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Journal articles on the topic 'Leptin Physiological effect'

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Published: 4 June 2021
Last updated: 28 January 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Zouhar, Petr, Günaj Rakipovski, Muhammad Hamza Bokhari, Oliver Busby, Johan F. Paulsson, Kilian W. Conde-Frieboes, Johannes J. Fels, et al. "UCP1-independent glucose-lowering effect of leptin in type 1 diabetes: only in conditions of hypoleptinemia." American Journal of Physiology-Endocrinology and Metabolism 318, no. 1 (January 1, 2020): E72—E86. http://dx.doi.org/10.1152/ajpendo.00253.2019.

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The possibility to use leptin therapeutically for lowering glucose levels in patients with type 1 diabetes has attracted interest. However, earlier animal models of type 1 diabetes are severely catabolic with very low endogenous leptin levels, unlike most patients with diabetes. Here, we aim to test glucose-lowering effects of leptin in novel, more human-like murine models. We examined the glucose-lowering potential of leptin in diabetic models of two types: streptozotocin-treated mice and mice treated with the insulin receptor antagonist S961. To prevent hypoleptinemia, we used combinations o
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12

Herrid, Muren, Yin Xia, Tim O'Shea, and James R. McFarlane. "Leptin inhibits basal but not gonadotrophin-stimulated testosterone production in the immature mouse and sheep testis." Reproduction, Fertility and Development 20, no. 4 (2008): 519. http://dx.doi.org/10.1071/rd07062.

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The mechanisms whereby leptin regulates testosterone secretion are complex and are likely to involve actions at different levels of the hypothalamus–pituitary–gonadal axis. In the present study, the effect of leptin on testicular steroidogenesis at different developmental stages in mice and sheep was investigated. Testosterone data from testicular slice and Leydig cells of immature and adult mice testes demonstrated that the action of leptin in the regulation of steroidogenesis appears to be dependent on the developmental stage of the testis. Leptin biphasically modulates basal testosterone pr
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13

Mistry, Anahita M., Andrew Swick, and Dale R. Romsos. "Leptin alters metabolic rates before acquisition of its anorectic effect in developing neonatal mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 3 (September 1, 1999): R742—R747. http://dx.doi.org/10.1152/ajpregu.1999.277.3.r742.

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Leptin inhibits food intake and increases metabolic rates in adult mice. Neonatal mice need to maximize food intake and also maintain high thermoregulatory metabolic rates to optimize survival, suggesting that leptin may function differentially in neonatal versus adult animals. The efficacy of exogenous leptin to alter these two physiological functions during development was thus examined in C57BL/6J lean (+/+ or ob/+) and ob/ ob(leptin-deficient) mice. Intraperitoneal leptin administration (1 mg/kg body wt) to lean and ob/ obpups from 7 to 10 days of age did not affect milk intake, oxygen con
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14

Ortiga-Carvalho, TM, KJ Oliveira, BA Soares, and CC Pazos-Moura. "The role of leptin in the regulation of TSH secretion in the fed state: in vivo and in vitro studies." Journal of Endocrinology 174, no. 1 (July 1, 2002): 121–25. http://dx.doi.org/10.1677/joe.0.1740121.

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Leptin has been shown to stimulate the hypothalamus-pituitary-thyroid axis in fasting rodents; however, its role in thyroid axis regulation under physiological conditions is still under investigation. Here it was investigated in freely fed rats whether leptin modulates thyrotroph function in vivo and whether leptin has direct pituitary effects on TSH release. Since leptin is produced in the pituitary, the possibility was also investigated that leptin may be a local regulator of TSH release. TSH was measured by specific RIA. Freely fed adult rats 2 h after being injected with a single s.c. inje
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15

Kendall, N. R., C. G. Gutierrez, R. J. Scaramuzzi, D. T. Baird, R. Webb, and B. K. Campbell. "Direct in vivo effects of leptin on ovarian steroidogenesis in sheep." Reproduction 128, no. 6 (December 2004): 757–65. http://dx.doi.org/10.1530/rep.1.00256.

