Готові списки джерел за темами / Leptin receptors

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Добірка наукової літератури з теми "Leptin receptors"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 31 січня 2023

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Статті в журналах з теми "Leptin receptors"

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 obesity because of increased adipocyte mass, but obese subjects exhibit resistance to the anorexic and metabolic effects of leptin. However, multiple studies have shown that leptin can increase sympathetic nerve activity to non-thermogenic tissues in rodents causing obesity-related hypertension. One potential explanation of this paradox is selective leptin resistance. Compared with large and persuasive number of studies on the sympathetic and blood pressure effects of leptin in experimental animals, relatively little attention was given to these effects of leptin in humans. This review article presents recent findings related to leptin and its mechanism of action, and also the role of leptin in patophysiological conditions.

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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 main binding protein is the extracellular domain (ECD) of leptin receptor (Liu et al., 1997). One of the established functions of leptin, is its attenuating effect on the expression of NPY and other neuropeptides in hypothalamus that subsequently leads to decreased food intake (Campfield, 2000). Therefore it seems logical that blocking leptin receptors that are responsible for transferring it through the blood-brain barrier or for its action in hypothalamus will lead to increase in food intake. Leptin receptor belongs to cytokine receptor superfamily. Its ECD consists of ∷ 800 amino acids but it was suggested that only the cytokine homology subdomain II (CHD) consisting of ∷ 200 amino acids is responsible for binding (Fong et al., 1997). The objective of the present work is to prepare recombinant proteins aimed to block leptin action. We suggest two approaches (a) preparation of leptin antagonists capable of binding but not homodimerizing leptin receptors and (b) subcloning and preparing CHD II of leptin receptor responsible for binding of the hormone.

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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 obesity and expression of leptin receptors in the skeletal muscles. It is also important to investigate the contribution of fatty tissue of different localization to leptin secretion regulation and activity of its receptors. The term «leptin resistence» reflects a complex pathophysiological phenomenon with broad perspectives for study. In this review, we analyze methods of diagnosing leptin resistance.

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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 within the hindbrain remains unexplored. Here rats implanted with telemetric devices for recording energetic/cardiovascular responses were examined to determine whether: 1) hindbrain (fourth ventricular) leptin receptor stimulation triggers energetic and cardiovascular effects, 2) these effects are altered by a 6-wk high-fat diet maintenance, and 3) hindbrain MC-Rs mediate the thermogenic, cardiovascular, and anorexic effects of hindbrain leptin delivery. Results show that hindbrain leptin receptor stimulation produced long-lasting (>6 h) increases in core temperature and heart rate and also decreased food intake and body weight. These responses were not altered by high-fat maintenance, in contrast to what has been reported for forebrain leptin delivery. Fourth ventricular pretreatment with MC-R antagonist SHU 9119 completely abolished the hyperthermia, anorexia, and body weight loss seen with hindbrain-directed leptin but had no effects of its own. These data highlight a role for hindbrain leptin receptors in the initiation of energetic and anorexic responses and show that MCRs are part of the downstream mediation of hindbrain leptin-induced energy balance effects, paralleling effects observed for hypothalamic leptin receptors.

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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 receptor subtypes. In cerebral microvessels from neonates, ObRa, ObRb, ObRc, and ObRe mRNA were all higher than in adults, but ObRd was not detectable. Hypothalamus showed similar age-related changes except for ObRb, which was higher in adults. The homologous receptor gp130 did not show significant age-related changes in either region. Despite the increase of leptin receptors, leptin permeation across the BBB after iv injection was less in the neonates. In situ brain perfusion with blood-free buffer showed no significant difference in the brain uptake of leptin between neonates and adults, indicating an antagonistic role of leptin-binding proteins in the circulation, especially the soluble receptor ObRe. The results are consistent with our previous finding that ObRe antagonizes leptin endocytosis in cultured endothelia and transport from blood to brain in mice. Overall, the developmental changes observed for leptin receptors unexpectedly failed to correlate with the entry of leptin into brain, and this may indicate different functions of the receptors in neonates and adults.

