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Articles de revues sur le sujet « Leptin receptors »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 31 janvier 2023

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1

Panić, Anastasija, Sanja Soskić, and Esma Isenović. "Leptin and its mechanism of action." Medicinska istrazivanja 49, no. 3 (2015): 36–41. http://dx.doi.org/10.5937/medist1502036p.

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Leptin is a hormone produced by the adipose tissue, which has effects on the central nervous system. Leptin is bound to its Ob receptor on hypo-thalamic neurons to inhibit feeding behavior and to increase sympathetically-mediated thermogenesis. In addition to anorexia and thermogenesis, leptin also has direct peripheral and central nervous system-mediated effects on the endocrine, vascular, hematopoietc, immune and musculoskeletal systems. Leptin accomplishes its effects using distributed network of leptin receptors and differential molecular signaling pathways. Leptinemia is increased in obes

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Gertler, A., Y. Sandowski, and N. Raver. "Recombinant leptin mutants and leptin binding proteins aimed to block leptin action in vivo." Proceedings of the British Society of Animal Science 2002 (2002): 48. http://dx.doi.org/10.1017/s1752756200007043.

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Obese protein (OB) also known as leptin serves as a protein signal secreted from adipose tissue and acts on a central nervous system that regulate ingestive behavior and energy balance (Campfield, 2000). The sequence of various leptins from 10 mammalian species was compiled and the 3D structure of human leptin mutant W100E was elucidated (Zhang et al., 1997). We have prepared recombinant leptins of sheep, chicken, cow and pig. Mammalian and chicken leptins are respectively 146 and 145 amino acid containing proteins found in circulation. Leptin in blood is found in both free and bound form; the

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Borodkina, Daria A., Olga V. Gruzdeva, Olga E. Akbasheva, Ekaterina V. Belik, Elena I. Palicheva, and Olga L. Barbarash. "Leptin resistance: unsolved diagnostic issues." Problems of Endocrinology 64, no. 1 (April 9, 2018): 62–66. http://dx.doi.org/10.14341/probl201864162-66.

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Leptin and its receptors are key regulators of body weight and energy homeostasis. A decrease in tissue sensitivity to leptin leads to the development of obesity, insulin resistance, dyslipidemia, etc. Currently, the phenomenon of leptin resistance is explained by a number of mechanisms, including impairment of gene structure, leptin transport through the blood-brain barrier, and leptin receptor signaling. However, it is not known, a decrease in the number of receptors of which area leads to the development of leptin resistance. No relationship has been found between the basal leptin level in

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Borodkina, Daria A., Olga V. Gruzdeva, Olga E. Akbasheva, Ekaterina V. Belik, Elena I. Palicheva, and Olga L. Barbarash. "Leptin resistance: unsolved diagnostic issues." Problems of Endocrinology 64, no. 1 (April 9, 2018): 62–66. http://dx.doi.org/10.14341/probl8740.

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Leptin and its receptors are key regulators of body weight and energy homeostasis. A decrease in tissue sensitivity to leptin leads to the development of obesity, insulin resistance, dyslipidemia, etc. Currently, the phenomenon of leptin resistance is explained by a number of mechanisms, including impairment of gene structure, leptin transport through the blood-brain barrier, and leptin receptor signaling. However, it is not known, a decrease in the number of receptors of which area leads to the development of leptin resistance. No relationship has been found between the basal leptin level in

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Skibicka, Karolina P., and Harvey J. Grill. "Hindbrain Leptin Stimulation Induces Anorexia and Hyperthermia Mediated by Hindbrain Melanocortin Receptors." Endocrinology 150, no. 4 (September 10, 2008): 1705–11. http://dx.doi.org/10.1210/en.2008-1316.

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Of the central nervous system receptors that could mediate the energy balance effects of leptin, those of the hypothalamic arcuate nucleus receive the greatest attention. Melanocortin receptors (MC-Rs) contribute to the feeding and energetic effects of hypothalamically delivered leptin. Energy balance effects of leptin are also mediated by extrahypothalamic neurons including the hindbrain nucleus tractus solitarius. Hindbrain leptin receptors play a role in leptin’s anorectic effects, but their contribution to its energetic effects and their functional interaction with melanocortin systems wit

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Pan, Weihong, Hung Hsuchou, Hong Tu, and Abba J. Kastin. "Developmental Changes of Leptin Receptors in Cerebral Microvessels: Unexpected Relation to Leptin Transport." Endocrinology 149, no. 3 (November 26, 2007): 877–85. http://dx.doi.org/10.1210/en.2007-0893.