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Leptin, the metabolic fat hormone, has been shown to have effects on reproduction in mice and to modulate steroid production by cultured ovarian somatic cells in a number of species. However, a direct role of leptin on normal ovarian function in vivo has not been shown. In this paper the effect of passive immunisation against leptin (experiment 1; 20 ml antiserum or non-immune plasma i.v.; n = 6/treatment) and direct ovarian infusion of leptin (experiment 2; 0, 2 or 20 μg recombinant ovine leptin; n = 4/treatment) during the early follicular phase was investigated in sheep with ovarian autotra
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16

Breslow, Michael J., Kyoung Min-Lee, Daniel R. Brown, V. P. Chacko, David Palmer, and Dan E. Berkowitz. "Effect of leptin deficiency on metabolic rate inob/obmice." American Journal of Physiology-Endocrinology and Metabolism 276, no. 3 (March 1, 1999): E443—E449. http://dx.doi.org/10.1152/ajpendo.1999.276.3.e443.

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Reduced metabolic rate may contribute to weight gain in leptin-deficient ( ob/ob) mice; however, available studies have been criticized for referencing O2 consumption (V˙o 2) to estimated rather than true lean body mass. To evaluate whether leptin deficiency reduces energy expenditure, four separate experiments were performed: 1) NMR spectroscopy was used to measure fat and nonfat mass, permittingV˙o 2 to be referenced to true nonfat mass; 2) dietary manipulation was used in an attempt to eliminate differences in body weight and composition between ob/ob and C57BL/6J mice; 3) short-term effect
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17

Heintges, U., M. Hennies, A. Gertler, and H. Sauerwein. "Leptin and its effect on glucose and insulin metabolism in pregnant and lactating goats." Proceedings of the British Society of Animal Science 2002 (2002): 96. http://dx.doi.org/10.1017/s1752756200007523.

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Pregnancy and lactation are phases during which major adaptations in maternal metabolism are necessary to meet the requirements of foetal growth and of lactation. Leptin, an adipocyte derived hormone, involved in regulation of energy metabolism, has been implicated in the coordination of these adaptive processes. Similar to monogastric species, increased leptin blood concentrations are reported for sheep at mid-pregnancy when compared to prebreeding, late pregnancy or early lactation (Ehrhardt et al., 2001). In sheep, the changes of leptin concentrations showed no obvious relation with the abi
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18

Leury, Brian J., Lance H. Baumgard, Stephanie S. Block, Nthabisheng Segoale, Richard A. Ehrhardt, Robert P. Rhoads, Dale E. Bauman, Alan W. Bell, and Yves R. Boisclair. "Effect of insulin and growth hormone on plasma leptin in periparturient dairy cows." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 5 (November 2003): R1107—R1115. http://dx.doi.org/10.1152/ajpregu.00320.2003.

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After parturition, dairy cows suffer from an intense energy deficit caused by the onset of copious milk secretion and an inadequate increase in voluntary food intake. We previously showed that this energy deficit contributes to a decline in plasma leptin. This decline mirrors that of plasma insulin but is reciprocal to the profile of plasma growth hormone (GH), suggesting that both hormones may regulate plasma leptin in periparturient dairy cows. To study the role of insulin, hyperinsulinemic-euglycemic clamps were performed on six dairy cows in late pregnancy (LP, 31 days prepartum) and early
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19

Rosenbaum, Michael, and Rudolph L. Leibel. "20 YEARS OF LEPTIN: Role of leptin in energy homeostasis in humans." Journal of Endocrinology 223, no. 1 (July 25, 2014): T83—T96. http://dx.doi.org/10.1530/joe-14-0358.