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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 response at 0.3 μg leptin/day. To test whether hindbrain receptors opposed activity of hypothalamic receptors, rats received peripheral infusions of 40 μg leptin/day and increasing 4th ventricle doses of the leptin receptor antagonist mutein protein. Mutein (3.0 μg/day) reduced body fat in PBS-infused rats to the same level as leptin-infused rats and reduced lean tissue in all rats. Leptin, but not mutein, inhibited food intake. By contrast, 3.0 μg/day mutein in the 3rd ventricle increased food intake and body fat in both PBS- and leptin-infused rats. In basal conditions, hindbrain leptin receptors may antagonize activity of forebrain receptors to protect lean and fat tissue, but there is no evidence for an anabolic role for hindbrain receptors when leptin is elevated. In a dietary study, rats increased energy intake when offered lard and 30% sucrose solution in addition to chow. Peripheral leptin infusion exaggerated the gain in body fat without altering energy intake confirming the potential for leptin to increase adiposity.

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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 protein kinase) phosphorylation, and PI3K activity. Insulin or leptin pre-treatment of SH-SY5Y cells increased basal STAT-3 phosphorylation, but abolished the acute effect of these hormones, and, interestingly, leptin pre-treatment abolished insulin effect and vice versa. Similar results were obtained for MAPK phosphorylation, but leptin or insulin pre-treatment did not completely abolish the acute effect of insulin or leptin. We have also showed that insulin and leptin are able to activate PI3K through IRS-1 (insulin receptor substrate 1) and IRS-2 respectively. Furthermore, leptin or insulin pre-treatment increased basal PI3K activity and IRS-1 or IRS-2 association with p85 and abolished acute insulin or leptin effect, in addition to the down-regulation of IRS-1 and IRS-2. Finally, insulin pre-treatment reduced leptin binding by approx. 60%, and leptin pre-treatment reduced the expression of insulin receptor by 40% in SH-SY5Y cells, which most likely accounts for the cross down-regulation of leptin and insulin receptors. These results provide evidence to suggest cross down-regulation of leptin and insulin receptors at both receptor and downstream signalling levels. This finding may contribute to the understanding of the complex relationship between leptin resistance and insulin resistance at the neuronal level.

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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 30 without cancer. Microarrays were used to assess the expression profile of leptin-related genes. Then, the expression of leptin (LEP), leptin receptor (LEPR), leptin receptor overlapping transcript (LEPROT), and leptin receptor overlapping transcript-like 1 (LEPROTL1) was determined by the Real-Time Quantitative Reverse Transcription Reaction (RT-qPCR). The serum leptin concentration was evaluated using Enzyme-linked immunosorbent assay (ELISA). Leptin and its receptors were overexpressed both at the mRNA and protein levels. Furthermore, there were strong positive correlations between leptin levels and patient Body Mass Index (BMI). Elevated levels of leptin and its receptors may potentially contribute to the progression of endometrial cancer. These observations may be useful in designing endometrial cancer treatment strategies.

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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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Дисертації з теми "Leptin receptors"

Yang, Seung Hak. "Gene expression of leptin and leptin receptors in beef cattle." Kyoto University, 2007. http://hdl.handle.net/2433/136511.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(農学)
甲第13091号
農博第1596号
新制||農||938(附属図書館)
学位論文||H19||N4217(農学部図書室)
UT51-2007-H364
京都大学大学院農学研究科応用生物科学専攻
(主査)教授矢野秀雄, 教授今井裕, 教授久米新一
学位規則第4条第1項該当

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Duggal, Priya S. "Leptin action on ovulation and leptin receptors across the rat oestrous cycle /." Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phd866.pdf.

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Chikani, Gentle P. "LEPTIN RECEPTORS IN CAVEOLAE: REGULATION OF LIPOLYSIS IN 3T3-L1 ADIPOCYTES." UKnowledge, 2004. http://uknowledge.uky.edu/gradschool_theses/382.