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The adipokine leptin participates not only in the regulation of feeding and obesity in adults but also in neonatal development. It crosses the blood-brain barrier (BBB) by receptor-mediated transport. Leptin concentrations in blood differ between neonates and adults. We determined the developmental changes of leptin receptor subtypes in the cerebral microvessels composing the BBB and examined their expected correlation with leptin transport across the BBB. Total RNA was extracted from enriched cerebral microvessels of mice 1, 7, 14, and 60 d of age for real-time RT-PCR analysis of leptin recep

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Harris, Ruth B. S. "Leptin-induced increase in body fat content of rats." American Journal of Physiology-Endocrinology and Metabolism 304, no. 3 (February 1, 2013): E267—E281. http://dx.doi.org/10.1152/ajpendo.00251.2012.

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We previously reported that peripheral leptin infusions in chronically decrebrate rats, in which the forebrain is neurally isolated from the hindbrain, increased body fat and decreased energy expenditure. Any central leptin response in decerebrate rats would depend upon the hindbrain. Here, we tested whether selective activation of hindbrain leptin receptors increased body fat. Fourth ventricle infusion of 0.6 μg leptin/day for 12 days increased body fat by 13% with no increase in food intake. Third ventricle leptin infusions decreased food intake, body fat, and lean tissue with a maximal resp

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BENOMAR, Yacir, Anne-France ROY, Alain AUBOURG, Jean DJIANE, and Mohammed TAOUIS. "Cross down-regulation of leptin and insulin receptor expression and signalling in a human neuronal cell line." Biochemical Journal 388, no. 3 (June 7, 2005): 929–39. http://dx.doi.org/10.1042/bj20041621.

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Leptin and insulin are major signals to the hypothalamus to regulate energy homoeostasis and body adiposity. IR (insulin receptors) and leptin receptors (long isoform, ObRb) share a number of signalling cascades, such as JAK2/STAT-3 (Janus kinase 2/signal transduction and activator of transcription 3) and PI3K (phosphoinositide 3-kinase); the cross-talk between IR and ObRb have been described previously in non-neuronal cells. Differentiated human neuroblastoma (SH-SY5Y) cells express endogenous ObR and IR, and respond to leptin and insulin with stimulation of STAT-3 and MAPK (mitogen-activated

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Boroń, Dariusz, Robert Nowakowski, Beniamin Oskar Grabarek, Nikola Zmarzły, and Marcin Opławski. "Expression Pattern of Leptin and Its Receptors in Endometrioid Endometrial Cancer." Journal of Clinical Medicine 10, no. 13 (June 24, 2021): 2787. http://dx.doi.org/10.3390/jcm10132787.

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The identification of novel molecular markers and the development of cancer treatment strategies are very important as cancer incidence is still very high. Obesity can contribute to cancer progression, including endometrial cancer. Adipocytes secrete leptin, which, when at a high level, is associated with an increased risk of cancer. The aim of this study was to determine the expression profile of leptin-related genes in the endometrial tissue samples and whole blood of patients. The study material included tissue samples and whole blood collected from 30 patients with endometrial cancer and 3

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Wada, Nobuhiro, Satoshi Hirako, Fumiko Takenoya, Haruaki Kageyama, Mai Okabe, and Seiji Shioda. "Leptin and its receptors." Journal of Chemical Neuroanatomy 61-62 (November 2014): 191–99. http://dx.doi.org/10.1016/j.jchemneu.2014.09.002.

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Fernandez-Galaz, C., T. Fernandez-Agullo, F. Campoy, C. Arribas, N. Gallardo, A. Andres, M. Ros, and JM Carrascosa. "Decreased leptin uptake in hypothalamic nuclei with ageing in Wistar rats." Journal of Endocrinology 171, no. 1 (October 1, 2001): 23–32. http://dx.doi.org/10.1677/joe.0.1710023.

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Leptin interacts with specific receptors in hypothalamic nuclei and modulates energy balance. Growing evidence has shown the association of obesity and hyperleptinaemia with non-insulin-dependent diabetes mellitus and insulin resistance. The aged Wistar rat shows peripheral insulin resistance in the absence of obesity and alterations of glucose homeostasis. However, it is not known whether, in these animals, the leptin action is altered. Here we studied the effect of ageing on plasma leptin concentration and the ability of hypothalamic nuclei to capture i.c.v.-injected digoxigenin-labelled lep

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Sahin, Gulcan Semra, Jose Luis Rodriguez-Llamas, Crystal Dillon, Igor Medina, Suzanne M. Appleyard, Jean-Luc Gaiarsa та Gary A. Wayman. "Leptin increases GABAergic synaptogenesis through the Rho guanine exchange factor β-PIX in developing hippocampal neurons". Science Signaling 14, № 683 (18 травня 2021): eabe4111. http://dx.doi.org/10.1126/scisignal.abe4111.

