because of the secretion of adipose-specific factors, called adipokines. Adiponectin is a well-described homeostatic adipokine with metabolic properties. It regulates whole-body energy status through the induction of fatty acid oxidation and glucose uptake. Adiponectin also has anti-inflammatory and antidiabetic properties, making it an interesting subject of biomedical studies. Perivascular adipose tissue (PVAT) is a fat depot that is conterminous to the vascular wall and acts on it in a paracrine manner through adipokine secretion. PVAT-derived adiponectin can act on the vascular wall through endothelial cells and vascular smooth muscle cells. The present review describes adiponectin’s structure, receptors, and main signaling pathways. We further discuss recent studies of the extent and nature of crosstalk between PVAT-derived adiponectin and endothelial cells, vascular smooth muscle cells, and atherosclerotic plaques. Furthermore, we argue whether adiponectin and its receptors may be considered putative therapeutic targets.
21
Fain, John N. "Release of Inflammatory Mediators by Human Adipose Tissue Is Enhanced in Obesity and Primarily by the Nonfat Cells: A Review." Mediators of Inflammation 2010 (2010): 1–20. http://dx.doi.org/10.1155/2010/513948.
Full textAbstract:
This paper considers the role of putative adipokines that might be involved in the enhanced inflammatory response of human adipose tissue seen in obesity. Inflammatory adipokines [IL-6, IL-10, ACE, TGFβ1, TNFα, IL-1β, PAI-1, and IL-8] plus one anti-inflammatory [IL-10] adipokine were identified whose circulating levels as well as in vitro release by fat are enhanced in obesity and are primarily released by the nonfat cells of human adipose tissue. In contrast, the circulating levels of leptin and FABP-4 are also enhanced in obesity and they are primarily released by fat cells of human adipose tissue. The relative expression of adipokines and other proteins in human omental as compared to subcutaneous adipose tissue as well as their expression in the nonfat as compared to the fat cells of human omental adipose tissue is also reviewed. The conclusion is that the release of many inflammatory adipokines by adipose tissue is enhanced in obese humans.
22
Josephs, Tracy, Hayley Waugh, Ilona Kokay, David Grattan, and Mary Thompson. "Fasting-induced adipose factor identified as a key adipokine that is up-regulated in white adipose tissue during pregnancy and lactation in the rat." Journal of Endocrinology 194, no. 2 (August 2007): 305–12. http://dx.doi.org/10.1677/joe-07-0158.
Full textAbstract:
Adipokines, which are expressed and secreted from white adipose tissue (WAT), are potential factors that could contribute to the changes in energy homeostasis that occurs in pregnancy and lactation to meet the nutrient demands of fetal growth and milk production. The aim was to identify adipokines that could be involved by measuring the pattern of their mRNA expression in adipose tissue. Adipokine mRNAs were measured by quantitative RT-PCR in RNA isolated from white and brown adipose tissue (BAT) of rats at days 7, 14 and 21 of pregnancy, day 7 of lactation and virgin at dioestrus phase. The results for leptin, adiponectin and resistin expression in WAT essentially confirmed previous studies and it is unlikely that they are directly involved in the metabolic adaptations. The relative amounts of the mRNAs of the adipokines in BAT were comparable with those in WAT, but the patterns of expression did not follow those in WAT, except for apelin. Visfatin mRNA in WAT was elevated 2.5-fold only at day 21 of pregnancy. Apelin mRNA in WAT was increased 2.2-fold at day 7 of pregnancy. Retinol-binding protein 4 mRNA in WAT decreased to 46% of control at day 14 of pregnancy. Fasting-induced adipose factor (FIAF) mRNA in WAT was 2.2- to 2.5-fold higher throughout pregnancy and lactation. The marked induction of FIAF identifies this adipokine as a potential regulator of the metabolic adaptations that occur during pregnancy and lactation.
23
Plasko, George, Sijia He, Jingjing Zhang, Fen Liu, Juli Bai, Lily Dong, and Feng Liu. "34646 DEFICIENCY OF NOVEL ADIPOKINE TETRANECTIN INCREASES OBESITY AND INSULIN RESISTANCE IN FEMALES." Journal of Clinical and Translational Science 5, s1 (March 2021): 19. http://dx.doi.org/10.1017/cts.2021.453.
Full textAbstract:
ABSTRACT IMPACT: Novel adipokines like tetranectin help explain why some people progress from obesity to diseases like diabetes, atherosclerosis, and dislipidemia OBJECTIVES/GOALS: Obesity has an established association with diabetes, dyslipidemia, and atherosclerosis. Preventing progression from obesity to insulin resistance requires understanding of the regulatory mechanisms involved in the loss of insulin sensitivity. Adipose tissue is well known to function as an endocrine organ that produces many kinds of adipokines. METHODS/STUDY POPULATION: Blood sample analysis from human patients and mice was used to determine associations between tetranectin and obesity. Samples were tested with a monoclonal anti-tetranectin antibody for detection with western blot. A tetranectin mutant knock out mouse line was compared to wild type littermates on high fat diet for 4 months. Insulin tolerance tests and glucose tolerance were used to determine progression to insulin resistance and glucose intolerance. Histological analysis of metabolic tissue was used to demonstrate adipocyte hypertrophy and liver steatosis. RESULTS/ANTICIPATED RESULTS: In the current study, we report the identification and initial characterization of a novel adipokine tetranectin. Tetranectin, which is coded by the C-type lectin domain family 3 member B (CLEC3B) gene, is ubiquitously expressed in various mouse tissues, whereas it is highly enriched in white adipose tissue. We found that the serum level of tetranectin was much higher in both obese and diabetic patients. Knocking out the tetranectin gene in mice protected against glucose intolerance in males but reduced insulin and glucose tolerance in females, without effects on food intake and body weight for either sex. Mechanistically, tetranectin targets liver tissues and its deficiency increases lipid accumulation in hepatocytes in females. DISCUSSION/SIGNIFICANCE OF FINDINGS: We have identified a novel adipokine which mediates a different metabolic crosstalk among tissues to maintain systemic glucose and lipid metabolism in different genders. Further investigation of tetranectin’s function could yield a new target for precise therapeutic treatment for obesity and its associated metabolic diseases in different genders
24
Drew, Janice E. "Molecular mechanisms linking adipokines to obesity-related colon cancer: focus on leptin." Proceedings of the Nutrition Society 71, no. 1 (October 21, 2011): 175–80. http://dx.doi.org/10.1017/s0029665111003259.