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The present study has tested the hypothesis that leptin receptors are localized in caveolae and that caveolae are involved in the leptin-induced stimulation of lipolysis in 3T3-L1 adipocytes. Leptin, a peptide hormone, is secreted primarily by adipocytes and has been postulated to regulate food intake and energy expenditure via hypothalamic-mediated effects. Exposure to leptin increases the lipolytic activity in 3T3-L1 adipocytes. We isolated caveolae from 3T3-L1 adipocytes using a detergent free sucrose gradient centrifugation method. Leptin receptors were localized in the same gradient fraction as caveolin-1. Confocal microscopic studies demonstrated the colocalization of leptin receptors with caveolin-1 in the plasma membrane, indicating distribution of leptin receptors in the caveolae. We disrupted caveolae by treating cells with methyl--cyclodextrin and found that leptin induced lipolytic activity was reduced after caveolae disruption, indicating an important role of caveolae in the signaling mechanism of leptin.

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De, Silva Andrea, and mikewood@deakin edu au. "The role of leptin receptors in the development of obesity." Deakin University. School of Health Sciences, 1999. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20051125.111246.

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The focus of this dissertation was leptin and the leptin receptor, and the role of these genes (OB and OB-R) in the development of obesity and type 2 diabetes in humans and Psammomys obesus, a polygenic rodent model of obesity and type 2 diabetes. Studies in humans showed that circulating leptin concentrations were positively associated with adiposity, and independently associated with circulating insulin and triglyceride concentrations. Analysis of two leptin receptor sequence polymorphisms in a Caucasian Australian population and a population of Nauruan males, with very high prevalence rates of obesity, showed no associations between sequence variation within the OB-R gene and obesity- or diabetes-related phenotypic measures. In addition, these two OB-R polymorphisms were not associated with longitudinal changes in body mass or composition in either of the populations examined. A unique analysis of the effects of multiple gene defects in the Nauruan population, demonstrated that the presence of sequence alterations in both the OB and OB-R genes were associated with insulin resistance. Psammomys obesus is regarded as an excellent rodent model in which to study the development of obesity and type 2 diabetes in humans. Examination of circulating leptin concentrations in Psammomys revealed that, as in humans, leptin concentrations were associated with adiposity, and independently associated with circulating insulin concentrations. This animal model was utilised to examine expression of OB-R, and the regulation of expression of this gene after dietary manipulation. OB-R is known to have several isoforms, and in particular, OB-RA and OB-RB gene expression were examined. OB-RB is the main signalling isoform of the leptin receptors. It has a long intracellular domain and has previously been shown to play an important role in energy balance and body weight regulation in rodents and humans. OB-RA is a much shorter isoform of OB-R, and although it lacks the long intracellular domain necessary to activate the JAK/STAT pathway, OB-RA is also capable of signalling, although to a lesser degree than OB-RB. OB-RA is found to be expressed almost ubiquitously throughout the body, and this isoform may be involved in transport of leptin into the cell, although its role remains unclear. OB-RA and OB-RB were both found to be expressed in a large number of tissues in Psammomys obesus. Interestingly, obese Psammomys were found to have lower levels of expression of OB-RA and OB-RB in the hypothalamus, compared to lean animals. This finding raises the possibility that decreased leptin signalling in the brain of obese, hyperleptinemic Psammomys obesus may contribute to the leptin resistance previously described in this animal model. However, the primary defect is unclear, as alternatively, increased circulating leptin concentrations may lead to down-regulation of leptin receptors. The effect of fasting on leptin concentrations and gene expression of OB-RA and OB-RB was also examined. A 24-hour fast resulted in no change in body weight, but a reduction in circulating leptin concentrations, and an increase in hypothalamic OB-RB gene expression in lean Psammomys. In obese animals, fasting again did not alter body weight, but resulted in an increase in both circulating leptin concentrations and hypothalamic OB-RB gene expression. In the liver, fasting resulted in a large increase in OB-RA gene expression in both lean and obese animals. These results highlighted the fact that regulation of leptin receptor gene expression in polygenic models of obesity and type 2 diabetes is complex, and not solely under the control of circulating leptin concentrations. Sucrose-feeding is an established method of inducing obesity and type 2 diabetes in rodents, and this experimental paradigm was utilised to examine the effects of longer term perturbations of energy balance on the leptin signalling pathway in Psammomys obesus. Addition of a 5% sucrose solution to the diet of lean and obese Psammomys resulted in increased body weight in both groups of animals, however only obese Psammomys showed increased fat mass and the development of type 2 diabetes. The changes in body mass and composition with sucrose-feeding were accompanied by decreased circulating leptin concentrations in both groups of animals, as well as a range of changes in leptin receptor gene expression. Sucrose-feeding increased hypothalamic OB-RB gene expression in obese Psammomys only, while in the liver there was evidence of a reduction in OB-RA and OB-RB gene expression in both lean and obese animals. The direct effects of sucrose on the leptin signalling pathway are unclear, however it is possible to speculate that the effect of sucrose to decrease leptin concentrations may have been involved in the exacerbation of obesity and the development of type 2 diabetes in obese Psammomys, From these studies, it appears that sequence variation in the OB and OB-R genes is unlikely to be a major factor in the etiology of obesity in human populations. The ability to examine regulation of expression of these genes in Psammomys obesus, however, has demonstrated that the effects of nutritional modifications on leptin receptor gene expression need closer attention. The role of the OB and OB-R genes in metabolism and the development of type 2 diabetes also warrants further examination, with particular attention on the differential effects of dietary modifications on leptin receptor gene expression across a range of tissues.