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The hyperphagia, low sympathetic nervous system tone, and decreased circulating concentrations of bioactive thyroid hormones that are common to states of congenital leptin deficiency and hypoleptinemia following and during weight loss suggest that the major physiological function of leptin is to signal states of negative energy balance and decreased energy stores. In weight-reduced humans, these phenotypes together with pronounced hypometabolism and increased parasympathetic nervous system tone create the optimal circumstance for weight regain. Based on the weight loss induced by leptin admini
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20

Yang, Meng-Jie, Fang Wang, Jiang-Hua Wang, Wen-Ning Wu, Zhuang-Li Hu, Jin Cheng, Dan-Fang Yu, et al. "PI3K integrates the effects of insulin and leptin on large-conductance Ca2+-activated K+ channels in neuropeptide Y neurons of the hypothalamic arcuate nucleus." American Journal of Physiology-Endocrinology and Metabolism 298, no. 2 (February 2010): E193—E201. http://dx.doi.org/10.1152/ajpendo.00155.2009.

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The adipocyte-derived hormone leptin and the pancreatic β-cell-derived hormone insulin function as afferent signals to the hypothalamus in an endocrine feedback loop that regulates body adiposity. They act in hypothalamic centers to modulate the function of specific neuronal subtypes, such as neuropeptide Y (NPY) neurons, by modifying neuronal electrical activity. To investigate the intrinsic activity of these neurons and their responses to insulin and leptin, we used a combination of morphological features and immunocytochemical technique to identify the NPY neurons of hypothalamic arcuate nu
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21

Morton, Gregory J., Karl J. Kaiyala, Jonathan D. Fisher, Kayoko Ogimoto, Michael W. Schwartz, and Brent E. Wisse. "Identification of a physiological role for leptin in the regulation of ambulatory activity and wheel running in mice." American Journal of Physiology-Endocrinology and Metabolism 300, no. 2 (February 2011): E392—E401. http://dx.doi.org/10.1152/ajpendo.00546.2010.

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Mechanisms regulating spontaneous physical activity remain poorly characterized despite evidence of influential genetic and acquired factors. We evaluated ambulatory activity and wheel running in leptin-deficient ob/ob mice and in wild-type mice rendered hypoleptinemic by fasting in both the presence and absence of subcutaneous leptin administration. In ob/ob mice, leptin treatment to plasma levels characteristic of wild-type mice acutely increased both ambulatory activity (by 4,000 ± 200 beam breaks/dark cycle, P < 0.05) and total energy expenditure (TEE; by 0.11 ± 0.01 kcal/h during the d
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22

Mostyn, A., D. H. Keisler, R. Webb, T. Stephenson, and M. E. Symonds. "The role of leptin in the transition from fetus to neonate." Proceedings of the Nutrition Society 60, no. 2 (May 2001): 187–94. http://dx.doi.org/10.1079/pns200086.

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Leptin is a 16 kDa hormone which has been shown to have a major physiological role in the control of energy balance. Leptin is produced primarily in white adipose tissue, although there is evidence for its production in brown adipose tissue (BAT) and the placenta. BAT is critically important for the initiation of non-shivering thermogenesis in the newborn through the BAT-specific uncoupling protein (UCP), UCP1. This factor is particularly important in lambs in which levels of UCP1 peak at birth, concomitant with a rapid decline in plasma leptin levels. Our studies have examined the effect of a
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23

McAlister, Edward D., and Dean A. Van Vugt. "Effect of leptin administration versus re-feeding on hypothalamic neuropeptide gene expression in fasted male rats." Canadian Journal of Physiology and Pharmacology 82, no. 12 (December 1, 2004): 1128–34. http://dx.doi.org/10.1139/y04-122.

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Adipocytes are the primary source of circulating leptin. Leptin inhibits eating, increases metabolism, and stimulates the reproductive axis. Numerous hypothalamic neuropeptides have been implicated in leptin's behavioral and neuroendocrine effects, including neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART). The aim of this study was to investigate the physiological relevance of leptin's signaling of nutritional status by comparing the effects of leptin with the effects of re-feeding on fasting-induced changes in the expression of the long form of the leptin recepto
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Balland, Eglantine, Weiyi Chen, Tony Tiganis, and Michael A. Cowley. "Persistent Leptin Signaling in the Arcuate Nucleus Impairs Hypothalamic Insulin Signaling and Glucose Homeostasis in Obese Mice." Neuroendocrinology 109, no. 4 (2019): 374–90. http://dx.doi.org/10.1159/000500201.

