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Letteratura scientifica selezionata sul tema "Leptin Physiological effect"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 28 gennaio 2023

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Articoli di riviste sul tema "Leptin Physiological effect"

Misch, Monica, and Prasanth Puthanveetil. "The Head-to-Toe Hormone: Leptin as an Extensive Modulator of Physiologic Systems." International Journal of Molecular Sciences 23, no. 10 (May 13, 2022): 5439. http://dx.doi.org/10.3390/ijms23105439.

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Leptin is a well-known hunger-sensing peptide hormone. The role of leptin in weight gain and metabolic homeostasis has been explored for the past two decades. In this review, we have tried to shed light upon the impact of leptin signaling on health and diseases. At low or moderate levels, this peptide hormone supports physiological roles, but at chronically higher doses exhibits detrimental effects on various systems. The untoward effects we observe with chronically higher levels of leptin are due to their receptor-mediated effect or due to leptin resistance and are not well studied. This revi

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Flatow, Elizabeth A., Evilin N. Komegae, Monique T. Fonseca, Camila F. Brito, Florin M. Musteata, José Antunes-Rodrigues, and Alexandre A. Steiner. "Elucidating the role of leptin in systemic inflammation: a study targeting physiological leptin levels in rats and their macrophages." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 313, no. 5 (November 1, 2017): R572—R582. http://dx.doi.org/10.1152/ajpregu.00171.2017.

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To elucidate the role of leptin in acute systemic inflammation, we investigated how its infusion at low, physiologically relevant doses affects the responses to bacterial lipopolysaccharide (LPS) in rats subjected to 24 h of food deprivation. Leptin was infused subcutaneously (0–20 μg·kg−1·h−1) or intracerebroventricularly (0–1 μg·kg−1·h−1). Using hypothermia and hypotension as biomarkers of systemic inflammation, we identified the phase extending from 90 to 240 min post-LPS as the most susceptible to modulation by leptin. In this phase, leptin suppressed the rise in plasma TNF-α and accelerat

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Wisse, Brent E., Kayoko Ogimoto, Gregory J. Morton, Charles W. Wilkinson, R. Scott Frayo, David E. Cummings та Michael W. Schwartz. "Physiological regulation of hypothalamic IL-1β gene expression by leptin and glucocorticoids: implications for energy homeostasis". American Journal of Physiology-Endocrinology and Metabolism 287, № 6 (грудень 2004): E1107—E1113. http://dx.doi.org/10.1152/ajpendo.00038.2004.

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Interleukin-1β (IL-1β) is synthesized in a variety of tissues, including the hypothalamus, where it is implicated in the control of food intake. The current studies were undertaken to investigate whether hypothalamic IL-1β gene expression is subject to physiological regulation by leptin and glucocorticoids (GCs), key hormones involved in energy homeostasis. Adrenalectomy (ADX) increased hypothalamic IL-1β mRNA levels twofold, measured by real-time PCR ( P < 0.05 vs. sham-operated controls), and this effect was blocked by subcutaneous infusion of a physiological dose of corticosterone. Conve

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Powis, Jeff E., Jaideep S. Bains, and Alastair V. Ferguson. "Leptin depolarizes rat hypothalamic paraventricular nucleus neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 5 (May 1, 1998): R1468—R1472. http://dx.doi.org/10.1152/ajpregu.1998.274.5.r1468.

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Leptin, the protein product of the ob/ obgene, is thought to have a central site of action, presumably within the hypothalamus, through which it regulates feeding behavior. The paraventricular nucleus (PVN) is one structure that has been implicated in regulating feeding behavior. Using patch-clamp recording techniques, this study examines the direct membrane effects of leptin on neurons in a coronal PVN slice. Bath application of the physiologically active leptin fragment (amino acids 22–56) elicited dose-related depolarizations in 82% of the type I cells tested ( n = 17) and 67% of the type I

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Linnemann, K., A. Malek, H. Schneider, and C. Fusch. "Physiological and pathological regulation of feto/placento/maternal leptin expression." Biochemical Society Transactions 29, no. 2 (May 1, 2001): 86–90. http://dx.doi.org/10.1042/bst0290086.

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There is clear evidence of placental leptin production, as shown recently in trophoblast cultures and by dual in vitro placenta perfusion (median production of 225 pg/min per g of tissue; 98.4% released into the maternal and 1.6% into the fetal circulation). However, the physiological impact for the mother and the fetus is unclear. The classical role of leptin is to provide information about energy stores to the central nervous system, and to reduce appetite if the energy stores are full. In pregnancy, maternal plasma leptin concentrations are elevated, and lack the well established correlatio

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Ghizzoni, Lucia, George Mastorakos, Mariangela Ziveri, Mariangela Furlini, Angela Solazzi, Alessandra Vottero, and Sergio Bernasconi. "Interactions of Leptin and Thyrotropin 24-Hour Secretory Profiles in Short Normal Children." Journal of Clinical Endocrinology & Metabolism 86, no. 5 (May 1, 2001): 2065–72. http://dx.doi.org/10.1210/jcem.86.5.7452.