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Xu, Jialin, and 徐嘉林. "B lymphocyte development and function in leptin receptor-deficient mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45011096.

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Chikani, Gentle. "Leptin receptors in caveolae regulation of lipolysis in 3T3-L1 adipocytes /." Lexington, Ky. : [University of Kentucky Libraries], 2004. http://lib.uky.edu/ETD/ukynusc2004t00203/thesis.pdf.

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Thesis (m.s.)--University of Kentucky, 2004.
Title from document title page (viewed Jan. 7, 2005). Document formatted into pages; contains 70 p. : ill. Includes abstract and vita. Includes bibliographical references (p. 58-68).

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Mak, Amy, and 麥安美. "Expression and regulation of leptin receptor in human and mouse oviduct." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45010869.

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Soedling, Helen. "The role of leptin receptors in the endocrine pancreas and nucleus tractus solitarius." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/63933.

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The highly controlled regulation of pancreatic hormone secretion is vital to keep the body’s glucose concentration at a constant level. Defects in the regulation of glucose levels are involved in several metabolic diseases, including type 2 diabetes and obesity. Leptin is a satiety hormone with important roles in the maintenance of body weight and glucose homeostasis. Mice that lack leptin (ob/ob) or the leptin receptor (db/db) are massively obese and have diabetes symptoms. Leptin has been demonstrated to have an effect on glucose homeostasis that is suggested to be secondary to the obesity these animals are suffering from. Currently, it is unclear how leptin regulates glucose homeostasis. Leptin mediates its effects by interaction with its leptin receptor (LepRb), which is highly expressed in the hypothalamus, and at lower levels in the periphery. Leptin’s effect on glucose homeostasis has been proposed to be mediated via its receptor expressed on pancreatic cells affecting insulin secretion. Previous animal studies have deleted the leptin receptor in pancreatic β- and α-cells using either “leaky” or inefficient Cre-drivers resulting in conflicting results on glucose homeostasis. In this study, we use a β-cell selective Ins1Cre promoter in mice to investigate the role of leptin receptor expressed on pancreatic cells effect on glucose homeostasis. Deletion of LepRb was found to have minor effects on glucose tolerance in female animals an effect that was only detected in 8 weeks old animals. No effect was observed in male animals or in females above the age of 8 weeks. It is well established that the LepRb in hypothalamus plays an important role in regulation of energy balance. However, the LepRb is expressed in several areas outside hypothalamus, such as the nucleus of the solitary tract (NTS). GLP-1-expressing neurons in this area express the LepRb and it is therefore possible that these neurons mediate an effect on energy homeostasis or glucose homeostasis. We have therefore deleted LepRb in GLP-1 expressing neurons with a proglucagon specific promoter iGluCre. In this study, we found no effect on body weight or glucose homeostasis in animals deleted for LepRb in GLP-1 expressing neurons. Hypothalamus is the brain region that plays a key role in the regulation of feeding and energy homeostasis. This area contains anorexigenic and orexigenic neurons and intermingled with these neurons are subpopulation of neurons named RIP2Cre neurons expressing insulin. Due to the neurons location in the feeding area of the brain they are most likely having a role in energy homeostasis. Previous studies have suggested that tumour suppressor LKB1 plays a role on body weight and food intake in these neurons. Therefore, we deleted LKB1 selectively in the RIP2Cre neurons but failed to see a difference in body weight.