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Background: Obesity is associated with reduced physiological responses to leptin and insulin, leading to the concept of obesity-associated hormonal resistance. Objectives: Here, we demonstrate that contrary to expectations, leptin signaling not only remains functional but also is constantly activated in the arcuate nucleus of the hypothalamus (ARH) neurons of obese mice. This state of persistent response to endogenous leptin underpins the lack of response to exogenous leptin. Methods and Results: The study of combined leptin and insulin signaling demonstrates that there is a common pool of ARH
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25

Wilsey, Jared, Michael K. Matheny, and Philip J. Scarpace. "Oral Vanadium Enhances the Catabolic Effects of Central Leptin in Young Adult Rats." Endocrinology 147, no. 1 (January 1, 2006): 493–501. http://dx.doi.org/10.1210/en.2004-1358.

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Recently, vanadium has been shown to enhance leptin signal transduction in vitro. We hypothesized that chronic oral administration of an organic vanadium complex would enhance both leptin signaling and physiological responsiveness in vivo. Three-month-old F344 × Brown Norway male rats were provided a solution containing escalating doses of vanadyl acetoacetonate (V), peaking at 60 mg/liter elemental vanadium in drinking water on the 11th d of V treatment. Although V treatment tended to suppress weight gain, absolute body weights did not significantly differ between groups after 62 d of treatme
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Arvaniti, Konstantinia, Denis Richard, Frédéric Picard, and Yves Deshaies. "Lipid deposition in rats centrally infused with leptin in the presence or absence of corticosterone." American Journal of Physiology-Endocrinology and Metabolism 281, no. 4 (October 1, 2001): E809—E816. http://dx.doi.org/10.1152/ajpendo.2001.281.4.e809.

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The aim of the present study was to assess whether the glucocorticoid corticosterone (Cort) modulates the effects of leptin on food intake and lipid deposition. Rats were subjected to a 6-day intracerebroventricular infusion of leptin and were either sham-adrenalectomized (Sham-ADX) or ADX and supplemented with 0 (C0), 40 (C40), or 80 mg (C80) of Cort. Investigation of potential peripheral sites of interaction of leptin and Cort included liver and plasma triglyceride (TG) content and lipoprotein lipase (LPL) activity in adipose and muscle tissues. The study confirmed the respective anorectic a
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Dawson, R., M. A. Pelleymounter, W. J. Millard, S. Liu, and B. Eppler. "Attenuation of leptin-mediated effects by monosodium glutamate-induced arcuate nucleus damage." American Journal of Physiology-Endocrinology and Metabolism 273, no. 1 (July 1, 1997): E202—E206. http://dx.doi.org/10.1152/ajpendo.1997.273.1.e202.

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Leptin is a protein secreted by adipocytes that is important in regulating appetite and adiposity. Recent studies have suggested the presence of leptin receptors in the arcuate nucleus of the hypothalamus (ANH). Neonatal administration of monosodium glutamate (MSG) damages the ANH, resulting in obesity and neuroendocrine dysfunction. Neonatal administration of MSG was utilized to test the hypothesis that the anatomic site for many of leptin's actions is the ANH. Female control (n = 6) and MSG-treated rats (n = 7) were implanted for 14 days with osmotic minipumps containing phosphate-buffered s
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Fan, WuQiang, Toshihiko Yanase, Yoshihiro Nishi, Seiichi Chiba, Taijiro Okabe, Masatoshi Nomura, Hironobu Yoshimatsu, Shigeaki Kato, Ryoichi Takayanagi, and Hajime Nawata. "Functional Potentiation of Leptin-Signal Transducer and Activator of Transcription 3 Signaling by the Androgen Receptor." Endocrinology 149, no. 12 (August 14, 2008): 6028–36. http://dx.doi.org/10.1210/en.2008-0431.