Full textAbstract:
Obesity is linked to increased risk of colon cancer, currently the third most common cancer. Consequently rising levels of obesity worldwide are likely to significantly impact on obesity-related colon cancers in the decades to come. Understanding the molecular mechanisms whereby obesity increases colon cancer risk is thus a focus for research to inform strategies to prevent the increasing trend in obesity-related cancers. This review will consider research on deregulation of adipokine signalling, a consequence of altered adipokine hormone secretion from excess adipose tissue, with a focus on leptin, which has been studied extensively as a potential mediator of obesity-related colon cancer. Numerous investigations using colon cell lines in vitro, in vivo studies in rodents and investigations of colon cancer patients illuminate the complexity of the interactions of leptin with colon tissues via leptin receptors expressed by the colon epithelium. Although evidence indicates a role for leptin in proliferation of colon epithelial cells in vitro, this has been contradicted by studies in rodent models. However, recent studies have indicated that leptin may influence inflammatory mediators linked with colon cancer and also promote cell growth dependent on genotype and is implicated in growth promotion of colon cancer cells. Studies in human cancer patients indicate that there may be different tumour sub-types with varying levels of leptin receptor expression, indicating the potential for leptin to induce variable responses in the different tumour types. These studies have provided insights into the complex interplay of adipokines with responsive tissues prone to obesity-related colon cancer. Deregulation of adipokine signalling via adipokine receptors located in the colon appears to be a significant factor in obesity-related colon cancer. Molecular profiling of colon tumours will be a useful tool in future strategies to characterise the influence that adipokines may have on tumour development and subsequent therapeutic intervention. Study of the molecular mechanisms linking obesity with cancer also supports recommendations to maintain a normal body weight to reduce the risk of colon cancer.
25
Ameen, Gulizar Issa, and Silvia Mora. "Cbl downregulation increases RBP4 expression in adipocytes of female mice." Journal of Endocrinology 236, no. 1 (January 2018): 29–41. http://dx.doi.org/10.1530/joe-17-0359.
Full textAbstract:
Obesity leads to adipose tissue dysfunction, insulin resistance and diabetes. Adipose tissue produces adipokines that contribute to regulate insulin sensitivity. In turn, insulin stimulates the production and release of some adipokines. Casitas-b-lymphoma proteins (c-Cbl, Cbl-b and Cbl3) are intracellular adaptor signalling proteins that are rapidly phosphorylated by activation of tyrosine kinase receptors. c-Cbl is rapidly phosphorylated by insulin in adipocytes. Here, we tested the hypothesis that Cbl signalling regulates adipokine expression in adipose tissue. We determined the adipokine profile of WAT of Cbl−/− and Cbl+/+ mice in the C57BL6 background. Female Cbl−/− mice exhibited altered expression of adiponectin, leptin and RBP4 in visceral adipose tissue, while no significant changes were seen in male mice. TNFα and IL6 levels were unaffected by Cbl depletion. RBP4 expression was unchanged in liver. Adipose tissue of Cbl−/− animals showed increased basal activation of extracellular regulated kinases (ERK1/2) compared to Cbl+/+. c-Cbl knockdown in 3T3L1 adipocytes also increased basal ERK phosphorylation and RBP4 expression. Inhibition of ERK1/2 phosphorylation in Cbl-depleted 3T3L1 adipocytes or in adipose tissue explants of Cbl−/− mice reduced RBP4 mRNA. 17β-Estradiol increased RBP4 mRNA in adipocytes. Cbl depletion did not change ER expression but increased phosphorylation of ERα at S118, a target site for ERK1/2. ERK1/2 inhibition reduced phosphoER and RBP4 levels. These findings suggest that Cbl contributes to regulate RBP4 expression in adipose of female mice through ERK1/2-mediated activation of ERα. Since Cbl signalling is compromised in diabetes, these data highlight a novel mechanism that upregulates RBP4 locally.
26
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.
Full textAbstract:
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.
27
Khudyakov, Jane I., Eileen Abdollahi, Angela Ngo, Gureet Sandhu, Alicia Stephan, Daniel P. Costa, and Daniel E. Crocker. "Expression of obesity-related adipokine genes during fasting in a naturally obese marine mammal." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 317, no. 4 (October 1, 2019): R521—R529. http://dx.doi.org/10.1152/ajpregu.00182.2019.