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Thyroid hormones and leptin have effects on similar aspects of body homeostasis, such as energy expenditure, thermogenesis, and metabolic efficiency. Thus, the cross-talk between the thyrostat and the lipostat might play a crucial role in the maintenance of body homeostasis. To investigate the relationship between the hypothalamic-pituitary-thyroid (HPT) axis and leptin under physiological conditions, we evaluated the pulsatility and circadian rhythmicity and time-cross-correlated the 24-h secretory patterns of leptin and TSH in 12 short normal prepubertal children (6 girls and 6 boys). In bot

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Shebl, M. M. "Effect of leptin on LH and FSH release in ovariectomized rats." Eastern Mediterranean Health Journal 08, no. 01 (March 15, 2002): 105–13. http://dx.doi.org/10.26719/2002.8.1.105.

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We compared the estradiol/progesterone-induced luteinizing hormone [LH] and follicle-stimulating hormone [FSH] release between normally fed and leptin-supplemented starved ovariectomized female rats and studied also the effect of hyper-leptinaemia on the steroid-induced hormonal release in normally fed ovariectomized rats. Three days’ starvation completely abolished steroid-induced LH and FSH release. Significant recovery of the hormonal release was shown in the leptin-supplemented starved group. The magnitudes of LH and FSH release in the normally fed animals with a higher dose of leptin were

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Jethwa, Preeti H., Caroline J. Small, Kirsty L. Smith, Asha Seth, Sarah J. Darch, Caroline R. Abbott, Kevin G. Murphy, Jeannie F. Todd, Mohammad A. Ghatei, and Stephen R. Bloom. "Neuromedin U has a physiological role in the regulation of food intake and partially mediates the effects of leptin." American Journal of Physiology-Endocrinology and Metabolism 289, no. 2 (August 2005): E301—E305. http://dx.doi.org/10.1152/ajpendo.00404.2004.

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Intracerebroventricular (ICV) administration of Neuromedin U (NMU), a hypothalamic neuropeptide, or leptin, an adipostat hormone released from adipose tissue, reduces food intake and increases energy expenditure. Leptin stimulates the release of NMU in vitro, and NMU expression is reduced in models of low or absent leptin. We investigated the role of NMU in mediating leptin-induced satiety. ICV administration of anti-NMU immunoglobulin G (IgG) (5 nmol) to satiated rats significantly increased food intake 4 h after injection, an effect seen for ≤8 h after injection. ICV administration of NMU (1

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Agarwal, Sanjay K., Klara Vogel, Stacy R. Weitsman, and Denis A. Magoffin. "Leptin Antagonizes the Insulin-Like Growth Factor-I Augmentation of Steroidogenesis in Granulosa and Theca Cells of the Human Ovary1." Journal of Clinical Endocrinology & Metabolism 84, no. 3 (March 1, 1999): 1072–76. http://dx.doi.org/10.1210/jcem.84.3.5543.

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There is increasing evidence that leptin is a physiological link between obesity and infertility. Although leptin receptors have been demonstrated in human ovaries, there is no information regarding the effects of leptin on cells from developing ovarian follicles. To test the direct effects of leptin on human ovarian cells, granulosa cells (GC) and theca cells were isolated from the ovaries of regularly cycling women. Serum was obtained at the time of surgery, and follicular fluid was aspirated from the follicles before isolation of the ovarian cells. Leptin concentrations were similar in foll

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Deem, Jennifer D., Kenjiro Muta, Kayoko Ogimoto, Jarrell T. Nelson, Kevin R. Velasco, Karl J. Kaiyala, and Gregory J. Morton. "Leptin regulation of core body temperature involves mechanisms independent of the thyroid axis." American Journal of Physiology-Endocrinology and Metabolism 315, no. 4 (October 1, 2018): E552—E564. http://dx.doi.org/10.1152/ajpendo.00462.2017.

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The ability to maintain core temperature within a narrow range despite rapid and dramatic changes in environmental temperature is essential for the survival of free-living mammals, and growing evidence implicates an important role for the hormone leptin. Given that thyroid hormone plays a major role in thermogenesis and that circulating thyroid hormone levels are reduced in leptin-deficient states (an effect partially restored by leptin replacement), we sought to determine the extent to which leptin’s role in thermogenesis is mediated by raising thyroid hormone levels. To this end, we 1) quant

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Più fonti

Tesi sul tema "Leptin Physiological effect"

Hillard, Kynlee, Matthew Zahner, David Kyle Mounger, Brooke Tipton, and Grayson Jo White. "The effect of leptin on metabolic- and cardiovascular-related pre-sympathetic hypothalamic neurons in mice." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/11.