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Hypogonadism is associated with increased fat mass and dysregulation of metabolic homeostasis in men. Our previous study revealed that androgen receptor (AR)-null male mice (ARL-/Y) develop late-onset obesity and are leptin-resistant. The present study evaluated how hypothalamic AR contributes to central leptin-signal transducer and activator of transcription 3 (STAT3) signaling. We evaluated leptin action in wild-type and ARL-/Y mice, the anatomic co-relationship between AR and leptin signaling in the hypothalamus, and the effects of AR on leptin-mediated STAT3 transactivation and nuclear tra
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Maymó, Julieta L., Antonio Pérez Pérez, José L. Dueñas, Juan Carlos Calvo, Víctor Sánchez-Margalet, and Cecilia L. Varone. "Regulation of Placental Leptin Expression by Cyclic Adenosine 5′-Monophosphate Involves Cross Talk between Protein Kinase A and Mitogen-Activated Protein Kinase Signaling Pathways." Endocrinology 151, no. 8 (May 19, 2010): 3738–51. http://dx.doi.org/10.1210/en.2010-0064.

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Leptin, a 16-kDa protein mainly produced by adipose tissue, has been involved in the control of energy balance through its hypothalamic receptor. However, pleiotropic effects of leptin have been identified in reproduction and pregnancy, particularly in placenta, where it was found to be expressed. In the current study, we examined the effect of cAMP in the regulation of leptin expression in trophoblastic cells. We found that dibutyryl cAMP [(Bu)2cAMP], a cAMP analog, showed an inducing effect on endogenous leptin expression in BeWo and JEG-3 cell lines when analyzed by Western blot analysis an
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Irani, Boman G., Christelle Le Foll, Ambrose Dunn-Meynell, and Barry E. Levin. "Effects of Leptin on Rat Ventromedial Hypothalamic Neurons." Endocrinology 149, no. 10 (June 12, 2008): 5146–54. http://dx.doi.org/10.1210/en.2008-0357.

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Neurons in the ventromedial and arcuate hypothalamic nuclei (VMN and ARC, respectively) mediate many of leptin’s effects on energy homeostasis. Some are also glucosensing, whereby they use glucose as a signaling molecule to regulate their firing rate. We used fura-2 calcium (Ca2+) imaging to determine the interactions between these two important mediators of peripheral metabolism on individual VMN neurons and the mechanisms by which leptin regulates neuronal activity in vitro. Leptin excited 24%, inhibited 20%, and had a biphasic response in 10% of VMN neurons. Excitation occurred with a EC50
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Hernández Morante, Juan José, Inmaculada Díaz Soler, Joaquín S. Galindo Muñoz, Horacio Pérez Sánchez, Mª del Carmen Barberá Ortega, Carlos Manuel Martínez, and Juana Mª Morillas Ruiz. "Moderate Weight Loss Modifies Leptin and Ghrelin Synthesis Rhythms but Not the Subjective Sensations of Appetite in Obesity Patients." Nutrients 12, no. 4 (March 27, 2020): 916. http://dx.doi.org/10.3390/nu12040916.

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Obesity is characterized by a resistance to appetite-regulating hormones, leading to a misalignment between the physiological signals and the perceived hunger/satiety signal. A disruption of the synthesis rhythm may explain this situation. The aim of this study was to evaluate the effect of dietary-induced weight loss on the daily rhythms of leptin and ghrelin and its influence on the daily variability of the appetite sensations of patients with obesity. Twenty subjects with obesity underwent a hypocaloric dietary intervention for 12 weeks. Plasma leptin and ghrelin were analyzed at baseline a
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32

Kata, Faris, Saad W. Alsulaitti, and Muneera M. Adlan. "Leptin and Vascular Cell Adhesion Protein 1 as Physiological Biomarkers in Serum of Women Suffering from Rheumatoid Arthritis." Open Access Macedonian Journal of Medical Sciences 10, A (January 19, 2022): 164–69. http://dx.doi.org/10.3889/oamjms.2022.8208.