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Developing hippocampal neurons undergo rapid synaptogenesis in response to neurotrophic signals to form and refine circuit connections. The adipokine leptin is a satiety factor with neurotrophic actions, which potentiates both glutamatergic and GABAergic synaptogenesis in the hippocampus during neonatal development. Brief exposure to leptin enhances GABAA receptor–dependent synaptic currents in hippocampal neurons. Here, using molecular and electrophysiological techniques, we found that leptin increased the surface localization of GABAA receptors and the number of functional GABAergic synapses

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Taildeman, Jasmien, Claudina A. Pérez-Novo, Isabelle Rottiers, Liesbeth Ferdinande, Anouk Waeytens, Veerle De Colvenaer, Claus Bachert, et al. "Human mast cells express leptin and leptin receptors." Histochemistry and Cell Biology 131, no. 6 (February 25, 2009): 703–11. http://dx.doi.org/10.1007/s00418-009-0575-3.

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Lin, Yen-Chang, Jianying Huang, Stan Hileman, Karen H. Martin, Robert Hull, Mary Davis, and Han-Gang Yu. "Leptin decreases heart rate associated with increased ventricular repolarization via its receptor." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 10 (November 15, 2015): H1731—H1739. http://dx.doi.org/10.1152/ajpheart.00623.2015.

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Leptin has been proposed to modulate cardiac electrical properties via β-adrenergic receptor activation. The presence of leptin receptors and adipocytes in myocardium raised a question as to whether leptin can directly modulate cardiac electrical properties such as heart rate and QT interval via its receptor. In this work, the role of local direct actions of leptin on heart rate and ventricular repolarization was investigated. We identified the protein expression of leptin receptors at cell surface of sinus node, atrial, and ventricular myocytes isolated from rat heart. Leptin at low doses (0.

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Moult, Peter R., and Jenni Harvey. "Regulation of glutamate receptor trafficking by leptin." Biochemical Society Transactions 37, no. 6 (November 19, 2009): 1364–68. http://dx.doi.org/10.1042/bst0371364.

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It is well established that leptin is a circulating hormone that enters the brain and regulates food intake and body weight via its hypothalamic actions. However, it is also known that leptin receptors are widely expressed in the CNS (central nervous system), and evidence is accumulating that leptin modulates many neuronal functions. In particular, recent studies have indicated that leptin plays an important role in the regulation of hippocampal synaptic plasticity. Indeed leptin-insensitive rodents display impairments in hippocampal synaptic plasticity and defects in spatial memory tasks. We

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Al-Shibli, Saad M., Norra Harun, Abdelkader E. Ashour, Mohd Hanif B. Mohd Kasmuri, and Shaikh Mizan. "Expression of leptin and leptin receptors in colorectal cancer—an immunohistochemical study." PeerJ 7 (October 2, 2019): e7624. http://dx.doi.org/10.7717/peerj.7624.

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Obesity is demonstrated to be a risk factor in the development of cancers of various organs, such as colon, prostate, pancreas and so on. Leptine (LEP) is the most renowned of the adipokines. As a hormone, it mediates its effect through leptin receptor (LEPR), which is widely expressed in various tissues including colon mucosa. In this study, we have investigated the degree of expression of LEP and LEPR in colorectal cancer (CRC). We collected 44 surgically resected colon cancer tissues along with normal adjacent colon tissue (NACT) from a sample of CRC patients from the Malaysian population a

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Hossner, Kim L. "Cellular, molecular and physiological aspects of leptin: Potential application in animal production." Canadian Journal of Animal Science 78, no. 4 (December 1, 1998): 463–72. http://dx.doi.org/10.4141/a98-061.

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This review encompasses the biochemistry and physiology of the newly discovered adipose hormone, leptin. Leptin appears to fulfill the role of the long sought after "lipostat", which functions to regulate energy intake in relation to body stores in the form of fat. Leptin is a 16 000 Dalton polypeptide which interacts with specific receptors in the hypothalamus to regulate food intake and body fat stores. Leptin receptors exist in several forms, which can be divided into those with small cytoplasmic domains and one with a single long cytoplasmic tail. The latter is thought to mediate most of l

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Madiehe, Abram M., Tiffany D. Mitchell та Ruth B. S. Harris. "Hyperleptinemia and reduced TNF-α secretion cause resistance of db/db mice to endotoxin". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, № 3 (1 березня 2003): R763—R770. http://dx.doi.org/10.1152/ajpregu.00610.2002.

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Leptin deficiency in ob/ob mice increases susceptibility to endotoxic shock, whereas leptin pretreatment protects them against LPS-induced lethality. Lack of the long-form leptin receptor (Ob-Rb) in db/db mice causes resistance. We tested the effects of LPS in C57BL/6J db3J/db3J (BL/3J) mice, which express only the circulating leptin receptors, compared with C57BL/6J db/db (BL/6J) mice, which express all short-form and circulating isoforms of the leptin receptor. Intraperitoneal injections of LPS significantly decreased rectal temperature and increased leptin, corticosterone, and free TNF-α in

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Harvey, J., L. J. Shanley, D. O'Malley, and A. J. Irving. "Leptin: a potential cognitive enhancer?" Biochemical Society Transactions 33, no. 5 (October 26, 2005): 1029–32. http://dx.doi.org/10.1042/bst0331029.

