Relevant bibliographies by topics / Adipocyte hormones

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Adipocyte hormones'

Author: Grafiati
Published: 28 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Adipocyte hormones"

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Vernon, R. G. "Adipocyte studies: systems for investigating effects of growth hormone and other chronically acting hormones." Biochemical Society Transactions 28, no. 2 (February 1, 2000): 126–31. http://dx.doi.org/10.1042/bst0280126.

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Adipose tissue is very amenable to study in vitro. Collagenase digestion yields free adipocytes which usually respond well to acute stimulation/inhibition by hormones and other factors. Chronic effects of hormones are best studied using explants of adipose tissue which, from some species (e.g. sheep), can be maintained in culture for up to a week without loss of function. Alternatively, pre-adipocytes can be readily isolated from adipose tissue and induced to proliferate and differentiate in culture, while various adipocyte-like cell-lines have been established, which can be used for chronic studies. Use of these various systems for investigating the mechanisms of action of growth hormone are described.
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Lafontan, Max. "FAT CELLS: Afferent and Efferent Messages Define New Approaches to Treat Obesity." Annual Review of Pharmacology and Toxicology 45, no. 1 (September 22, 2005): 119–46. http://dx.doi.org/10.1146/annurev.pharmtox.45.120403.095843.

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For a long time neural and endocrine messages were studied for their impact on adipocyte metabolism and control of storage/release of fatty acids. In fact, bidirectional communication exists between adipocytes and other tissues. Several molecules secreted from adipocytes are involved in fat cell signaling to other tissues. Adipocyte products could initiate antagonistic effects on target tissues. Fat cells produce peptides that can elicit insulin resistance, such as tumor necrosis factor-α and resistin, as well as hormones that can improve insulin resistance, such as leptin and adiponectin. Secretion of complement proteins, proinflammatory cytokines, procoagulant, and acute phase reactant proteins have also been observed in adipocytes. There is much to learn about how these signals function. It is unlikely that all the adipocyte's endocrine and paracrine signals have been identified. Putative pharmacological strategies aiming at modulation of afferent and efferent fat cell messages are reviewed and discussed.
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Phillips, Kevin J. "Beige Fat, Adaptive Thermogenesis, and Its Regulation by Exercise and Thyroid Hormone." Biology 8, no. 3 (July 31, 2019): 57. http://dx.doi.org/10.3390/biology8030057.

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While it is now understood that the proper expansion of adipose tissue is critically important for metabolic homeostasis, it is also appreciated that adipose tissues perform far more functions than simply maintaining energy balance. Adipose tissue performs endocrine functions, secreting hormones or adipokines that affect the regulation of extra-adipose tissues, and, under certain conditions, can also be major contributors to energy expenditure and the systemic metabolic rate via the activation of thermogenesis. Adipose thermogenesis takes place in brown and beige adipocytes. While brown adipocytes have been relatively well studied, the study of beige adipocytes has only recently become an area of considerable exploration. Numerous suggestions have been made that beige adipocytes can elicit beneficial metabolic effects on body weight, insulin sensitivity, and lipid levels. However, the potential impact of beige adipocyte thermogenesis on systemic metabolism is not yet clear and an understanding of beige adipocyte development and regulation is also limited. This review will highlight our current understanding of beige adipocytes and select factors that have been reported to elicit the development and activation of thermogenesis in beige cells, with a focus on factors that may represent a link between exercise and ‘beiging’, as well as the role that thyroid hormone signaling plays in beige adipocyte regulation.
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Burrell, Jasmine A., Anik Boudreau, and Jacqueline M. Stephens. "Latest advances in STAT signaling and function in adipocytes." Clinical Science 134, no. 6 (March 2020): 629–39. http://dx.doi.org/10.1042/cs20190522.

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Abstract Adipocytes and adipose tissue are not inert and make substantial contributions to systemic metabolism by influencing energy homeostasis, insulin sensitivity, and lipid storage. In addition to well-studied hormones such as insulin, there are numerous hormones, cytokines, and growth factors that modulate adipose tissue function. Many endocrine mediators utilize the JAK–STAT pathway to mediate dozens of biological processes, including inflammation and immune responses. JAKs and STATs can modulate both adipocyte development and mature adipocyte function. Of the seven STAT family members, four STATs are expressed in adipocytes and regulated during adipogenesis (STATs 1, 3, 5A, and 5B). These STATs have been shown to play influential roles in adipose tissue development and function. STAT6, in contrast, is highly expressed in both preadipocytes and mature adipocytes, but is not considered to play a major role in regulating adipose tissue function. This review will summarize the latest research that pertains to the functions of STATs in adipocytes and adipose tissue.
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Ahima, Rexford S. "Central actions of adipocyte hormones." Trends in Endocrinology & Metabolism 16, no. 7 (September 2005): 307–13. http://dx.doi.org/10.1016/j.tem.2005.07.010.