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BACKGROUND: Rheumatoid arthritis is defining as a common chronic and inflammatory disorder of systematic autoimmune disease. Leptin is a small peptide hormone involved in the inflammatory and immunomodulators processes of several diseases. AIM: The study aimed at evaluating the level of leptin and Vascular Cell Adhesion Protein 1 (VCAM-1) and proves that they act as vital markers in the serum of rheumatoid arthritis. MATERIALS AND METHODS: In this study, 80 serum samples from women were obtains (56 serum samples were distributing for women with rheumatoid arthritis and 24 serum samples for uni
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33

Wójcik, Maciej, Andrzej Przemysław Herman, Dorota Anna Zieba, and Agata Krawczyńska. "The Impact of Photoperiod on the Leptin Sensitivity and Course of Inflammation in the Anterior Pituitary." International Journal of Molecular Sciences 21, no. 11 (June 10, 2020): 4153. http://dx.doi.org/10.3390/ijms21114153.

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Leptin has a modulatory impact on the course of inflammation, affecting the expression of proinflammatory cytokines and their receptors. Pathophysiological leptin resistance identified in humans occurs typically in sheep during the long-day photoperiod. This study aimed to determine the effect of the photoperiod with relation to the leptin-modulating action on the expression of the proinflammatory cytokines and their receptors in the anterior pituitary under physiological or acute inflammation. Two in vivo experiments were conducted on 24 blackface sheep per experiment in different photoperiod
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34

Xiao, Ennian, Linna Xia-Zhang, Nicolas R. Vulliémoz, Michel Ferin, and Sharon L. Wardlaw. "Leptin Modulates Inflammatory Cytokine and Neuroendocrine Responses to Endotoxin in the Primate." Endocrinology 144, no. 10 (October 1, 2003): 4350–53. http://dx.doi.org/10.1210/en.2003-0532.

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Leptin, which plays a crucial role in regulating energy balance, can also modulate the inflammatory response. Although leptin-deficient rodents are more sensitive to the toxic effects of bacterial endotoxin, it is unknown if leptin can modulate inflammatory cytokine or neuroendocrine responses to inflammation in a primate model. We have therefore studied the effects of leptin on plasma cytokine and hypothalamic-pituitary-adrenal responses to endotoxin (5 μg iv) in nine ovariectomized rhesus monkeys. Human leptin (50 μg/h) or saline was infused iv for 16 h before and 4 h after endotoxin injecti
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35

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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36

Rooks, Cherie R., Dawn M. Penn, Emily Kelso, Robert R. Bowers, Timothy J. Bartness, and Ruth B. S. Harris. "Sympathetic denervation does not prevent a reduction in fat pad size of rats or mice treated with peripherally administered leptin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 1 (July 2005): R92—R102. http://dx.doi.org/10.1152/ajpregu.00858.2004.

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Leptin increases sympathetic nervous system (SNS) activity in brown adipose tissue and renal nerves. Experiments described here tested whether SNS innervation is required for peripheral, physiological concentrations of leptin to reduce body fat. In experiment 1, one epididymal (EPI) fat pad was sympathectomized by local injection of 6-hydroxydopamine (6OHDA) in C57BL/6 mice that were then infused for 13 days with PBS or 10 μg leptin/day from an intraperitoneal miniosmotic pump. Surprisingly, EPI denervation increased total body fat of PBS-infused mice but leptin decreased the size of both inje
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37

Ngai, Ying Fai, Whitney L. Quong, Melissa B. Glier, Maria M. Glavas, Sandra L. Babich, Sheila M. Innis, Timothy J. Kieffer, and William T. Gibson. "Ldlr−/− Mice Display Decreased Susceptibility to Western-Type Diet-Induced Obesity Due to Increased Thermogenesis." Endocrinology 151, no. 11 (September 29, 2010): 5226–36. http://dx.doi.org/10.1210/en.2010-0496.