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Håkansson, Ovesjö Marie-Louise. "Leptin targets in the brain regulating body weight : receptors and down-stream mediators of leptin in neurons of the hypothalamus and brainstem /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4178-5/.

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Vaughan, Tamisha Y. "Novel Mechanisms Underlying the Inflammatory Effects of Leptin and Low Dose Endotoxin." Diss., Virginia Tech, 2010. http://hdl.handle.net/10919/28013.

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Obesity over the last several has become a major health concern in our country as well as the world. Obesity is also one of the risk factors which lead to several inflammatory complications such as diabetes, artherosclerosis, etc. Two leading factors involved in the causes of inflammatory complications include leptin and low dose endotoxin lipopolysaccharide (LPS). However, the mechanism underlying the involvement of these two mediators is not clearly understood. The purpose of this study is to understand the mechanism underlying inflammatory complications caused by leptin and low dose endotoxin most recently coined metabolic endotoxemia. Interleukin-Receptor Associated Kinase 1 (IRAK-1) is an intracellular signaling component shown to activate NFÎºB which leads to the induction of proinflammatory mediators. Deletion of IRAK-1 in mice has beneficial effects in alleviating inflammatory complications and human variations in IRAK-1 gene are correlated with higher risks for inflammatory diseases. Therefore, we hypothesized that IRAK-1 is critically involved for the induction of proinflammatory mediators induced by leptin and low dose LPS. IL-6 mRNA levels were measured in THP-1 (human monocytic cells) and wild type and IRAK-deficient bone marrow derived macrophages (BMDM) challenged with different combinations of leptin and LPS. Data shows that leptin alone will not induce inflammatory mediators. However, increased induction of IL-6 was observed in a synergistic manner involving both LPS and leptin in an IRAK-1 dependent manner causing a robust inflammatory response. With regard to the effect of low dose LPS, we observed that human monocytic cells treated with low concentrations of LPS showed a mild yet sustained induction of proinflammatory cytokines, which is contrast to the robust and transient induction of cytokines by a high dose LPS. To further determine the molecular mechanisms, we measured several key signaling molecules that include IRAK-1, IKKepsilon, and C/EBPdelta. Our study revealed a novel mechanism that appears to be distinct from the traditional NFï «B pathway responsible for the effect of low dose LPS.
Ph. D.

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Книги з теми "Leptin receptors"

Leptin and leptin antagonists. Austin, Tex: Landes Bioscience, 2009.

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Oliveira, Maria Nubia Gama. Marcadores de obesidade na avaliação do estado nutricional em adolescente. Edited by Marcia Alessandra Arantes Marques. Bookerfield Editora, 2021. http://dx.doi.org/10.53268/bkf21110300.