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Vannucci, S. J., C. M. Klim, L. F. Martin, and K. F. LaNoue. "A1-adenosine receptor-mediated inhibition of adipocyte adenylate cyclase and lipolysis in Zucker rats." American Journal of Physiology-Endocrinology and Metabolism 257, no. 6 (December 1, 1989): E871—E878. http://dx.doi.org/10.1152/ajpendo.1989.257.6.e871.

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Hormone-stimulated lipolysis is reduced in genetically obese rodents and may contribute to the increased adiposity characteristic of the obese state. Endogenously released adenosine, acting via the A1 receptor coupled to the inhibitory guanosine 5'-triphosphate binding protein, Gi, provides a tonic inhibition of lipolysis in rat adipocytes. Removal of this inhibition by the addition of adenosine deaminase frequently results in maximal lipolytic activity. Adipocytes isolated from lean Zucker (Fa/?) rats responded normally to adenosine deaminase, where lipolysis in adipocytes from obese Zucker (fa/fa) rats remained approximately 50% inhibited. Adipocyte adenylate cyclase was equally responsive to activation by forskolin, but lipolytic hormones were significantly less effective in stimulating adenosine 3',5'-cyclic monophosphate (cAMP) production in the obese adipocytes. These cells also exhibited an increased sensitivity to inhibition by the adenosine agonist, N6-(L-2-phenylisopropyl)-adenosine, either in combination with forskolin or beta-adrenergic hormone stimulation. Treatment of isolated adipocytes with pertussis toxin, which uncouples receptor-mediated Gi function, had little effect in cells from lean rats but increased isoproterenol stimulated cAMP production of cells from obese rats to levels observed in the lean cells. In addition, the adenosine A1 antagonist, 8-phenyltheophylline, increased cAMP and lipolytic activity in the obese adipocytes while having little significant effect in the lean adipocytes. These results suggest that hormonal control of lipolysis is altered in the obese Zucker rat because of an alteration in A1-adenosine receptor-mediated inhibition of adenylate cyclase.
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GREGOIRE, FRANCINE M., CYNTHIA M. SMAS, and HEI SOOK SUL. "Understanding Adipocyte Differentiation." Physiological Reviews 78, no. 3 (January 7, 1998): 783–809. http://dx.doi.org/10.1152/physrev.1998.78.3.783.

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Gregoire, Francine M., Cynthia M. Smas, and Hei Sook Sul. Understanding Adipocyte Differentiation. Physiol. Rev. 78: 783–809, 1998. — The adipocyte plays a critical role in energy balance. Adipose tissue growth involves an increase in adipocyte size and the formation of new adipocytes from precursor cells. For the last 20 years, the cellular and molecular mechanisms of adipocyte differentiation have been extensively studied using preadipocyte culture systems. Committed preadipocytes undergo growth arrest and subsequent terminal differentiation into adipocytes. This is accompanied by a dramatic increase in expression of adipocyte genes including adipocyte fatty acid binding protein and lipid-metabolizing enzymes. Characterization of regulatory regions of adipose-specific genes has led to the identification of the transcription factors peroxisome proliferator-activated receptor-γ (PPAR-γ) and CCAAT/enhancer binding protein (C/EBP), which play a key role in the complex transcriptional cascade during adipocyte differentiation. Growth and differentiation of preadipocytes is controlled by communication between individual cells or between cells and the extracellular environment. Various hormones and growth factors that affect adipocyte differentiation in a positive or negative manner have been identified. In addition, components involved in cell-cell or cell-matrix interactions such as preadipocyte factor-1 and extracellular matrix proteins are also pivotal in regulating the differentiation process. Identification of these molecules has yielded clues to the biochemical pathways that ultimately result in transcriptional activation via PPAR-γ and C/EBP. Studies on the regulation of the these transcription factors and the mode of action of various agents that influence adipocyte differentiation will reveal the physiological and pathophysiological mechanisms underlying adipose tissue development.
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Rondinone, Cristina M. "Adipocyte-Derived Hormones, Cytokines, and Mediators." Endocrine 29, no. 1 (2006): 81–90. http://dx.doi.org/10.1385/endo:29:1:81.