Full textAbstract:
Northern elephant seals ( Mirounga angustirostris) are exceptional among fasting-adapted animals in coupling prolonged fasting with energetically costly activities, relying on oxidation of fat stores accrued during foraging to power metabolic demands of reproduction and molting. We hypothesized that high rates of energy expenditure, insulin resistance, and immune responses to colonial breeding in fasting seals are mediated by adipokines, or signaling molecules secreted by adipose tissue that are associated with obesity and inflammation in humans. We measured mRNA expression of 10 adipokine genes in blubber tissue of adult female elephant seals sampled early and late during their lactation and molting fasts and correlated gene expression with adiposity and circulating levels of corticosteroid and immune markers. Expression of adiponectin ( ADIPOQ) and its receptor ADIPOR2, leptin receptor ( LEPR), resistin ( RETN), retinol binding protein 4 ( RBP4), and visfatin/nicotinamide phosphoribosyltransferase ( NAMPT) was increased, whereas that of fat mass and obesity-associated protein ( FTO) was decreased in late-fasted compared with early-fasted groups. Abundance of adipokine transcripts that increased in late fasting was negatively associated with body mass and positively associated with cortisol, suggesting that they may mediate local metabolic effects of cortisol in blubber during fasting. Expression of several adipokines was correlated with the immune markers IL-6, haptoglobin, IgM, and IgE, suggesting a potential role in modulating immune responses to colonial breeding and molting. Since many of these adipokines have not been measured in other wild animals, this study provides preliminary insights into their local regulation in fat tissue and targeted assays for future studies.
28
Gruzdeva, O. V., A. D. Borodkina, O. E. Akbasheva, Yu A. Dileva, L. V. Antonova, V. G. Matveeva, E. G. Uchasova, et al. "Influence of visceral obesity on the secretion of adipokines with epicardial adipocytes in patients with coronary heart disease." Terapevticheskii arkhiv 90, no. 10 (October 15, 2018): 71–78. http://dx.doi.org/10.26442/terarkh201890104-78.
Full textAbstract:
Aim. To study adipokine-cytokine profile of epicardial adipocytes (EAT) and subcutaneous adipose tissue (SAT) in conjunction with the area of visceral adipose tissue (VAT), biochemical and clinical characteristics of patients with coronary heart disease. Materials and methods. Examined 84 patients (70 men and 14 women) with coronary artery disease. In fact the presence of visceral obesity (VO) the patients were divided into two groups. Patients VO the sampling of adipocytes of EAT and SAT, with subsequent cultivation and evaluation of adipokine and provospalitelna activity. Carried out the determination of carbohydrate and lipid metabolism, adipokine and pro-inflammatory status in the blood serum. Results and discussion. It was found that adipokine-cytokine profile of adipocytes of EAT and SAT differ. Adipocytes art of the disease on the background characterized by an increase IL-1, TNF-α, leptin-adiponectin relationships and a decrease in the content of protective factors: adiponectin and anti-inflammatory cytokine IL-10. While the SAT adipocytes was characterized by a decrease in the concentration of soluble receptor for leptin and the more pronounced leptinresistance, and the increase in proinflammatory cytokines was offset by the increase in the concentration of IL-10. The presence associated with multi-vessel coronary bed lesion, multifocal atherosclerosis, insulin resistance, atherogenic dyslipidemia, an imbalance of adipokines and markers of inflammation. So the value of the square VAT determined higher concentrations of leptin, TNF-α in adipocytes and serum, lipid and carbohydrate metabolism and a lower content of soluble receptor for leptin. Conclusion. Thus, the disease on the background of the status of the adipocytes of EAT characterized as a "metabolic inflammation", and may indicate the direct involvement of adipocytes in the pathogenesis of coronary artery disease, due to the formation of adipokine imbalance and the activation of proinflammatory reactions.
29
Saxton, Sophie N., Ben J. Clark, Sarah B. Withers, Etto C. Eringa, and Anthony M. Heagerty. "Mechanistic Links Between Obesity, Diabetes, and Blood Pressure: Role of Perivascular Adipose Tissue." Physiological Reviews 99, no. 4 (October 1, 2019): 1701–63. http://dx.doi.org/10.1152/physrev.00034.2018.
Full textAbstract:
Obesity is increasingly prevalent and is associated with substantial cardiovascular risk. Adipose tissue distribution and morphology play a key role in determining the degree of adverse effects, and a key factor in the disease process appears to be the inflammatory cell population in adipose tissue. Healthy adipose tissue secretes a number of vasoactive adipokines and anti-inflammatory cytokines, and changes to this secretory profile will contribute to pathogenesis in obesity. In this review, we discuss the links between adipokine dysregulation and the development of hypertension and diabetes and explore the potential for manipulating adipose tissue morphology and its immune cell population to improve cardiovascular health in obesity.
30
Neumann, Elena, Rebecca Hasseli, Selina Ohl, Uwe Lange, Klaus W. Frommer, and Ulf Müller-Ladner. "Adipokines and Autoimmunity in Inflammatory Arthritis." Cells 10, no. 2 (January 22, 2021): 216. http://dx.doi.org/10.3390/cells10020216.