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It is well documented that the hormone leptin signals information regarding the status of fat stores to hypothalamic nuclei, which in turn control feeding behaviour and body weight. However, leptin and its receptor are widely expressed in many extra-hypothalamic brain regions, including hippocampus, brain stem and cerebellum. Moreover, evidence is accumulating that leptin has other neuronal functions that are unrelated to its effects on energy homeostasis. Indeed a role for leptin in neuronal development has been suggested as leptin-deficient rodents display abnormal brain development and lept

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Cammisotto, Philippe G., Diane Gingras, Christian Renaud, Emile Levy, and Moïse Bendayan. "Secretion of soluble leptin receptors by exocrine and endocrine cells of the gastric mucosa." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 2 (February 2006): G242—G249. http://dx.doi.org/10.1152/ajpgi.00334.2005.

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Leptin is a hormone secreted by the gastric mucosa into the lumen of the stomach. It is present in its intact form in the intestine where it regulates nutrient absorption and intestinal mucosa integrity. We have identified the binding protein that protects leptin from the harsh conditions of the gastric juice. Immunoprecipitations and Western blot analyses demonstrated that leptin is present in the gastric mucosa and the gastric juice, bound to a protein corresponding to the extracellular domain of the leptin receptor. In the absence of this soluble receptor, leptin is rapidly degraded. Immuno

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Karlsson, Cecilia, Kajsa Lindell, Eva Svensson, Christina Bergh, Peter Lind, Håkan Billig, Lena M. S. Carlsson, and Björn Carlsson. "Expression of Functional Leptin Receptors in the Human Ovary1." Journal of Clinical Endocrinology & Metabolism 82, no. 12 (December 1, 1997): 4144–48. http://dx.doi.org/10.1210/jcem.82.12.4446.

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The size of body fat stores is known to influence fertility, indicating a link between adipose tissue and the reproductive system. Studies in mice have identified the adipocyte-derived hormone, leptin (Ob protein), as a possible mediator of this effect. The aim of this study was to investigate the possibility that leptin may have direct effects on the human ovary. To probe this hypothesis we first analyzed the expression of leptin receptors in the human ovary. Transcripts encoding both the long and short isoforms of the leptin receptor were present in human granulosa cells and thecal cells; ho

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Ricci, A. G., M. P. Di Yorio, and A. G. Faletti. "Inhibitory effect of leptin on the rat ovary during the ovulatory process." Reproduction 132, no. 5 (November 2006): 771–80. http://dx.doi.org/10.1530/rep.1.01164.

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The aims of this study were to investigate the negative action of leptin on some intraovarian ovulatory mediators during the ovulatory process and to assess whether leptin is able to alter the expression of its ovarian receptors. Immature rats primed with gonadotrophins were used to induce ovulation. Serum leptin concentration was diminished 4 h after human chorionic gonadotrophin (hCG) administration, whereas the ovarian expression of leptin receptors, measured by western blot, was increased by the gonadotrophin treatment. Serum progesterone level, ovulation rate and ovarian prostaglandin E (

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Uddin, Shahab, and Ramzi M. Mohammad. "Role of leptin and leptin receptors in hematological malignancies." Leukemia & Lymphoma 57, no. 1 (July 7, 2015): 10–16. http://dx.doi.org/10.3109/10428194.2015.1063145.

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Friedman, Jeffrey M. "Leptin, Leptin Receptors, and the Control of Body Weight." Nutrition Reviews 56 (April 27, 2009): S38—S46. http://dx.doi.org/10.1111/j.1753-4887.1998.tb01685.x.

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Li, Raymond H. W., Sandy C. S. Poon, Mei Y. Yu, and Y. F. Wong. "Expression of Placental Leptin and Leptin Receptors in Preeclampsia." International Journal of Gynecological Pathology 23, no. 4 (October 2004): 378–85. http://dx.doi.org/10.1097/01.pgp.0000139647.40620.c8.

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Pulido-Mendez, Magdalena, Juan De Sanctis, and Alexis Rodriguez-Acosta. "Leptin and leptin receptors during malaria infection in mice." Folia Parasitologica 49, no. 4 (December 1, 2002): 249–51. http://dx.doi.org/10.14411/fp.2002.046.

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Seeley, Randy J., Keith A. Yagaloff, Stewart L. Fisher, Paul Burn, Todd E. Thiele, Gertjan van Dijk, Denis G. Baskin, and Michael W. Schwartz. "Melanocortin receptors in leptin effects." Nature 390, no. 6658 (November 1997): 349. http://dx.doi.org/10.1038/37016.