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Este livro é resultado da pesquisa de doutorado em um Centro de Referência de Adolescente. O que se destaca a recomendação da leitura do livro marcadores de obesidade na avalição do estado nutricional em adolescente é o método científico, trazendo à tona, à proposta, à pesquisa científica, à faixa etária de 10 a 19 anos. Estudar e atender adolescente são desafiadores, dado que, neste segmento observa-se uma fase de mudanças biológicas importantes, o consumo de refeições nem sempre satisfatória em nutrientes como vitamina A, E e β─caroteno. Somando-se a tudo isto, o excesso de calorias corrobora a ocorrência de dislipidemia, hiperleptinemia e obesidade, acelerando o risco para a doença cardiovascular. Alguns fatores de risco da DCV têm sido associados ao estresse oxidativo, por essa razão o aporte de nutrientes antioxidantes, dentre os quais, a vitamina A (retinol e β─caroteno) e a vitamina E foram estudados como marcadores metabólicos. Variáveis clínicas e laboratoriais são instrumentos aplicados na prática e anamnese clínica, contudo o polimorfismo Q223R do gene do receptor da leptina, vitaminas antioxidantes e leptina sérica, ainda, são ferramentas não tão bem conhecidas, porém valiosas, a fim de traçar o estado nutricional em adolescente obeso. É indubitavelmente importante destacar que, a medida que esta geração de adolescente é exposta a alimentação precária em nutrientes, se aumenta a incidência e prevalência de obesidade e doenças metabólicas em adultos jovens. Concebe-se que, os resultados observados reforçam à necessária busca de diagnóstico precoce de obesidade e as comorbidades associadas. Com efeito, é relevante formular propostas de ações públicas, a fim de amenizar estes impactos negativos à saúde desta população, assim como das futuras. Por fim, espero que ao final, o leitor tenha sido instigado a querer conhecer cada vez mais sobre a saúde do adolescente. Boa leitura!

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Частини книг з теми "Leptin receptors"

Cottrell, Elizabeth C., and Julian G. Mercer. "Leptin Receptors." In Handbook of Experimental Pharmacology, 3–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-24716-3_1.

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Dam, Julie, Ralf Jockers, Michèle Guerre-Millo, and Karine Clément. "Leptin Receptors and Mechanism of Action." In Leptin, 15–24. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09915-6_2.

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Considine, Robert V. "Measurement of Circulating Leptin and Soluble Leptin Receptors." In Leptin, 39–43. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09915-6_4.

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Gouilleux, Fabrice. "Erythropoietin, Thrombopoietin and Leptin Receptors." In Hormone Signaling, 145–78. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3600-7_8.

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Lubrano, Cécile, Béatrice Dubern, and Karine Clément. "Obesity-related mutations of leptin and melanocortin receptors." In Insights into Receptor Function and New Drug Development Targets, 35–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-34447-0_3.

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Zabeau, Lennart, Frank Peelman, and Jan Tavernier. "Leptin and Leptin Receptor." In Encyclopedia of Signaling Molecules, 2839–45. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101679.

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Zabeau, Lennart, Frank Peelman, and Jan Tavernier. "Leptin and Leptin Receptor." In Encyclopedia of Signaling Molecules, 1–6. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101679-1.

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Gorska, E., K. Popko, and M. Wasik. "Leptin Receptor in Childhood Acute Leukemias." In Advances in Experimental Medicine and Biology, 155–61. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4549-0_20.

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Castracane, V. Daniel, and Michael C. Henson. "Regulation of Leptin and Leptin Receptor in the Human Uterus: Possible Roles in Implantation and Uterine Pathology." In Leptin and Reproduction, 111–15. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0157-2_7.

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Otvos, Laszlo, Marco Cassone, Marianna Terrasi, Sandra Cascio, George D. Mateo, Daniel Knappe, Ralf Hoffmann, Predrag Cudic, John D. Wade, and Eva Surmacz. "Agonists and Partial Antagonists Acting on the Leptin—Leptin Receptor Interface." In Advances in Experimental Medicine and Biology, 497–98. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-73657-0_215.

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Тези доповідей конференцій з теми "Leptin receptors"

Ahmed, Sumaya, and Nasser Rizk. "The Expression of Bile Acid Receptor TGR5 in Adipose Tissue in Diet-Induced Obese Mice." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0212.