Full textAbstract:
Adipokines are adipose tissue-derived factors not only playing an important role in metabolism but also influencing other central processes of the body, such as inflammation. In autoimmune diseases, adipokines are involved in inflammatory pathways affecting different cell types. Many rheumatic diseases belong to the group of autoimmune diseases, for example rheumatoid arthritis (RA) and psoriatic arthritis. Due to the autoimmune responses, a chronic inflammatory milieu develops, which affects the whole body, including adipose tissue. Metabolic alterations such as obesity influence inflammatory responses in autoimmune diseases. Adipokines are bioactive mediators mainly produced by adipose tissue. Due to alterations of systemic adipokine levels, their role as biomarkers with diagnostic potential has been suggested in the context of rheumatic diseases. In the affected joints of RA patients, different synoviocytes but also osteoclasts, osteoblasts, and chondrocytes produce several adipokines, contributing to the unique inflammatory microenvironment. Adipokines have been shown to be potent modulatory effectors on different cell types of the immune system but also local cells in synovial tissue, cartilage, and bone. This review highlights the most recent findings on the role of adipokines in the pathophysiology of inflammatory arthritis with a distinct focus on RA in the quickly developing research field.
31
Romacho, Tania, Carlos F. Sánchez-Ferrer, and Concepción Peiró. "Visfatin/Nampt: An Adipokine with Cardiovascular Impact." Mediators of Inflammation 2013 (2013): 1–15. http://dx.doi.org/10.1155/2013/946427.
Full textAbstract:
Adipose tissue is acknowledged as an endocrine organ that releases bioactive factors termed adipokines. Visfatin was initially identified as a novel adipokine with insulin-mimetic properties in mice. This adipokine was identical to two previously described molecules, namely, pre-B cell colony-enhancing factor (PBEF) and the enzyme nicotinamide phosphoribosyltransferase (Nampt). Enhanced circulating visfatin/Nampt levels have been reported in metabolic diseases, such as obesity and type 2 diabetes. Moreover, visfatin/Nampt circulating levels correlate with markers of systemic inflammation. In cardiovascular diseases, visfatin/Nampt was initially proposed as a clinical marker of atherosclerosis, endothelial dysfunction, and vascular damage, with a potential prognostic value. Nevertheless, beyond being a surrogate clinical marker, visfatin/Nampt is an active player promoting vascular inflammation, and atherosclerosis. Visfatin/Nampt effects on cytokine and chemokine secretion, macrophage survival, leukocyte recruitment by endothelial cells, vascular smooth muscle inflammation and plaque destabilization make of this adipokine an active factor in the development and progression of atherosclerosis. Further research is required to fully understand the mechanisms mediating the cellular actions of this adipokine and to better characterize the factors regulating visfatin/Nampt expression and release in all these pathologic scenarios. Only then, we will be able to conclude whether visfatin/Nampt is a therapeutical target in cardiometabolic diseases.
32
Schlich, Raphaela, Miriam Willems, Sabrina Greulich, Florian Ruppe, Wolfram Trudo Knoefel, D. Margriet Ouwens, Bujar Maxhera, Artur Lichtenberg, Jürgen Eckel, and Henrike Sell. "VEGF in the Crosstalk between Human Adipocytes and Smooth Muscle Cells: Depot-Specific Release from Visceral and Perivascular Adipose Tissue." Mediators of Inflammation 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/982458.
Full textAbstract:
Adipose tissue secrets adipokines and fatty acids, which may contribute to obesity-associated vascular dysfunction and cardiovascular risk. This study investigated which factors are responsible for the synergistic effect of adipokine and oleic acid- (OA-) induced proliferation of human vascular smooth muscle cells (VSMC). Adipocyte-conditioned medium (CM) from human adipocytes induces proliferation of VSMC in correlation to its vascular endothelial growth factor (VEGF) content. CM increases VEGF-receptor (VEGF-R) 1 and 2 expression and VEGF secretion of VSMC, while OA only stimulates VEGF secretion. VEGF neutralization abrogates CM- and OA-induced proliferation and considerably reduces proliferation induced by CM and OA in combination. VEGF release is higher from visceral adipose tissue (VAT) of obese subjects compared to subcutaneous adipose tissue (SAT) and VAT from lean controls. Furthermore, VEGF release from VAT correlates with its proliferative effect. Perivascular adipose tissue (PAT) from type 2 diabetic patients releases significantly higher amounts of VEGF and induces stronger proliferation of VSMC as compared to SAT and SAT/PAT of nondiabetics. In conclusion, VEGF is mediating CM-induced proliferation of VSMC. As this adipokine is released in high amounts from VAT of obese patients and PAT of diabetic patients, VEGF might link adipose tissue inflammation to increased VSMC proliferation.
33
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.
Full textAbstract:
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.
34
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.
Full textAbstract:
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.
35
Maury, E., K. Ehala-Aleksejev, Y. Guiot, R. Detry, A. Vandenhooft, and S. M. Brichard. "Adipokines oversecreted by omental adipose tissue in human obesity." American Journal of Physiology-Endocrinology and Metabolism 293, no. 3 (September 2007): E656—E665. http://dx.doi.org/10.1152/ajpendo.00127.2007.