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Hall, Michael E., Grant Smith, John E. Hall, and David E. Stec. "Cardiomyocyte-specific deletion of leptin receptors causes lethal heart failure in Cre-recombinase-mediated cardiotoxicity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 12 (December 15, 2012): R1241—R1250. http://dx.doi.org/10.1152/ajpregu.00292.2012.

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Although disruption of leptin signaling is associated with obesity as well as cardiac lipid accumulation and dysfunction, it has been difficult to separate the direct effects of leptin on the heart from those associated with the effects of leptin on body weight and fat mass. Using Cre-loxP recombinase technology, we developed tamoxifen-inducible, cardiomyocyte-specific leptin receptor-deficient mice to assess the role of leptin in regulating cardiac function. Cre recombinase activation in the heart resulted in transient reduction in left ventricular systolic function which recovered to normal

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Cottrell, E. C., R. L. Cripps, J. S. Duncan, P. Barrett, J. G. Mercer, A. Herwig, and S. E. Ozanne. "Developmental changes in hypothalamic leptin receptor: relationship with the postnatal leptin surge and energy balance neuropeptides in the postnatal rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 3 (March 2009): R631—R639. http://dx.doi.org/10.1152/ajpregu.90690.2008.

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In the adult brain, leptin regulates energy homeostasis primarily via hypothalamic circuitry that affects food intake and energy expenditure. Evidence from rodent models has demonstrated that during early postnatal life, leptin is relatively ineffective in modulating these pathways, despite the high circulating levels and the presence of leptin receptors within the central nervous system. Furthermore, in recent years, a neurotrophic role for leptin in the establishment of energy balance circuits has emerged. The precise way in which leptin exerts these effects, and the site of leptin action, i

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Guerra, Borja, Alfredo Santana, Teresa Fuentes, Safira Delgado-Guerra, Alfredo Cabrera-Socorro, Cecilia Dorado, and Jose A. L. Calbet. "Leptin receptors in human skeletal muscle." Journal of Applied Physiology 102, no. 5 (May 2007): 1786–92. http://dx.doi.org/10.1152/japplphysiol.01313.2006.

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Human skeletal muscle expresses leptin receptor mRNA; however, it remains unknown whether leptin receptors (OB-R) are also expressed at the protein level. Fourteen healthy men (age = 33.1 ± 2.0 yr, height = 175.9 ± 1.7 cm, body mass = 81.2 ± 3.8 kg, body fat = 22.5 ± 1.9%; means ± SE) participated in this investigation. The expression of OB-R protein was determined in skeletal muscle, subcutaneous adipose tissue, and hypothalamus using a polyclonal rabbit anti-human leptin receptor. Three bands with a molecular mass close to 170, 128, and 98 kDa were identified by Western blot with the anti-OB

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Hileman, Stanley M., Jens Tornøe, Jeffrey S. Flier, and Christian Bjørbæk. "Transcellular Transport of Leptin by the Short Leptin Receptor Isoform ObRa in Madin-Darby Canine Kidney Cells*." Endocrinology 141, no. 6 (June 1, 2000): 1955–61. http://dx.doi.org/10.1210/endo.141.6.7450.

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Abstract Leptin is an adipocyte-derived hormone that acts in specific regions of the brain to regulate body weight and neuroendocrine function. The mechanism by which leptin enters the brain is unknown. We previously reported that rat brain microvessels, which constitute the blood-brain barrier, contain large amounts of messenger RNA encoding a short form of the leptin receptor (ObRa), suggesting that this site may be important for receptor-mediated transport of leptin into the brain. The purpose of this study was to determine whether ObRa is capable of transcellular transport of intact leptin

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Cao, G. Y., R. V. Considine, and R. B. Lynn. "Leptin receptors in the adrenal medulla of the rat." American Journal of Physiology-Endocrinology and Metabolism 273, no. 2 (August 1, 1997): E448—E452. http://dx.doi.org/10.1152/ajpendo.1997.273.2.e448.

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Leptin is the protein product of the recently cloned obesity gene. Leptin receptor mRNA is found in a number of central and peripheral locations. The hypothalamus is a presumed site of action. However, little is known about the specific locations of the receptor in peripheral organs. Epinephrine has potent anorectic effects and can cause weight loss by a variety of mechanisms. Excretion of epinephrine is reduced in the ob/ob mouse, which lacks leptin, suggesting an effect by leptin on the adrenal medulla. In the current study, the presence of the leptin receptor was identified on epinephrine-s

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AL-Barzinji, Ruqaya M., and Ahmed A. AL-Naqshbandi. "Estimation of Leptin and Leptin Receptor Concentrations in Seminal Plasma of Primary Infertile Men." Journal of the Faculty of Medicine Baghdad 59, no. 2 (July 2, 2017): 160–64. http://dx.doi.org/10.32007/jfacmedbagdad.592129.