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Bile acids are significant physiological factors for digestion, solubilization, absorption, toxic metabolites and xenobiotics. In addition, bile acids are responsible of signal transduction as well as metabolic regulation that activate several receptors such as farnesoid X receptor (FXR) and the membrane G-protein receptor 5 (TGR5). Activation of TGR5 by bile acids is associated with prevention of obesity as well as ameliorating the resistance to insulin via increasing energy expenditure. The objective of this research is to investigate TGR5 gene expression level in different fat depots including visceral or epididymal adipose tissue (eWAT), brown adipose tissue and inguinal adipose tissue (iWAT) and to study the response of TGR5 gene expression to the antiobesity treatment (SFN). Three groups of male CD1 mice were used in this study; lean group fed with SCD, DIO mice on HFD and DIO obese mice treated with anti-obesity treatment. Body weight (BW) and phenotype data were evaluated by weekly including blood samples for analysis of glucose, insulin, leptin, triglycerides (TG). Total RNA was extracted from different fat depots and RT-PCR profiler array technology was used to in order to assess the mRNA expression of TGR5 and leptin. There was significant downregulation of TGR5 gene expression level in obese (DIO) mice and remarkable upregulation of TGR5 gene expression after successful weight loss in DIO mice treated with SFN in time dependent manner at 1 weeks and 4 weeks of ip applications. In conclusion, obesity is associated with decrease in expression of TGR5 in different fat depots and treatment with anti-obesity drug (Sulforaphane) causes stepwise upregulation of TGR5 gene expression in epididymal white adipose tissue parallel stepwise decrease in body weight. Increase of expression of TGR5 in DIO mice in eWAT is accompanied by improvement in glucose homeostasis and insulin action.

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Zheng, Qiao, Sarah Smith, Jinling Zhu, Erin Downs-Kelly, Stephen D. Hursting, Jeremy N. Rich, Nathan A. Berger, and Ofer Reizes. "Abstract 3327: Leptin receptors are expressed in breast cancer stem cells and leptin promotes their self-renewal and survival in mice." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3327.

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Yom, Cha Kyong, Jun Ho Kim, Hee Sung Kim, and Yong Lai Park. "Abstract B50: Leptin and leptin receptor expression in breast cancer." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b50.

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Bruno, Andreina, Antonella Ballacchino, Liboria Siena, Domenica Russo, Salvatore Gallina, Francesco Lorusso, Giuseppina Chiappara, Mark Gjomarkaj, and Elisabetta Pace. "Impairment of leptin/leptin receptor pathway in nasal epithelium from allergic turbinates." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa905.

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Wazir, U., Sarakbi W. Al, WG Jiang, and K. Mokbel. "Abstract P6-05-11: Leptin and Leptin receptor expression in human breast cancer." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-p6-05-11.

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Karampela, Irene, Evangelia Kandri, George Skyllas, Evangelia Chrysanthopoulou, Gerasimos-Socrates Christodoulatos, Georgios Antonakos, Evangelos Vogiatzakis, Apostolos Armaganidis, and Maria Dalamaga. "Serum kinetics of total leptin and soluble leptin receptor as prognostic tools in sepsis." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2260.

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Ahasic, Amy, Yang Zhao, Li Su, B. T. Thompson, and David Christiani. "Leptin Receptor Gene (LEPR) Polymorphism And ARDS Susceptibility." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2099.

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Yabushita, Hiromitsu, Keita Iwasaki, Taiki Ueno, and Akihiko Wakatsuki. "Abstract 4738: Clinicopathological roles of adiponectin receptor and leptin receptor in endometrial carcinoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4738.

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Llanos, Adana A. M., Baichen Xu, Bo Qin, Wenjin Chen, Marina A. Chekmareva, Lei Cong, Chi-Chen Hong, et al. "Abstract C063: Associations of leptin and leptin receptor protein and gene expression with breast cancer clinicopathologic features." In Abstracts: Eleventh AACR Conference on The Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; November 2-5, 2018; New Orleans, LA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7755.disp18-c063.

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Gu, Fangyi, Peter Kraft, Megan Rice, and Karin B. Michels. "Abstract A104: Leptin and leptin receptor genes in relation to premenopausal breast cancer incidence and grade in Caucasian women." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Oct 22-25, 2011; Boston, MA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1940-6207.prev-11-a104.