Full textAbstract:
Central-omental obesity plays a causative role in the pathogenesis of the metabolic syndrome. Adipokines are involved in the pathogenesis of this syndrome. However, adipokines secreted by omental adipose tissue (OAT) are still poorly characterized in human obesity. Therefore, we searched for novel adipokines abnormally secreted by OAT in obesity and examined their relationships with some features of metabolic syndrome and the respective contribution of adipocytes vs. stromal-vascular cells. OAT from obese and nonobese men was fractionated into adipocytes and SV cells, which were then cultured. Medium was screened by medium-scale protein arrays and ELISAs. Adipokine mRNA levels were measured by real-time RT-qPCR. We detected 16 cytokines secreted by each cellular fraction of lean and obese subjects. Of the 16 cytokines, six adipokines were newly identified as secretory products of OAT, which were dysregulated in obesity: three chemokines (growth-related oncogen factor, RANTES, macrophage inflammatory protein-1β), one interleukin (IL-7), one tissue inhibitor of metalloproteinases (TIMP-1), and one growth factor (thrombopoietin). Their secretion and expression were enhanced in obesity, with a relatively similar contribution of the two fractions. The higher proportion of macrophages and endothelial cells in obesity may contribute to this enhanced production as well as changes in intrinsic properties of hypertrophied adipocytes. Accordingly, mRNA concentrations of most of these adipokines increased during adipocyte differentiation. Eventually, expression of the investigated adipokines did correlate with several features of the metabolic syndrome. In conclusion, six adipokines were newly identified as oversecreted by OAT in obesity. These adipokines may link obesity to its cardiovascular or metabolic comorbidities.
36
Yazigi Solis, Marina, Guilherme Giannini Artioli, Eduardo Montag, Vitor de Salles Painelli, Fábio Lopes Saito, Fernanda Rodrigues Lima, Hamilton Roschel, Bruno Gualano, Antonio Herbert Lancha Junior, and Fabiana Braga Benatti. "The Liposuction-Induced Effects on Adiponectin and Selected Cytokines Are Not Affected by Exercise Training in Women." International Journal of Endocrinology 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/315382.
Full textAbstract:
It has been suggested that the abrupt liposuction-induced decrease in adipose tissue could affect adipokine secretion pattern. We hypothesized that exercise training could positively impact adipokine metabolism following liposuction. The aim of this study was to investigate the effects of liposuction on inflammation-related adipokines in women who were either exercise-trained or remained sedentary after surgery. Thirty-six healthy normal-weight women underwent an abdominal liposuction and two months after surgery were randomly allocated into two groups: trained (TR,n=18, four-month exercise program) and nontrained (NT,n=18). Inflammation-related adipokine serum levels (TNF-α, IL-6, IL-10, and adiponectin) and abdominal and thigh subcutaneous adipose tissue (scAT) mRNA levels were assessed before (PRE) and six months after surgery (POST6). TNF-α, IL-6, and IL-10 serum levels were unchanged in both groups. In contrast, TNF-α, IL-6, and IL-10 mRNA levels in scAT were increased, whereas adiponectin scAT mRNA and serum levels were decreased at POST6 (P<0.05, main effect for time). No changes were observed in mRNA levels of MCP-1, CD14, and CD68 in any of the groups. In conclusion, liposuction downregulates adiponectin scAT gene expression and serum levels and upregulates scAT gene expression of inflammation-related genes six months after surgery in normal-weight women, irrespective of exercise training.
37
Askari, Alireza, Peyman Arasteh, Reza Homayounfar, Mohamad Mehdi Naghizadeh, Elham Ehrampoush, Seyyede Makiye Mousavi, and Reza Alipoor. "The role of adipose tissue secretion in the creation and pain level in osteoarthritis." Endocrine Regulations 54, no. 1 (January 1, 2020): 6–13. http://dx.doi.org/10.2478/enr-2020-0002.
Full textAbstract:
AbstractObjectives. With increasing evidence regarding the metabolic basis of osteoarthritis (OA), we studied the relationship between adipose tissue and OA.Methods. This study is part of an OA registry in the eastern part of Fars Province, Iran. Overall, 150 patients with OA and 300 sex matched individuals were selected as a control group. They were compared regarding adipokine concentration (leptin, adiponectin, resistin and visfatin), anthropo-metric indices, the Western Ontario and McMaster universities arthritis index score (WOMAC).Results. All adipokine levels were higher among OA patients (p<0.001). After adjusting for age, sex, and body mass index (BMI), adipokines showed a significant and positive association with OA (B: 14.12, B: 9.92, B: 24.71 and B: 12.29 for leptin, adiponectin, visfatin, and resistin, respectively; p<0.001). Except the adiponectin that had a negative relationship with BMI in the OA group (r=–0.570, p<0.001), other adipokines had positive relationships with BMI (r=0.781, p<0.001; r=0.530, p<0.001; r=0.549, p<0.001 for leptin, visfatin, and resistin, respectively). Only leptin and adiponectin levels were correlated with pain (B: 0.045, –0.079 and p<0.05).Conclusion. The present study shows that aside to the well-known role of mechanical stress in OA pathogenesis (weight load), leptin, adiponectin, visfatin, and resistin, which represent the adi-pose tissue independent on the weight, may play a chemical role in OA pathogenesis. In addition, leptin and adiponectin may be involved in the pain levels among patients with OA.
38
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.
Full textAbstract:
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.
39
Kurowska, Patrycja, Ewa Mlyczyńska, Monika Dawid, Małgorzata Jurek, Dominika Klimczyk, Joelle Dupont, and Agnieszka Rak. "Review: Vaspin (SERPINA12) Expression and Function in Endocrine Cells." Cells 10, no. 7 (July 6, 2021): 1710. http://dx.doi.org/10.3390/cells10071710.