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Background: There are many sources for Leptin secretion, and it is activated by binding with its receptor known as leptin receptor, that play a role in male infertility.Objective: To assess the levels of leptin and leptin receptors in seminal plasma among primary infertile men and its impact on semen parameters.Patients and Methods: A case control study of 75 primary infertile males and 40 healthy individuals who were enrolled in this study during March 2013 to May 2013. Estimation of age, body mass index (BMI), semen analysis, seminal plasma leptin, leptin receptor and testosterone hormone co

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Guo, Zhihong, Haiyang Jiang, Xiangru Xu, Wenzhen Duan, and Mark P. Mattson. "Leptin-mediated Cell Survival Signaling in Hippocampal Neurons Mediated by JAK STAT3 and Mitochondrial Stabilization." Journal of Biological Chemistry 283, no. 3 (November 9, 2007): 1754–63. http://dx.doi.org/10.1074/jbc.m703753200.

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Leptin plays a pivotal role in the regulation of energy homeostasis and metabolism, primarily by acting on neurons in the hypothalamus that control food intake. However, leptin receptors are more widely expressed in the brain suggesting additional, as yet unknown, functions of leptin. Here we show that both embryonic and adult hippocampal neurons express leptin receptors coupled to activation of STAT3 and phosphatidylinositol 3-kinase-Akt signaling pathways. Leptin protects hippocampal neurons against cell death induced by neurotrophic factor withdrawal and excitotoxic and oxidative insults. T

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Schulz, Solveig, Carsten Hackel, and Wolfgang Weise. "Hormonal regulation of neonatal weight: placental leptin and leptin receptors." BJOG: An International Journal of Obstetrics and Gynaecology 107, no. 12 (December 2000): 1486–91. http://dx.doi.org/10.1111/j.1471-0528.2000.tb11672.x.

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Li, Raymond H. W., May M. Y. Yu, Annie N. Y. Cheung, and Y. F. Wong. "Expression of leptin and leptin receptors in gestational trophoblastic diseases." Gynecologic Oncology 95, no. 2 (November 2004): 299–306. http://dx.doi.org/10.1016/j.ygyno.2004.06.040.

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Wasim, Muhammad, Fazli Rabbi Awan, Syeda Sadia Najam, Abdul Rehman Khan, and Haq Nawaz Khan. "Role of Leptin Deficiency, Inefficiency, and Leptin Receptors in Obesity." Biochemical Genetics 54, no. 5 (June 16, 2016): 565–72. http://dx.doi.org/10.1007/s10528-016-9751-z.

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Seamon, Marissa, WonMo Ahn, Ai-Jun Li, Sue Ritter, and Ruth B. S. Harris. "Leptin receptor-expressing neurons in ventromedial nucleus of the hypothalamus contribute to weight loss caused by fourth ventricle leptin infusions." American Journal of Physiology-Endocrinology and Metabolism 317, no. 4 (October 1, 2019): E586—E596. http://dx.doi.org/10.1152/ajpendo.00205.2019.

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Leptin administration into the hindbrain, and specifically the nucleus of the solitary tract, increases phosphorylated signal transducer and activator of transcription 3 (pSTAT3), a marker of leptin receptor activation, in hypothalamic nuclei known to express leptin receptors. The ventromedial nucleus of the hypothalamus (VMH) shows the greatest response, with a threefold increase in pSTAT3. This experiment tested the importance of VMH leptin receptor-expressing neurons in mediating weight loss caused by fourth ventricle (4V) leptin infusion. Male Sprague-Dawley rats received bilateral VMH 75-

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Glasow, A., W. Kiess, U. Anderegg, A. Berthold, A. Bottner, and J. Kratzsch. "Expression of Leptin (Ob) and Leptin Receptor (Ob-R) in Human Fibroblasts: Regulation of Leptin Secretion by Insulin." Journal of Clinical Endocrinology & Metabolism 86, no. 9 (September 1, 2001): 4472–79. http://dx.doi.org/10.1210/jcem.86.9.7792.

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Leptin, a hormone of the cytokine family, is mainly synthesized by white adipocytes. As fibroblasts and adipocytes share a common stem cell origin, we hypothesized that connective tissue may be another candidate for leptin synthesis. We demonstrated leptin receptors, inclusive of all isoforms, on cultured fibroblasts (n = 13) by RT-PCR and immunohistochemistry. In contrast to its receptor, basal leptin mRNA expression and protein secretion were found in 8 of 13 cultures, reaching 1.4 ng/350,000 cells·24 h. Incubation with physiological insulin concentrations (1 nmol/liter) increased leptin sec

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Almabhouh, Fayez A., Faizatul Isyraqiah Ahmad Muhammad, Hisham Ibrahim, and Harbindarjeet Singh. "Leptin: a pleitropic factor in physiology." Journal of Clinical and Health Sciences 4, no. 2 (December 31, 2019): 31. http://dx.doi.org/10.24191/jchs.v4i2.7551.