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Obesity has risen 75% in the United States since 1980 and an estimated 80 million American adults are considered obese. Obesity activates the sympathetic nervous system and is associated with neurogenic hypertension. Leptin is an obesity-related neuropeptide released from fat cells which reduces appetite and increases metabolism. Leptin activates metabolic and cardiovascular responsive pre‑sympathetic neurons within the hypothalamus. Although leptin increases metabolism and curbs appetite, it also increases blood pressure. Considering that one main goal of obesity treatments is to diminish t

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Lampiao, Fanuel. "Effects of insulin and leptin on human spermatozoa function and their cross-talk with nitric oxide and cytokines." Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/1083.

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Thesis (PhD (Biomedical Sciences. Medical Physiology))--University of Stellenbosch, 2009. ENGLISH ABSTRACT: In recent years there has been an increase in obesity and diabetes mellitus (DM). These conditions have for a long time been associated with infertility. Obesity is characterized by high levels of circulating leptin and cytokines as well as insulin resistance. Type I DM is associated with low or no insulin whereas, Type II DM is characterised by insulin resistance. As the prevalence of obesity and DM continues to rise, it is likely that the incidence of infertility associated wit

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Pye, Richard Laurence. "Measuring the Acute Physiological Effects of Leptin in the Carotid Body." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1449583350.

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孔兆偉. "急性和長期運動對血淸瘦素的影響及內分泌和免疫機理之硏究 = Effects of acute and chronic exercise on serum leptin and the regulation mechanism of endocrine and immune functions". HKBU Institutional Repository, 2002. http://repository.hkbu.edu.hk/etd_ra/469.

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

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Duggal, Priya S. (Priya Sunanda). "Leptin action on ovulation and leptin receptors across the rat oestrous cycle / Priya S. Duggal." Thesis, 2001. http://hdl.handle.net/2440/21675.

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"The relationship of leptin and leptin bioavailability with body composition, bone quality and osteoblast functions in adolescent idiopathic scoliosis." 2014. http://library.cuhk.edu.hk/record=b6116400.

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引言: 青少年突發性脊柱側彎(Adolescent Idiopathic Scoliosis, AIS)是一種複雜的脊柱三維畸形，而目前病因未明。這病主要出現於11-14歲的青少年女性，罹患率約為四個百分比。未經治療的側彎可能逐漸加重並導致明顯的外觀畸形，嚴重者可導致心肺功能異常等其他併發症。目前對AIS的治療方法包括觀察，支具和手術內固定矯形。然而因為這些治療並非針對病因而仍然存在一定缺陷，如支具治療失敗和手術的併發症等。因此明確AIS的發病機制仍然是制定有效治療的關鍵。 根據過往研究報告，AIS患者有低體重、身形高大、臂展增加、低體重指數，月經初潮推遲與低骨量，這顯示AIS患者或有全身性生長異常。因為瘦素的重要生理功能如影響骨骼發育、開始青春期，能量消耗和身體成分，所以瘦素被假設為AIS的病因之一。之前的研究報告指出，AIS患者對比相同年齡和性別的人擁有較低水平的循環瘦素。然而，瘦素信號的強度不僅由瘦素水平所決定的，它也有可能受到可溶性瘦素受體(sOB-R)所影響。sOB-R是循環系統中瘦素的結合蛋白，可以調節血清瘦素水平，並影響對目標組織的生物活性游離瘦素之生物利用度。游離瘦素指數(FLI)的開發是為了幫助數據的詮釋，並提供游離瘦素水平的估計。 瘦素對骨代謝的影響是間接地由中央神經系統和直接地由周緣組織來施加的。瘦素被發現通過下丘腦神經系統對骨形成有分解效果。而瘦

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Yuen, Bernard Sin Jee. "Energy balance and leptin in the fetus / Bernard Sin Jee Yuen." 2004. http://hdl.handle.net/2440/22040.

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Includes bibliographical references (leaves 165-225) xx, 298 leaves : ill. ; 30 cm. Title page, contents and abstract only. The complete thesis in print form is available from the University Library. Thesis (Ph.D.)--University of Adelaide, School of Molecular and Biological Sciences, Discipline of Physiology, 2004

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Yuen, Bernard Sin Jee. "Energy balance and leptin in the fetus / Bernard Sin Jee Yuen." Thesis, 2004. http://hdl.handle.net/2440/22040.

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Includes bibliographical references (leaves 165-225) xx, 298 leaves : ill. ; 30 cm. Thesis (Ph.D.)--University of Adelaide, School of Molecular and Biological Sciences, Discipline of Physiology, 2004

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Hart, Heather Anne Langford. "Effects of feed restriction on physiologic and metabolic parameters and leptin expression in adipose tissue in ovariectomized prepuberal gilts." 2005. http://purl.galileo.usg.edu/uga%5Fetd/hart%5Fheather%5Fa%5F200505%5Fms.