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Faraj, May, Hui Ling Lu, and Katherine Cianflone. "Diabetes, lipids, and adipocyte secretagogues." Biochemistry and Cell Biology 82, no. 1 (February 1, 2004): 170–90. http://dx.doi.org/10.1139/o03-078.

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That obesity is associated with insulin resistance and type II diabetes mellitus is well accepted. Overloading of white adipose tissue beyond its storage capacity leads to lipid disorders in non-adipose tissues, namely skeletal and cardiac muscles, pancreas, and liver, effects that are often mediated through increased non-esterified fatty acid fluxes. This in turn leads to a tissue-specific disordered insulin response and increased lipid deposition and lipotoxicity, coupled to abnormal plasma metabolic and (or) lipoprotein profiles. Thus, the importance of functional adipocytes is crucial, as highlighted by the disorders seen in both "too much" (obesity) and "too little" (lipodystrophy) white adipose tissue. However, beyond its capacity for fat storage, white adipose tissue is now well recognised as an endocrine tissue producing multiple hormones whose plasma levels are altered in obese, insulin-resistant, and diabetic subjects. The consequence of these hormonal alterations with respect to both glucose and lipid metabolism in insulin target tissues is just beginning to be understood. The present review will focus on a number of these hormones: acylation-stimulating protein, leptin, adiponectin, tumour necrosis factor α, interleukin-6, and resistin, defining their changes induced in obesity and diabetes mellitus and highlighting their functional properties that may protect or worsen lipid metabolism.Key words: C3adesarg, fatty acid trapping, lipolysis, lipogenesis.
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Hernandez, Arturo, Bibian Garcia, and Maria-Jesus Obregon. "Gene Expression from the Imprinted Dio3 Locus Is Associated with Cell Proliferation of Cultured Brown Adipocytes." Endocrinology 148, no. 8 (August 1, 2007): 3968–76. http://dx.doi.org/10.1210/en.2007-0029.

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Active thyroid hormones are critical for the differentiation and function of brown adipose tissue. However, we have observed high basal and induced levels of type 3 deiodinase (D3), an enzyme that inactivates thyroid hormones and is coded by the imprinted gene Dio3, in differentiating brown preadipocytes in primary culture. We find that D3 activity and mRNA expression strongly correlate with the rate of proliferation of undifferentiated precursor cells under various conditions. Furthermore, differentiation of precursor cells to adipocytes is associated with decreased levels of D3 expression, and only very low levels of D3 mRNA are found in mature adipocytes. Dlk1, an inhibitor of adipocyte differentiation and a paternally expressed gene located in the same imprinted domain as Dio3, displayed changes in expression that parallel those of Dio3. In contrast, a 4-kb transcript for Dio3os, an antisense gene also located in the same imprinted domain, is markedly up-regulated in differentiated adipocytes. We conclude that D3 expression in differentiating preadipocytes is primarily linked to proliferating cells, whereas Dio3os expression is associated with mature adipocytes. Our results suggest that genomic imprinting and gene expression at the Dlk1/Dio3 imprinted domain may play a role in the regulation of adipocyte proliferation and differentiation.
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Dissertations / Theses on the topic "Adipocyte hormones"

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Eriksson, Maria. "Adipocyte-derived hormones and cardiovascular disease." Doctoral thesis, Umeå universitet, Institutionen för folkhälsa och klinisk medicin, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-36679.