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Leptin, a 16 kDa protein and a product of the ob/ob gene, has a tertiary structure similar to that of a cytokine. It is primarily secreted by white adipose tissue and its levels in the blood correlate positively with percentage body fat. Leptin was first identified in 1994 as a major factor that regulated food intake and energy balance. Leptin in the circulation exists either as a free monomeric hormone or bound to its soluble receptor. Its serum levels usually range from 0.5 to 37.7 ng/ml in males and 2.0 to 45.2 ng/ml in females. The half-life of leptin is between 20 - 30 minutes and it is e

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Machinal-Quélin, F., M. N. Dieudonné, M. C. Leneveu, R. Pecquery, and Y. Giudicelli. "Proadipogenic effect of leptin on rat preadipocytes in vitro: activation of MAPK and STAT3 signaling pathways." American Journal of Physiology-Cell Physiology 282, no. 4 (April 1, 2002): C853—C863. http://dx.doi.org/10.1152/ajpcell.00331.2001.

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Because leptin has recently been shown to induce proliferation and/or differentiation of different cell types through different pathways, the aim of the present study was to investigate, in vitro, the influence of leptin on adipogenesis in rat preadipocytes. A prerequisite to this study was to identify leptin receptors (Ob-Ra and Ob-Rb) in preadipocytes from femoral subcutaneous fat. We observed that expressions of Ob-Ra and Ob-Rb increase during adipogenesis. Furthermore, leptin induces an increase of p42/p44 mitogen-activated protein kinase phosphorylated isoforms in both confluent and diffe

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Li, Ying, Xiaoyin Wu, Shiyi Zhou, and Chung Owyang. "Low-affinity CCK-A receptors are coexpressed with leptin receptors in rat nodose ganglia: implications for leptin as a regulator of short-term satiety." American Journal of Physiology-Gastrointestinal and Liver Physiology 300, no. 2 (February 2011): G217—G227. http://dx.doi.org/10.1152/ajpgi.00356.2010.

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The paradigm for the control of feeding behavior has changed significantly. Research has shown that leptin, in the presence of CCK, may mediate the control of short-term food intake. This interaction between CCK and leptin occurs at the vagus nerve. In the present study, we aimed to characterize the interaction between CCK and leptin in the vagal primary afferent neurons. Single neuronal discharges of vagal primary afferent neurons innervating the gastrointestinal tract were recorded from rat nodose ganglia. Three groups of nodose ganglia neurons were identified: group 1 responded to CCK-8 but

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Cammisotto, Philippe G., Moise Bendayan, Alain Sané, Michel Dominguez, Carole Garofalo, and Émile Levy. "Receptor-Mediated Transcytosis of Leptin through Human Intestinal Cells In Vitro." International Journal of Cell Biology 2010 (2010): 1–13. http://dx.doi.org/10.1155/2010/928169.

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Gastric Leptin is absorbed by duodenal enterocytes and released on the basolateral side towards the bloodstream. We investigated in vitro some of the mechanisms of this transport. Caco-2/15 cells internalize leptin from the apical medium and release it through transcytosis in the basal medium in a time- temperature-dependent and saturable fashion. Leptin receptors are revealed on the apical brush-border membrane of the Caco-2 cells. RNA-mediated silencing of the receptor led to decreases in the uptake and basolateral release. Leptin in the basal medium was found bound to the soluble form of it

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Niv-Spector, Leonora, Dana Gonen-Berger, Isabelle Gourdou, Eva Biener, Eugene E. Gussakovsky, Yackir Benomar, Krishnan V. Ramanujan, et al. "Identification of the hydrophobic strand in the A–B loop of leptin as major binding site III: implications for large-scale preparation of potent recombinant human and ovine leptin antagonists." Biochemical Journal 391, no. 2 (October 10, 2005): 221–30. http://dx.doi.org/10.1042/bj20050457.

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Interaction of leptin with its receptors resembles that of interleukin-6 and granulocyte colony-stimulating factor, which interact with their receptors through binding sites I–III. Site III plays a pivotal role in receptors' dimerization or tetramerization and subsequent activation. Leptin's site III also mediates the formation of an active multimeric complex through its interaction with the IGD (immunoglobulin-like domain) of LEPRs (leptin receptors). Using a sensitive hydrophobic cluster analysis of leptin's and LEPR's sequences, we identified hydrophobic stretches in leptin's A–B loop (amin

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Hurley, Matthew M., Eden M. Anderson, Christopher Chen, Brian Maunze, Evan M. Hess, Megan E. Block, Neerali Patel, et al. "Acute Blockade of PACAP-Dependent Activity in the Ventromedial Nucleus of the Hypothalamus Disrupts Leptin-Induced Behavioral and Molecular Changes in Rats." Neuroendocrinology 110, no. 3-4 (June 6, 2019): 271–81. http://dx.doi.org/10.1159/000501337.