Full textAbstract:
Proper functioning of the body depends on hormonal homeostasis. White adipose tissue is now known as an endocrine organ due to the secretion of multiple molecules called adipokines. These proteins exert direct effects on whole body functions, including lipid metabolism, angiogenesis, inflammation, and reproduction, whereas changes in their level are linked with pathological events, such as infertility, diabetes, and increased food intake. Vaspin-visceral adipose tissue-derived serine protease inhibitor, or SERPINA12 according to serpin nomenclature, is an adipokine discovered in 2005 that is connected to the development of insulin resistance, obesity, and inflammation. A significantly higher amount of vaspin was observed in obese patients. The objective of this review was to summarize the latest findings about vaspin expression and action in endocrine tissues, such as the hypothalamus, pituitary gland, adipose tissue, thyroid, ovary, placenta, and testis, as well as discuss the link between vaspin and pathologies connected with hormonal imbalance.
40
Taube, Annika, Raphaela Schlich, Henrike Sell, Kristin Eckardt, and Juergen Eckel. "Inflammation and metabolic dysfunction: links to cardiovascular diseases." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 11 (June 1, 2012): H2148—H2165. http://dx.doi.org/10.1152/ajpheart.00907.2011.
Full textAbstract:
Abdominal obesity is a major risk factor for cardiovascular disease, and recent studies highlight a key role of adipose tissue dysfunction, inflammation, and aberrant adipokine release in this process. An increased demand for lipid storage results in both hyperplasia and hypertrophy, finally leading to chronic inflammation, hypoxia, and a phenotypic change of the cellular components of adipose tissue, collectively leading to a substantially altered secretory output of adipose tissue. In this review we have assessed the adipo-vascular axis, and an overview of adipokines associated with cardiovascular disease is provided. This resulted in a first list of more than 30 adipokines. A deeper analysis only considered adipokines that have been reported to impact on inflammation and NF-κB activation in the vasculature. Out of these, the most prominent link to cardiovascular disease was found for leptin, TNF-α, adipocyte fatty acid-binding protein, interleukins, and several novel adipokines such as lipocalin-2 and pigment epithelium-derived factor. Future work will need to address the potential role of these molecules as biomarkers and/or drug targets.
41
Ukropec, Jozef, Adela Penesová, Martina Škopková, Mikuláš Pura, Miroslav Vlček, Žofia Rádiková, Richard Imrich, et al. "Adipokine Protein Expression Pattern in Growth Hormone Deficiency Predisposes to the Increased Fat Cell Size and the Whole Body Metabolic Derangements." Journal of Clinical Endocrinology & Metabolism 93, no. 6 (June 1, 2008): 2255–62. http://dx.doi.org/10.1210/jc.2007-2188.
Full textAbstract:
Abstract Context: GH deficiency (GHD) in adults is associated with central adiposity, dyslipidemia, and insulin resistance. Objective: The objective of the study was to test the hypothesis that GHD might change the spectrum of adipokines and thus influence the adipose tissue and the whole-body metabolic and inflammatory status leading to development of insulin resistance. Design: This was a single-center observational study with a cross-sectional design. Participants and Methods: Protein arrays were used to characterize adipokines expressed in the sc adipose tissue obtained from young GHD adults and compared with age-, gender-, and body mass index (BMI)-matched group of healthy individuals. All subjects underwent an oral glucose tolerance test, euglycemic hyperinsulinemic clamp, and magnetic resonance imaging examination. Results: Presence of abdominal obesity, enlarged adipocytes, increased circulating high-sensitivity C-reactive protein, impaired glucose tolerance, and decreased insulin action were found in GHD. Changes in adipokine protein expression due to GHD were highly dependent on the obesity phenotype. Lean GHD individuals (BMI ∼23 kg/m2) had decreased protein levels for stem cell factor and epithelial growth factor, indicating a possible defect in adipocyte differentiation and proliferation. Decrease of vascular endothelial growth factor, stromal cell-derived factor, angiopoietin-2, and brain-derived neurotrophic factor advocated for attenuated angiogenesis and neurogenesis. Presence of obesity (BMI ∼31 kg/m2) eliminated these inhibitory effects. However, adipose tissue expansion in GHD individuals was paralleled by an elevation of adipose tissue proinflammatory cytokines (IL-1β, interferon-γ) and chemoattractants (interferon-inducible T cell α-chemoattractant, monocyte chemotactic protein-2, monocyte chemotactic protein-3, eotaxin). Conclusion: Our data demonstrate that GHD modulates adipokine and cytokine protein expression pattern, which might influence the adipose tissue growth and differentiation and predispose to tissue hypoxia, inflammation, and a defect in the whole-body insulin action.
42
Gomez, Rodolfo, Francisca Lago, Juan Gomez-Reino, Carlos Dieguez, and Oreste Gualillo. "Adipokines in the skeleton: influence on cartilage function and joint degenerative diseases." Journal of Molecular Endocrinology 43, no. 1 (February 24, 2009): 11–18. http://dx.doi.org/10.1677/jme-08-0131.