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Obesity is increasing globally and related to major changes in lifestyle. This increase is associated with an increased risk of cardiovascular disease (CVD). Knowledge about adipose tissue as a metabolic-endocrine organ has increased during the last few decades. Adipose tissue produces a number of proteins with increased body weight, many of which are important for food intake and satiety, insulin sensitivity, and vessel integrity, and aberrations have been related to atherosclerosis. Notably, the risk for developing CVD over the course of a lifetime differs between men and women. In Northern Sweden, men have a higher risk for myocardial infarction (MI). However, the incidence is declining in men but not in women. These sex differences could be due to functional and anatomical differences in the fat mass and its functions. The primary aim of this thesis was to evaluate associations between the adipocyte-derived hormones leptin and adiponectin, and fibrinolysis and other variables associated with the metabolic syndrome, and particularly whether these associations differ between men and women. Another aim was to evaluate these associations during physical exercise and pharmacological intervention (i.e. enalapril). Finally, whether leptin and adiponectin predict a first MI or sudden cardiac death with putative sex differences was also investigated. The first study used a cross-sectional design and included 72 men and women  recruited from the WHO MONICA project. We found pronounced sex differences in the associations with fibrinolytic variables. Leptin was associated with fibrinolytic factors in men, whereas insulin resistance was strongly associated with all fibrinolytic factors in women. The second study was an experimental observational study with 20 men exposed to strenuous physical exercise. During exercise, leptin levels decreased and adiponectin levels increased, and both were strongly associated with an improved fibrinolytic capacity measured as decreased PAI-1 activity. Changes in insulin sensitivity were not associated with changing adiponectin levels. The third study was a randomised, double-blind, single centre clinical trial including 46 men and 37 women who had an earlier MI. The study duration was one year, and participating subjects were randomised to either placebo or ACE inhibitor (i.e. enalapril). Circulating leptin levels were not associated with enalapril treatment. During the one-year study, changes in leptin levels were associated with changes in circulating levels of tPA mass, PAI-1 mass, and tPA-PAI complex in men, but not vWF. These associations were found in all men and men on placebo treatment. In women on enalapril treatment there was an association between changes in leptin and changes in vWF. In the fourth study, the impact of leptin, adiponectin, and their ratio on future MI risk or sudden cardiac death was tested in a prospective nested casecontrol study within the framework of the WHO MONICA, Västerbotten Intervention Project (VIP), and Västerbotten  Mammary Screening Program (MSP). A total 564 cases (first-ever MI or sudden cardiac death) and 1082 matched controls were selected. High leptin, low adiponectin, and a high leptin/adiponectin ratio independently predicted a first-ever MI, possibly with higher risk in men in regards to leptin. The association was found for non-fatal cases with ST-elevation MI. Subjects with low adiponectin levels had their MI earlier than those with high levels. In conclusion, the adipocyte-derived hormones leptin and adiponectin are related to the development of CVD with a sex difference, and fibrinolytic mechanisms could be possible contributors to CVD risk.
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Lu, Buyu. "Hormones of stress and control of adipocyte biological "colour"." Thesis, University of Warwick, 2011. http://wrap.warwick.ac.uk/46849/.

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The family of “stress” peptides that includes CRH and UCNs are emerging as important regulators of the homeostatic mechanisms regulating energy balance and metabolism. These peptides exert well documented central anorectic and thermogenic actions in controlling food uptake and optimise energy losses. Furthermore, CRH acting through specific G-protein coupled receptors, CRH-R1 and R2 can target multiple peripheral tissues such as skeletal muscle and adipose tissue to influence important metabolic pathways. Two types of adipose tissue exist in mammals: WAT and BAT. Since WAT is the largest energy reserve in mammals and BAT can utilize energy through adaptive thermogenesis, one of the goals in this study was to identify the presence of CRH system components in adipose tissue. Real time RT-PCR and immunofluorescence demonstrated that CRH-Rs as well as CRH, UCN-I, and UCN-II are expressed in both WAT and BAT, raising the possibility that CRH and UCNs are important regulators of energy storage and adaptive thermogenesis. Also the functional roles of CRH-Rs in adipose tissue were investigated. Using an experimental paradigm the T37i fibroblast that can differentiate into brown adipocyte, it was demonstrated that CRH at low (nanomolar) but not high (submicromolar) concentrations stimulated a signaling pathway involving the AC/cAMP/PKA/AMPK signaling cascade that regulates downstream phosphorylation of HSL. This was associated with a significant translocation of HSL toward lipid droplets and association with perilipin, as demonstrated with immunofluorescence. Studies applying quantitative RT-PCR also suggested that CRH-R1 appears to regulate genes important for adaptive thermogenesis, whereas CRH-R2 likely regulates brown adipocyte formation. Further analysis using an experimental paradigm the 3T3L1 fibroblast that can differentiate into white adipocyte showed that exposure of 3T3L1 cells to UCN-II (a specific CRH-R2 agonist) or NBI-27914 (a CRH-R1 specific antagonist) were able to induce morphological and biochemical characteristics suggesting adipocyte differentiation to a “beige” phenotype in white preadipocytes/adipocytes. Thus, CRH-R1 and R2 could be of potential importance in maintenance of energy homeostasis. Moreover, in vivo analysis showed that CRH system seems to demonstrate a certain degree of plasticity in response to stress perturbation. For instance, HFD significantly repressed the expression of CRH-Rs and their agonists, whereas food deprivation dramatically increased their expression. The analysis of quantitative RTPCR demonstrated that this activation of CRH system might be associated with induction of ‘beige’ cells in white fat depots. Since CRH-R1 KO mice displayed a lean phenotype and resistance to HFD-induced fat accumulation and these phenotypes can be reversed by supplementation of corticosterone, role of CRH-R2 in adipose tissue of these KO mice was investigated. Data showed that CRH-R2 activation likely induced BAT activity and transdifferentiation from WAT to BAT in CRH-R1 KO mice. Corticosterone reversed these changes in KO mice via potential suppression of CRH-R2.
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Auffret, Julien. "Impact des hormones lactogènes sur la cellule β pancréatique et l’adipocyte." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T087/document.