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Leptin signaling pathways, stemming primarily from the hypothalamus, are necessary for maintaining normal energy homeostasis and body weight. In both rodents and humans, dysregulation of leptin signaling leads to morbid obesity and diabetes. Since leptin resistance is considered a primary factor underlying obesity, understanding the regulation of leptin signaling could lead to therapeutic tools and provide insights into the causality of obesity. While leptin actions in some hypothalamic regions such as the arcuate nuclei have been characterized, less is known about leptin activity in the hypot

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Houseknecht, K. L. "Leptin and its receptors: Modulation of the neuroendocrine axis." Proceedings of the British Society of Animal Science 2002 (2002): 229. http://dx.doi.org/10.1017/s1752756200008851.

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Leptin is a 16 kDa protein synthesized and secreted primarily by adipocytes. Leptin was discovered in 1994 as the gene product deficient in the obese ob/ob mouse. In addition to profound obesity, these animals are characterized by multiple, complex neuroendocrine disorders that manifest in severe insulin resistance and infertility. We now know that leptin is involved in the regulation of appetite, body weight, energy balance, reproduction and the neuroendocrine axis in animals and man. Additionally, leptin has been shown to regulate immune function and anorexia associated with disease.

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Knudson, Jarrod D., Ü. Deniz Dincer, Cuihua Zhang, Albert N. Swafford, Ryoji Koshida, Andrea Picchi, Marta Focardi, Gregory M. Dick, and Johnathan D. Tune. "Leptin receptors are expressed in coronary arteries, and hyperleptinemia causes significant coronary endothelial dysfunction." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 1 (July 2005): H48—H56. http://dx.doi.org/10.1152/ajpheart.01159.2004.

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Obesity is associated with marked increases in plasma leptin concentration, and hyperleptinemia is an independent risk factor for coronary artery disease. As a result, the purpose of this investigation was to test the following hypotheses: 1) leptin receptors are expressed in coronary endothelial cells; and 2) hyperleptinemia induces coronary endothelial dysfunction. RT-PCR analysis revealed that the leptin receptor gene is expressed in canine coronary arteries and human coronary endothelium. Furthermore, immunocytochemistry demonstrated that the long-form leptin receptor protein (ObRb) is pre

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Matheny, M., K. Y. E. Strehler, M. King, N. Tümer, and P. J. Scarpace. "Targeted leptin receptor blockade: role of ventral tegmental area and nucleus of the solitary tract leptin receptors in body weight homeostasis." Journal of Endocrinology 222, no. 1 (July 2014): 27–41. http://dx.doi.org/10.1530/joe-13-0455.

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The present investigation examined whether leptin stimulation of ventral tegmental area (VTA) or nucleus of the solitary tract (NTS) has a role in body weight homeostasis independent of the medial basal hypothalamus (MBH). To this end, recombinant adeno-associated viral techniques were employed to target leptin overexpression or overexpression of a dominant negative leptin mutant (leptin antagonist). Leptin antagonist overexpression in MBH or VTA increased food intake and body weight to similar extents over 14 days in rats. Simultaneous overexpression of leptin in VTA with antagonist in MBH re

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Morrison, Shaun F. "Activation of 5-HT1A receptors in raphe pallidus inhibits leptin-evoked increases in brown adipose tissue thermogenesis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 286, no. 5 (May 2004): R832—R837. http://dx.doi.org/10.1152/ajpregu.00678.2003.

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To elucidate the central neural pathways contributing to the thermogenic component of the autonomic response to intravenous administration of leptin, experiments were conducted in urethane-chloralose-anesthetized, ventilated rats to address 1) the role of neurons in the rostral ventromedial medulla, including raphe pallidus (RPa), in the leptin-evoked stimulation of brown adipose tissue (BAT) sympathetic nerve activity (SNA); and 2) the potential thermolytic effect of 5-hydroxytryptamine1A (5-HT1A) receptors on RPa neurons that influence BAT thermogenesis. Leptin (1 mg/kg) administration incre

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Minokoshi, Y., and B. B. Kahn. "Role of AMP-activated protein kinase in leptin-induced fatty acid oxidation in muscle." Biochemical Society Transactions 31, no. 1 (February 1, 2003): 196–201. http://dx.doi.org/10.1042/bst0310196.

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Leptin regulates energy homoeostasis through central and peripheral mechanisms. Initial steps in leptin action include signalling through a cytokine-like receptor which activates the JAK/STAT pathway. We investigated whether the metabolic effects of leptin in muscle could be mediated by the AMP-activated protein kinase (AMP kinase). Through studies involving leptin injection intrahypothalamically or intravenously, as well as incubation of soleus muscle or cultured muscle cells with leptin, we determined that leptin stimulates fatty acid oxidation in skeletal muscle by activating AMP kinase. Le

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