Full textAbstract:
The discovery of leptin in 1994 marked the beginning of a new understanding about white adipose tissue (WAT) and modified a static vision of this tissue which was viewed up to the end of the 20th century as an inert tissue, devoted to body protection from heat loss and to passively storing energy. The identification of the product of the gene obese accentuated the role of adipose tissue in the physiopathology of obesity-linked diseases, and led to the discovery of various adipokines, many of a pro-inflammatory nature. It has become progressively manifest that WAT-derived adipokines can now be considered as the fulcrum between obesity-related environmental causes, such as nutrition and lifestyle, and the biochemical shifts that lead to metabolic syndrome, inflammatory and/or autoimmune conditions, and rheumatic diseases. Herein, we review recent adipokine research, with particular emphasis to the role of leptin, adiponectin, resistin, and visfatin in chondrocyte function and skeleton, as well as in inflammatory and degenerative cartilage joint diseases.
43
Mirr, Małgorzata, and Maciej Owecki. "An Update to the WISP-1/CCN4 Role in Obesity, Insulin Resistance and Diabetes." Medicina 57, no. 2 (January 23, 2021): 100. http://dx.doi.org/10.3390/medicina57020100.
Full textAbstract:
Insulin resistance refers to the diminished response of peripheral tissues to insulin and is considered the major risk factor for type 2 diabetes. Although many possible mechanisms have been reported to develop insulin resistance, the exact underlying processes remain unclear. In recent years, the role of adipose tissue as a highly active metabolic and endocrine organ, producing proteins called adipokines and their multidirectional activities has gained interest. The physiological effects of adipokines include energy homeostasis and insulin sensitivity regulation. In addition, an excess of adipose tissue is followed by proinflammatory state which results in dysregulation of secreted cytokines contributing to insulin resistance. Wingless-type (Wnt) inducible signalling pathway protein-1 (WISP-1), also known as CCN4, has recently been described as a novel adipokine, whose circulating levels are elevated in obese and insulin resistant individuals. Growing evidence suggests that WISP-1 may participate in the impaired glucose homeostasis. In this review, we characterize WISP-1 and summarize the latest reports on the role of WISP-1 in obesity, insulin resistance and type 2 diabetes.
44
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.
Full textAbstract:
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.
45
Hoppmann, J., N. Perwitz, B. Meier, M. Fasshauer, D. Hadaschik, H. Lehnert, and J. Klein. "The balance between gluco- and mineralo-corticoid action critically determines inflammatory adipocyte responses." Journal of Endocrinology 204, no. 2 (November 25, 2009): 153–64. http://dx.doi.org/10.1677/joe-09-0292.
Full textAbstract:
Obesity is associated with chronic inflammation. Pro-inflammatory adipokines may promote metabolic disorders and cardiovascular morbidity. However, the key mechanisms leading to obesity-related inflammation are poorly understood. The corticosteroid metabolism in adipose tissue plays a crucial role in the pathogenesis of the metabolic syndrome. Both the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR) mediate corticosteroid action in adipose tissue. The significance of the interplay of these receptors in mediating an inflammatory adipokine response is virtually unexplored. In the present study, we investigated the differential roles of the GR and MR in controlling the key adipose tissue functions including inflammatory adipokine expression and adipogenesis using selective stimulation with receptor agonists, acute receptor knockdown via RNA interference and newly generated knockout adipose cell lines. Selective GR stimulation of white adipocytes with dexamethasone inhibited the expression of interleukin 6 (IL6), monocyte chemoattractant protein-1 (MCP1 or CCL2 as listed in the MGI Database), tumour necrosis factor-α, chemerin and leptin. By contrast, selective MR stimulation with aldosterone promoted the expression of IL6, plasminogen activator inhibitor 1, chemerin and leptin. Furthermore, in the presence of an acute GR knockdown as well as in GR knockout adipocytes, corticosterone increased the gene expression of the pro-inflammatory adipokines IL6 and MCP1. Whereas GR knockout adipocytes displayed a mildly impaired adipogenesis during early differentiation, MR knockout cells completely failed to accumulate lipids. Taken together, our data demonstrate a critical role for the balance between gluco- and mineralocorticoid action in determining adipocyte responses implicated in obesity-associated inflammation and cardiovascular complications.
46
Ambroszkiewicz, Jadwiga, Joanna Gajewska, Joanna Mazur, Witold Klemarczyk, Grażyna Rowicka, Mariusz Ołtarzewski, Małgorzata Strucińska, and Magdalena Chełchowska. "Does a Vegetarian Diet Affect the Levels of Myokine and Adipokine in Prepubertal Children?" Journal of Clinical Medicine 10, no. 17 (September 3, 2021): 3995. http://dx.doi.org/10.3390/jcm10173995.
Full textAbstract:
Myokines are cytokines secreted by muscle and exert autocrine, paracrine, or endocrine effects. Myokines mediate communication between muscle and other organs, including adipose tissue. The aim of the study was to assess serum myokines and their relationships with adipokines and anthropometric and nutritional parameters in children following vegetarian and omnivorous diets. One hundred and five prepubertal children were examined. Among them there were 55 children on a vegetarian diet and 50 children on an omnivorous diet. Concentrations of myokines (myostatin, irisin) and adipokines (leptin, adiponectin, omentin, visfatin) in serum were determined by enzyme-linked immunosorbent assay (ELISA). We observed comparable median values of serum myokines and adipokines (except of leptin concentration) in both of the studied groups of children. We also found several correlations between myokine and adipokine levels and certain nutritional parameters. Serum myostatin was positively correlated with omentin levels in vegetarians and omnivores (p = 0.002). Serum irisin was positively associated with omentin (p = 0.045) levels in omnivores and inversely with visfatin concentration (p = 0.037) in vegetarians. Myostatin concentration was negatively correlated with the percentage of energy from protein (p = 0.014), calcium (p = 0.046), and vitamin A (p = 0.028) intakes in vegetarians and with dietary vitamin C (p = 0.041) and vitamin E (p = 0.021) intakes in omnivores. In multivariate regression analyses, positive correlations of serum myostatin with omentin levels were revealed in both study groups (β = 0.437, p < 0.001 for vegetarians; and β = 0.359, p = 0.001 for omnivores). Consuming a lacto-ovo-vegetarian diet did not influence serum levels of myokines (myostatin, irisin) and adipokines such as adiponectin, visfatin, and omentin in prepubertal children. However, leptin levels were significantly lower in vegetarians compared with omnivores. The observed significant positive correlations between myostatin and omentin concentrations might suggest tissue cross-talk between skeletal muscle and fat tissue. Further studies, carried out in a larger group of children following different dietary patterns, could be important to fully understand the relations between muscle, adipose tissues, and nutrition.