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Pour étudier l’impact de la signalisation de la prolactine (PRL), une hormone impliquée dans la proliférationcellulaire sur l’adipocyte et la cellule β pancréatique, deux types cellulaires impliqués dans la balanceénergétique, nous avons caractérisé le phénotype de souris déficientes en récepteur de la PRL (R PRL-/-) sousdifférentes conditions physiopathologiques. Dans un premier temps, nous avons étudié l’impact du R PRL sur ledéveloppement d’une obésité induite par un régime obésogène. Dans un deuxième temps, nous nous sommesintéressés à l’impact du R PRL sur l’ontogenèse des cellules β durant les adaptations périnatales. Nous avonsaussi évalué son rôle sur la sécrétion d’insuline à l’âge adulte.Notre première étude montre que les souris R PRL-/- sous régime obésogène ont une prise de poids réduite etune augmentation de la dépense énergétique comparées à celles des souris sauvages. Nous montrons que desadipocytes beiges, une nouvelle classe d’adipocytes thermoactifs récemment caractérisés et exprimant laprotéine découplante UCP1, émergent dans le tissu adipeux blanc périrénal des souris R PRL-/- soumises à unrégime gras. Nous avons démontré que le R PRL contribue à l’apparition des adipocytes beiges en modulant lavoie de signalisation pRb/FoxC2 permettant la résistance à l’obésité induite par le régime gras.Notre deuxième étude montre que la souris R PRL-/- et le rat GK, un modèle de diabète de type 2, ont un défautd’adaptation de la masse des cellules β en période périnatale. Cette altération est corrélée à un défautd’expression d’igf2 (Insulin-like Growth Factor 2), une cible de la PRL. A partir d’îlots de Langherans de sourisadultes, nous avons confirmé que le R PRL est essentiel à la sécrétion d’insuline.Les résultats obtenus ont permis de mieux comprendre le rôle de la PRL sur la balance énergétique. Ces travauxouvrent des perspectives nouvelles pour le développement de stratégies thérapeutiques dans la lutte contrel’obésité et le diabète de type II
In order to study the impact of prolactin (PRL) signaling on pancreatic β-cell and adipocyte, two cell typesinvolved in energy balance, we characterized the phenotype of PRL receptor deficient mice (PRL R-/-) underdifferent physiopathological conditions. First, we studied the impact of PRL R on the development of obesityinduced by a high fat diet. Second, we investigated the impact of PRL R on β-cell ontogenesis during perinataladaptation and its role in insulin secretion during adulthood.Our first study shows that PRL R-/- mice under obesogenic diet have a reduced weight gain and an increase ofenergy expenditure as compared to those of wild-type mice. We showed that beige adipocytes, a new class ofthermogenic adipocytes recently characterized expressing uncoupling protein UCP1, emerged in the perirenalwhite adipose tissue of PRL R-/- mice challenged with a high fat diet. Altered expression of pRb/FoxC2 suggeststhat PRL R contributes to the development of beige adipocytes modulating this signaling pathway for resistanceto high fat diet induced obesity.Our second study shows that PRL R-/- mice do not adapt β-cell mass in perinatal period and this alteration isassociated with a lack of igf2 (Insulin-like Growth Factor 2) expression, a PRL target. We confirmed that R PRL isessential for insulin secretion using b islets in adult animals.These results lead to a better understanding of the PRL role on energy balance, and open new perspectives forthe development of therapeutic strategies in obesity and type II diabetes
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Ortega, Delgado Francisco José. "Mecanismos de regulación del anabolismo lipídico en el tejido adiposo del paciente obeso." Doctoral thesis, Universitat de Girona, 2012. http://hdl.handle.net/10803/83713.