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Звіти організацій з теми "Leptin receptors"

Boisclair, Yves R., and Arieh Gertler. Development and Use of Leptin Receptor Antagonists to Increase Appetite and Adaptive Metabolism in Ruminants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697120.bard.

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Objectives The original project had 2 major objectives: (1) To determine the effects of centrally administered leptin antagonist on appetite and adaptive metabolism in the sheep; (2) To develop and prepare second-generation leptin antagonists combining high binding affinity and prolonged in vivo half-life. Background Periods of suboptimal nutrition or exaggerated metabolic activity demands lead to a state of chronic energy insufficiency. Ruminants remain productive for a surprisingly long period of time under these circumstances by evoking adaptations sparing available energy and nutrients. The mechanism driving these adaptations in ruminant remains unknown, but could involve a reduction in plasma leptin, a hormone acting predominantly in the brain. In laboratory animals, reduced leptin signaling promotes survival during nutritional insufficiency by triggering energy sparing adaptations such as reduced thyroid hormone production and insulin resistance. Our overall hypothesis is that similar adaptations are triggered by reduced leptin signaling in the brain of ruminants. Testing of this hypothesis in ruminants has not been possible due to inability to block the actions of endogenous leptin and access to ruminant models where leptin antagonistic therapy is feasible and effective. Major achievements and conclusions The Israeli team had previously mutated 3 residues in ovine leptin, with no effect on receptor binding. This mutant was renamed ovine leptin antagonist (OLA) because it cannot activate signaling and therefore antagonizes the ability of wild type leptin to activate its receptor. To transform OLA into an effective in vivo antagonist, the Israeli made 2 important technical advances. First, it incorporated an additional mutation into OLA, increasing its binding affinity and thus transforming it into a super ovine leptin antagonist (SOLA). Second, the Israeli team developed a method whereby polyethylene glycol is covalently attached to SOLA (PEG-SOLA) with the goal of extending its half-life in vivo. The US team used OLA and PEG-SOLA in 2 separate animal models. First, OLA was chronically administered directly into the brain of mature sheep via a cannula implanted into the 3rdcerebroventricule. Unexpectedly, OLA had no effect of voluntary feed intake or various indicators of peripheral insulin action but reduced the plasma concentration of thyroid hormones. Second, the US team tested the effect of peripheral PEG-SOLA administration in an energy sensitive, rapidly growing lamb model. PEG-SOLA was administered for 14 consecutive days after birth or for 5 consecutive days before sacrifice on day 40 of life. Plasma PEG-SOLA had a half-life of over 16 h and circulated in 225- to 288-fold excess over endogenous leptin. PEG-SOLA administration reduced plasma thyroid hormones and resulted in a higher fat content in the carcass at slaughter, but had no effects on feed intake, body weight, plasma glucose or insulin. These results show that the team succeeded in developing a leptin antagonist with a long in vivo half-life. Moreover, in vivo results show that reduced leptin signaling promotes energy sparing in ruminants by repressing thyroid hormone production. Scientific and agricultural implications The physiological role of leptin in ruminants has been difficult to resolve because peripheral administration of wild type leptin causes little effects. Our work with leptin antagonists show for the first time in ruminants that reduced leptin signaling induces energy sparing mechanisms involving thyroid hormone production with little effect on peripheral insulin action. Additional work is needed to develop even more potent leptin antagonists, to establish optimal administration protocols and to narrow down phases of the ruminant life cycle when their use will improve productivity.

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Yuan, Qihang. Circulating Leptin Level, Soluble Leptin Receptor Level and Their Gene Polymorphism in Patients with Systemic Lupus Erythematosus: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0137.

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Nahta, Rita. Crosstalk between Leptin Receptor and Igf-Ir in Breast Cancer: A Potential Mediator of Chemoresistance. Fort Belvoir, VA: Defense Technical Information Center, April 2008. http://dx.doi.org/10.21236/ada486433.

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Nahta, Rita. Crosstalk Between Leptin Receptor and IGF-IR in Breast Cancer: A Potential Mediator of Chemoresistance. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada505199.

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