47
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.
Full textAbstract:
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.
48
Maury, E., and S. M. Brichard. "Adipokine dysregulation, adipose tissue inflammation and metabolic syndrome." Molecular and Cellular Endocrinology 314, no. 1 (January 15, 2010): 1–16. http://dx.doi.org/10.1016/j.mce.2009.07.031.
Full text
49
Tishinsky, Justine M. "Modulation of adipokines by n-3 polyunsaturated fatty acids and ensuing changes in skeletal muscle metabolic response and inflammation." Applied Physiology, Nutrition, and Metabolism 38, no. 3 (March 2013): 361. http://dx.doi.org/10.1139/apnm-2012-0447.
Full textAbstract:
Adipose tissue represents an important endocrine organ that secretes a multitude of adipokines known to mediate inflammation, lipid metabolism, and insulin sensitivity in peripheral tissues, such as skeletal muscle. Specifically, adiponectin stimulates skeletal muscle fatty acid oxidation and is associated with improvements in insulin response. Long-chain n-3 polyunsaturated fatty acids (PUFA) are well known for their anti-inflammatory and insulin-sensitizing properties, and their dietary consumption is associated with a more favourable circulating adipokine profile, including increased adiponectin. However, whether n-3 PUFA can directly stimulate adiponectin secretion from human adipocytes, as well as the underlying mechanisms involved, is unknown. In contrast to n-3 PUFA, diets high in saturated fatty acids (SFA) are thought to decrease adiponectin and increase pro-inflammatory adipokines, as well as blunt skeletal muscle response to both adiponectin and insulin, possibly via activation of inflammatory pathways. The role of n-3 PUFA in mediating the communication between adipose tissue and skeletal muscle, as well as preventing SFA-induced impairments in skeletal muscle function, has yet to be examined. In this thesis, it was found that long-chain n-3 PUFA increase adiponectin secretion from human adipocytes via a peroxisome proliferator-activated receptor γ-dependent mechanism. The effects of n-3 PUFA on adiponectin secretion were additive when combined with the thiazolidinedione, rosiglitazone. Second, incorporation of n-3 PUFA into a high SFA diet prevented impairments in adiponectin response and both prevented and restored impairments in insulin response in rodent skeletal muscle. Interestingly, these findings were paralleled by prevention of SFA-induced increases in toll-like receptor 4 expression by n-3 PUFA, suggesting inflammatory changes may be involved. Finally, dietary n-3 PUFA and SFA modulated the secretion of adipose tissue-derived factors from visceral rodent adipose tissue and subsequent exposure of isolated skeletal muscle to such factors induced acute changes in inflammatory gene expression without affecting insulin sensitivity. Together, the findings in this thesis suggest that n-3 PUFA modulate adipokine secretion from adipose tissue and that adipose-derived factors mediate skeletal muscle inflammation and response to adiponectin and insulin. Ultimately, this work highlights the importance of considering n-3 PUFA as a therapeutic strategy in the prevention and treatment of obesity and related pathologies.
50
Perego, Silvia, Veronica Sansoni, Ewa Ziemann, and Giovanni Lombardi. "Another Weapon against Cancer and Metastasis: Physical-Activity-Dependent Effects on Adiposity and Adipokines." International Journal of Molecular Sciences 22, no. 4 (February 18, 2021): 2005. http://dx.doi.org/10.3390/ijms22042005.
Full textAbstract:
Physically active behavior has been associated with a reduced risk of developing certain types of cancer and improved psychological conditions for patients by reducing anxiety and depression, in turn improving the quality of life of cancer patients. On the other hand, the correlations between inactivity, sedentary behavior, and overweight and obesity with the risk of development and progression of various cancers are well studied, mainly in middle-aged and elderly subjects. In this article, we have revised the evidence on the effects of physical activity on the expression and release of the adipose-tissue-derived mediators of low-grade chronic inflammation, i.e., adipokines, as well as the adipokine-mediated impacts of physical activity on tumor development, growth, and metastasis. Importantly, exercise training may be effective in mitigating the side effects related to anti-cancer treatment, thereby underlining the importance of encouraging cancer patients to engage in moderate-intensity activities. However, the strong need to customize and adapt exercises to a patient’s abilities is apparent. Besides the preventive effects of physically active behavior against the adipokine-stimulated cancer risk, it remains poorly understood how physical activity, through its actions as an adipokine, can actually influence the onset and development of metastases.