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Obesity is one of the most important public health problems facing the world today. Gene expression studies applied to fat depots from obese subjects have provided important clues about the pathophysiology of adipose tissue. The data collected in this thesis show that the synthesis of fatty acids (lipogenesis) is decreased in the adipose tissue of obese subjects, and describe the behavior of a new lipogenic factor. We also demonstrate that subcutaneous fat (beneath the skin of the buttocks, thighs and abdomen) is characterized by a greater responsiveness to thyroid hormones than the visceral (around the omentum, the intestines and the perirenal areas), and describe the increased activity of enzymes that activate thyroid hormones in adipose tissue of obese patients and the effects on the metabolism. According to these results, the local activation of thyroid hormone and the ability to synthesize fat are altered in adipose tissue from obese patients, and indicate significant differences between visceral and subcutaneous adipose tissue depots.
La obesidad es uno de los problemas de salud pública más importante. Los estudios de expresión aplicados a los depósitos de grasa en sujetos obesos han aportado importantes indicios sobre la fisiopatología del tejido adiposo. Los datos recogidos en esta tesis doctoral demuestran que la síntesis de grasa (lipogénesis) está disminuida en el tejido adiposo del paciente obeso, y describen el comportamiento de un nuevo factor lipogénicos. Se demuestra además que el tejido adiposo subcutáneo (situado bajo la piel de las nalgas , muslos y abdomen) está caracterizado por una mayor capacidad de respuesta a las hormonas tiroideas respecto al adiposo visceral (alrededor del epiplón, los intestinos y las áreas perirrenal) y se describe un incremento en la actividad de las enzimas que activan las hormonas tiroideas en el tejido adiposo del paciente obeso y los posibles efectos de esta eventualidad sobre el metabolismo. Según los resultados recopilados en esta tesis doctoral, la activación local de hormonas tiroideas y la capacidad para sintetizar acidos grasos del tejido adiposo del paciente obeso están alteradas, e indican importantes diferencias entre los depósitos de grasa visceral y subcutáneo.
L’obesitat és un dels problemes de salut pública més important. Els estudis d'expressió aplicats als dipòsits de greix en subjectes obesos han aportat importants indicis sobre la fisiopatologia del teixit adipós. Les dades recollides a aquesta tesi doctoral demostren que la síntesis de greix (lipogènesis) està disminuïda al teixit adipós del pacient obès, i descriuen el comportament d'un nou factor lipogènic. Es demostra, a més a més, que el teixit adipós subcutani (situat sota la pell de les natges, cuixes i abdomen) està caracteritzat per una major capacitat de resposta a les hormones tiroidees respecte a l'adipós visceral (al voltant de l’epipló, els intestins i las àrees perirenals) i es descriu un increment en l’activitat dels enzims que activen les hormones tiroidees al teixit adipós del pacient obès i els possibles efectes d'aquesta eventualitat sobre el metabolisme. Segons els resultats recopilats a aquesta tesi doctoral, l’activació local d'hormones tiroidees i la capacitat per sintetitzar greixos del teixit adipós del pacient obès estan alterades, i indiquen importants diferències entre els dipòsits de greix visceral i subcutani.
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Plee-Gautier, Emmanuelle. "Regulation par les hormones et les nutriments de l'expression de deux genes du metabolisme intermediaire de l'adipocyte ; la lipase hormono-sensible et l'aspartate aminotransferase." Paris 11, 1997. http://www.theses.fr/1997PA11T034.

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Christianson, Jennifer L. "Defining the Importance of Fatty Acid Metabolism in Maintaining Adipocyte Function: A Dissertation." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/415.