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The low-density lipoprotein receptor (Ldlr) is a key molecule involved with lipid clearance. The Ldlr−/− mouse has been used extensively as a model for studying atherosclerosis. This study sought to characterize the energy balance phenotype of Ldlr−/− mice with respect to weight gain, body composition, energy expenditure (EE), glucose homeostasis, and leptin sensitivity. Adult Ldlr−/− mice and Ldlr+/+ controls on a C57Bl/6J background were fed either a chow or a high-fat, high-sucrose Western-type diet (WTD) for eight wk. Physiological studies of food intake, EE, activity, insulin sensitivity,
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38

Zhang, Yiying, Kai-Ying Guo, Patricia A. Diaz, Moonseong Heo, and Rudolph L. Leibel. "Determinants of leptin gene expression in fat depots of lean mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 1 (January 1, 2002): R226—R234. http://dx.doi.org/10.1152/ajpregu.00392.2001.

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The relationship of leptin gene expression to adipocyte volume was investigated in lean 10-wk-old male C57BL/6J mice. mRNA levels for leptin, insulin receptor, glucocorticoid receptor, and tumor necrosis factor (TNF)-α in inguinal, epididymal, and retroperitoneal adipose tissues were quantified and related to adipocyte volume. Leptin mRNA levels were highly correlated with adipocyte volume within each fat depot. Multiple regression analysis of pooled data from the three depots showed that leptin mRNA levels were strongly correlated with adipocyte volumes (β = 0.84, P < 0.001) and, to a smal
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39

Maymó, Julieta L., Antonio Pérez Pérez, Víctor Sánchez-Margalet, José L. Dueñas, Juan Carlos Calvo, and Cecilia L. Varone. "Up-Regulation of Placental Leptin by Human Chorionic Gonadotropin." Endocrinology 150, no. 1 (September 11, 2008): 304–13. http://dx.doi.org/10.1210/en.2008-0522.

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Leptin, the 16,000 molecular weight protein product of the obese gene, was originally considered as an adipocyte-derived signaling molecule for the central control of metabolism. However, leptin has been suggested to be involved in other functions during pregnancy, particularly in placenta, in which it was found to be expressed. In the present work, we have found that recombinant human chorionic gonadotropin (hCG) added to BeWo choriocarcinoma cell line showed a stimulatory effect on endogenous leptin expression, when analyzed by Western blot. This effect was time and dose dependent. Maximal e
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40

Mehebik, Nadia, Anne-Marie Jaubert, Dominique Sabourault, Yves Giudicelli, and Catherine Ribière. "Leptin-induced nitric oxide production in white adipocytes is mediated through PKA and MAP kinase activation." American Journal of Physiology-Cell Physiology 289, no. 2 (August 2005): C379—C387. http://dx.doi.org/10.1152/ajpcell.00320.2004.

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Leptin injection increases plasma levels of nitrites and/or nitrates, an index of nitric oxide (NO) production. Because plasma levels of NO are correlated with fat mass and because adipose tissue is the main source of leptin, it seems that adipose tissue plays a major role in NO release induced by leptin. Adipocytes express both leptin receptors and nitric oxide synthase (NOS; including the endothelial isoform, NOS III, and the inducible isoform, NOS II). In this study, we have demonstrated that physiological concentrations of leptin stimulate NOS activity in adipocytes. This effect of leptin
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41

Penn, Dawn M., Lisa C. Jordan, Emily W. Kelso, Jessica E. Davenport, and Ruth B. S. Harris. "Effects of central or peripheral leptin administration on norepinephrine turnover in defined fat depots." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 6 (December 2006): R1613—R1621. http://dx.doi.org/10.1152/ajpregu.00368.2006.

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Leptin preserves lean tissue but decreases adipose tissue by increasing lipolysis and/or inhibiting lipogenesis. The sympathetic nervous system (SNS) is a primary regulator of lipolysis, but it is not known if leptin increases norepinephrine turnover (NETO) in white adipose tissue. In this study, we examined the effect of leptin administered either as a chronic physiological dose (40 μg/day for 4 days from ip miniosmotic pumps) or as an acute injection in the third ventricle (1.5 μg injected two times daily for 2 days) on NETO and the size of brown and white fat depots in male Sprague Dawley r
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42

Xu, Jing, Melissa A. Kirigiti, Kevin L. Grove, and M. Susan Smith. "Regulation of Food Intake and Gonadotropin-Releasing Hormone/Luteinizing Hormone during Lactation: Role of Insulin and Leptin." Endocrinology 150, no. 9 (May 21, 2009): 4231–40. http://dx.doi.org/10.1210/en.2009-0190.