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Libri sul tema "Leptin Physiological effect"

Chris, Henson Michael, and Castracane V. Daniel, eds. Leptin and reproduction. New York: Kluwer Academic/Plenum Publishers, 2003.

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Castracane, V. Daniel, and Michael C. Henson. Leptin. Springer, 2006.

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(Editor), V. Daniel Castracane, and Michael C. Henson (Editor), eds. Leptin (Endocrine Updates). Springer, 2006.

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Chris, Henson Michael, and Castracane V. Daniel, eds. Leptin and reproduction. New York: Kluwer Academic/Plenum Publishers, 2003.

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(Editor), Michael C. Henson, and V. Daniel Castracane (Editor), eds. Leptin and Reproduction. Springer, 2003.

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Mastering Leptin: The Leptin Diet, Solving Obesity and Preventing Disease, Second Edition. 2nd ed. Wellness Resources, 2004.

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The Leptin Diet: How Fit Is Your Fat? Truth In Wellness, 2006.

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Mastering Leptin: Your Guide to Permanent Weight Loss and Optimum Health. Wellness Resources, 2009.

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Mastering Leptin: The Key to Energetic Vitality, Youthful Hormonal Balance, Optimum Body Weight, and Disease Prevention. Wellness Resources Books, 2003.

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Claude, Kordon, ed. Brain somatic cross-talk and the central control of metabolism. Berlin: Springer, 2003.

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Capitoli di libri sul tema "Leptin Physiological effect"

Gelen, Volkan, Abdulsamed Kükürt, Emin Şengül, and Hacı Ahmet Devecı. "Leptin and Its Role in Oxidative Stress and Apoptosis: An Overview." In Role of Obesity in Human Health and Disease. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101237.

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Adipose tissue (AT) in the body plays a very important role in the regulation of energy metabolism. AT regulates energy metabolism by secreting adipokines. Some of the adipokines released are vaspin, resistin, adiponectin, visfatin and omentin, and leptin. In addition to regulating energy metabolism, leptin plays a role in the regulation of many physiological functions of the body such as regulation of blood pressure, inflammation, nutrition, appetite, insulin and glucose metabolism, lipid metabolism, coagulation, and apoptosis. Among all these physiological functions, the relationship between leptin, oxidative stress, and apoptosis has gained great importance recently due to its therapeutic effect in various types of cancer. For this reason, in this study, the release of leptin, its cellular effects and its effect on oxidative stress, and apoptosis are discussed in line with current information.

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Kayabekir, Murat. "Neurophysiology of Basic Molecules Affecting Sleep and Wakefulness Mechanisms, Fundamentals of Sleep Pharmacology." In Sleep Medicine and the Evolution of Contemporary Sleep Pharmacotherapy [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.100166.

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As part of the biological rhythm, the human brain has a healthy functioning with the ability to differentiate between day and night hours in any given day (sleep rhythm, life rhythm). From the control of hormone levels to muscle tonus, from the regulation of respiratory rate to the content of our thoughts, sleep has an impact on all bodily and cognitive functions. It is not surprising to see such effects of sleep on the body as it leads to significant changes in the electrical activity of the brain in general. Electrical signal changes in the brain (sleep-wakefulness rhythm) are regulated by neurohormonal molecules and their receptors in the body. Neurotransmitters that control sleep and wakefulness can be listed as “Glutamate, Acetylcholine, Histamine, Norepinephrine and GABA”. Main hormones are: Melatonin, Corticotropin Releasing Hormone (CRH), cortisol, prolactin, Growth Hormone (GH), Insulin like Growth Factor (IGF-1, Somatomedin-C), Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH), progesterone, estrogen, testosterone, catecholamines, leptin and neuropeptide Y″. The effects of pharmacological agents on sleep and wakefulness cycles are materialized through the following molecules and their receptors: Hypnotics (GABA A agonists, benzodiazepines, gabapentin, tiagabine), sedative antidepressants (tricyclic antidepressants, trazadone, mitrazapine), antihistamines, medications used for the treatment of sleeplessness (melatonin and melatonin analogues), amphetamine (most commonly used stimulant), secretion of monoamines (dopamine), non-amphetamine stimulants used in the treatment of hypersomnia and narcolepsy (modafinil, bupropion, selegiline, caffeine) and other substances (alcohol, nicotine, anesthetics). To the extent we can conceptualize the physiological mechanisms of these basic molecules listed above and the regions they affect, we can appreciate the effects of these substances on sleep physiology and sleep disorders.

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Rapporti di organizzazioni sul tema "Leptin Physiological effect"

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. Th

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