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Although once considered a simple energy storage depot, the adipose tissue is now known to be a powerful regulator of whole body insulin sensitivity and energy metabolism. This metabolically dynamic organ functions to safely store excess fatty acid as triglyceride, thereby preventing lipotoxicity in peripheral tissues and the development of insulin resistance. In addition, the adipose tissue acts as an endocrine organ and secretes factors, called adipokines, which influence whole body insulin sensitivity and glucose homeostasis. Therefore, understanding adipose tissue development and biology is essential to understanding whole body energy metabolism. A master regulator of adipose tissue development and whole body insulin sensitivity is the nuclear receptor, PPARγ. Due to the importance of this nuclear receptor in maintaining adipocyte function, disruptions in PPARγ activity result in severe metabolic abnormalities, such as insulin resistance and type 2 diabetes. Conversely, PPARγ activation by synthetic agonists ameliorates these conditions, demonstrating the potent control this nuclear receptor has on whole body metabolism. Therefore, understanding how PPARγ expression and activity are regulated, particularly in the adipose tissue, is paramount to understanding the pathogenesis of type 2 diabetes. While there are several synthetic PPARγ agonists available, identifying the endogenous ligand or ligands is still an area of intense investigation. Since fatty acids can induce PPARγ activation, in the first part of this thesis, I screened several fatty acid metabolizing enzymes present in the adipocyte to identify novel modulators of PPARγ activity. These studies revealed that the fatty acid Δ9 desaturase, Stearoyl CoA Desaturase 2 (SCD2), is absolutely required for 3T3-L1 adipogenesis and to maintain adipocyte-specific gene expression in fully differentiated cells. Although SCD2 does not appear to regulate PPARγ ligand production, it does potently regulate PPARγ activity by maintaining the synthesis of PPARγ protein. Surprisingly, this effect was found only with SCD2 and not with the highly homologous protein, SCD1. Therefore, these findings identify separate cellular functions for these SCD isoforms and reveal a novel and essential role for fatty acid desaturation in the adipocyte. Equally important to understanding PPARγ regulation is identifying the downstream mechanisms by which PPARγ activation improves insulin sensitivity. Evidence suggests that the PPARγ target gene, Cidea, is involved in mediating insulin sensitivity by binding to lipid droplets and promoting lipid storage in the adipocyte. Therefore, the second part of thesis provides mechanistic detail into Cidea function by showing that the carboxy terminal 104 amino acids is necessary and sufficient for lipid droplet targeting and the stimulation of triglyceride storage. However, these studies also identified a novel function for Cidea, which requires both the carboxy and amino termini: to induce larger and fewer droplets from smaller dispersed droplets, indicating the possible fusion of droplets. Perhaps this striking change in lipid droplet morphology allows tighter packing and more efficient storage of triglyceride and identifies a novel role for Cidea in lipid metabolism. The results presented in this thesis elucidate key aspects of lipid metabolism that maintain adipocyte function: SCD2 is required to maintain PPARγ protein expression in the mouse; Cidea is a downstream effector of PPARγ activity by promoting efficient triglyceride storage. Therefore, these findings enhance our understanding of adipocyte biology.
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Liu, Jing, and 刘静. "Investigation of the molecular mechanisms underlying the anti-breast cancer activity of an adipocyte-derived hormone, adiponectin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46503237.

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Lau, Tik-yan Ivy. "Macrophage-adipocyte cross-talk in the initiation of obesity-related insulin resistance and type 2 diabetes : role of adiponectin /." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B4129046X.

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Hoong, Isabelle Yoke Yien. "Expression of 11β-hydroxysteroid dehydrogenases in mice and the role of glucocorticoids in adipocyte function." Monash University, Dept. of Biochemistry and Molecular Biology, 2003. http://arrow.monash.edu.au/hdl/1959.1/9473.

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Lau, Tik-yan Ivy, and 劉荻茵. "Macrophage-adipocyte cross-talk in the initiation of obesity-related insulin resistance and type 2 diabetes: roleof adiponectin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B4129046X.

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Books on the topic "Adipocyte hormones"

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Steenbock Symposium (27th 1999 Madison, Wis.). Adipocyte biology and hormone signaling. Amsterdam, The Netherlands: IOS Press, 2000.

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Adipocyte Biology and Hormone Signaling (Biomedical and Health Research). Ios Pr Inc, 2000.

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Litwack, Gerald. Adiponectin. Elsevier Science & Technology Books, 2012.

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Book chapters on the topic "Adipocyte hormones"

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Goodman, H. Maurice, Genevieve Grichting, and Vittorio Coiro. "Growth Hormone Action on Adipocytes." In Human Growth Hormone, 499–512. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7201-5_39.

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Goodman, H. Maurice, Erela Gorin, Genevieve Grichting, Thomas W. Honeyman, Jaroslaw Szecowka, Lih-Ruey Tai, and Leonard R. Waice. "Growth Hormone Receptors in Rat Adipocytes." In Basic and Clinical Aspects of Growth Hormone, 189–98. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5505-2_17.

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Goodman, H. Maurice, G. Peter Frick, Tova Bick, Lih-Ruey Tai, and Jack L. Leonard. "Expression of the Short Isoform of the Growth Hormone Receptor in Adipocytes." In Growth Hormone II, 301–16. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4613-8372-7_23.

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Schwartz, J., C. Carter-Su, C. M. Foster, and J. A. Shafer. "Direct actions of growth hormone and insulin-like growth factor in cultured adipocytes." In Advances in Growth Hormone and Growth Factor Research, 85–100. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-11054-6_6.

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Hirako, Satoshi. "Adipocyte Hormones." In Handbook of Hormones, 304—e34–1. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801028-0.00034-9.

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Hirako, Satoshi. "Adipocyte hormones." In Handbook of Hormones, 571–72. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-820649-2.00145-5.

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Richard, Allison J., and Jacqueline M. Stephens. "Adipocyte-Derived Hormones." In Hormonal Signaling in Biology and Medicine, 461–86. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-813814-4.00020-1.

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Infante, Marco, Andrea Armani, Vincenzo Marzolla, Andrea Fabbri, and Massimiliano Caprio. "Adipocyte Mineralocorticoid Receptor." In Vitamins and Hormones, 189–209. Elsevier, 2019. http://dx.doi.org/10.1016/bs.vh.2018.10.005.

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Mir, Sajad Hussain, and Attiya Baddar. "Association between Urinary Bisphenol A Concentration and Obesity Prevalence in Children and Adolescents." In Handbook of Research on Environmental and Human Health Impacts of Plastic Pollution, 214–45. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-5225-9452-9.ch012.

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Abstract:
Bisphenol A is an organic compound that serves as a building block of polycarbonate plastics and epoxy resins. Being the world's highest-volume chemicals in use today in the form of medical devices, water and infant bottles, food cans, kitchen utensils, water supply pipes, compact devices, etc., this compound—after gaining an access to the body of an individual by way of leaching into food and water supplies—acts as an obesogen and disrupts the body weight regulation by either promoting adipogenesis or triggering the differentiation of fibroblasts into adipocytes. The other adverse effects of bisphenol A include insulin resistance, adipocyte differentiation or aromatase-mediated transformation of androgen into estrogen, cardiovascular diseases, liver function abnormalities, alterations in the circulating thyroid hormone levels, association with diabetes and carcinogenic effect. Its other aspects on health individually as well as in combination with other chemicals are worth mentioning.
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RINGOLD, GORDON M., ALGER B. CHAPMAN, DAVID M. KNIGHT, MARC NAVRE, and FRANK M. TORTI. "Hormonal Control of Adipocyte Differentiation and Adipocyte Gene Expression." In Proceedings of the 1987 Laurentian Hormone Conference, 115–40. Elsevier, 1988. http://dx.doi.org/10.1016/b978-0-12-571144-9.50008-9.

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Conference papers on the topic "Adipocyte hormones"

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Shimon, Naama, Orna Shaharabani-Yosef, Uri Zaretsky, and Amit Gefen. "Adipocytes Respond to Mechanical Stretch by Producing More Lipids." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53057.

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Obesity is a leading preventable cause of mortality and morbidity worldwide, with increasing prevalence in adults as well as in children [1]. Authorities often view obesity as one of the most serious public health problems of the 21st century. Treating obesity is aimed at decreasing the amount of excessive adipose tissue by changing the balance between intake and expenditure of energy, via physical exercise, diet control or both, under the assumption that if there are no hormonal disorders present, the obesity is caused by calorie consumption that is not counterbalanced by sufficient calorie burn.
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Liu, Chun, Seungik Baek, and Christina Chan. "The Complementary Effect of Mechanical and Chemical Stimuli on the Neural Differentiation of Mesenchymal Stem Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80131.

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Mesenchymal stem cells (MSCs), derived from bone marrow stroma, are a promising source for tissue repair and regeneration, due to their excellent abilities for proliferation and multipotent differentiation. While accumulated evidences during the past decade have shown that MSCs are able to differentiate into osteoblasts, chondrocytes, myoblasts and adipocytes, more recent research suggest their potential in neuronal differentiation [1]. Chemical stimuli, including growth factors, hormones, and other regulatory molecules, are used traditionally to direct MSC differentiation. Our group has previously shown that the intracellular second messenger, cAMP, is able to initiate early phase neuron-like morphology changes and late phase neural differentiation in MSCs [2]. Studies using chemical stimuli alone, however, have shown limited success in differentiating MSCs to mature neurons, thereby suggesting other factors are necessary for this process. In recent years, interest has grown on the impact of mechanical stimulation, such as stiffness, surface topography, and mechanical stretching, on cell fate decision [3].
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Zinser, Glendon M., Soumya Kashinkunti, and Matt Niehaus. "Abstract A57: Breast adipocytes bioactivate Vitamin D3and regulate hormone-induced epithelial cell growth." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Nov 7-10, 2010; Philadelphia, PA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-10-a57.

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