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Abstract Negative energy balance during lactation is reflected by low levels of insulin and leptin and is associated with chronic hyperphagia and suppressed GnRH/LH activity. We studied whether restoration of insulin and/or leptin to physiological levels would reverse the lactation-associated hyperphagia, changes in hypothalamic neuropeptide expression [increased neuropeptide Y (NPY) and agouti-related protein (AGRP) and decreased proopiomelanocortin (POMC), kisspeptin (Kiss1), and neurokinin B (NKB)] and suppression of LH. Ovariectomized lactating rats (eight pups) were treated for 48 h with
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43

Roy, A. F., Y. Benomar, V. Bailleux, C. M. Vacher, A. Aubourg, A. Gertler, J. Djiane, and M. Taouis. "Lack of cross-desensitization between leptin and prolactin signaling pathways despite the induction of suppressor of cytokine signaling 3 and PTP-1B." Journal of Endocrinology 195, no. 2 (November 2007): 341–50. http://dx.doi.org/10.1677/joe-07-0321.

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Hyperprolactinemia and hyperleptinemia occur during gestation and lactation with marked hyperphagia associated with leptin resistance. Prolactin (PRL) induces the expression of orexigenic neuropeptide Y (NPY) through the activation of JAK-2/STAT-3 signaling pathway in hypothalamic paraventricular nucleus (PVN) leading to hyperphagia. PRL may also act through the inhibition of anorexigenic effect of leptin via induction of suppressor of cytokine signaling 3 (SOCS-3). This paper aimed to co-localize PRL (PRL-R) and leptin (ObRb) receptors in the hypothalamus of female rats and investigate the po
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44

Fanjul, Carmen, Jaione Barrenetxe, Lorena De Pablo-Maiso, and María Pilar Lostao. "In vivo regulation of intestinal absorption of amino acids by leptin." Journal of Endocrinology 224, no. 1 (October 27, 2014): 17–23. http://dx.doi.org/10.1530/joe-14-0453.

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Leptin is secreted by the gastric mucosa and is able to reach the intestinal lumen and bind to its receptors located in the apical membranes of enterocytes. We have previously demonstrated that apical leptin inhibits uptake of amino acids in rat intestine in vitro and in Caco-2 cells. The aim of the present work was to investigate the effect of leptin on absorption of amino acids using in vivo techniques, which generate situations closer to physiological conditions. In vivo intestinal absorption of amino acids in rats was measured by isolating a jejunal loop and using the single-pass perfusion
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45

Roh, Cecilia, Galini Thoidis, Stephen R. Farmer, and Konstantin V. Kandror. "Identification and characterization of leptin-containing intracellular compartment in rat adipose cells." American Journal of Physiology-Endocrinology and Metabolism 279, no. 4 (October 1, 2000): E893—E899. http://dx.doi.org/10.1152/ajpendo.2000.279.4.e893.

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The major leptin-containing membrane compartment was identified and characterized in rat adipose cells by means of equilibrium density and velocity sucrose gradient centrifugation. This compartment appears to be different from peptide-containing secretory granules present in neuronal, endocrine, and exocrine cells, as well as from insulin-sensitive GLUT-4-containing vesicles abundant in adipocytes. Exocytosis of both leptin- and GLUT-4-containing vesicles can be induced by insulin; however, only leptin secretion is responsive to serum stimulation. This latter effect is resistant to cycloheximi
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46

Torday, J. S., and V. K. Rehan. "Stretch-stimulated surfactant synthesis is coordinated by the paracrine actions of PTHrP and leptin." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 1 (July 1, 2002): L130—L135. http://dx.doi.org/10.1152/ajplung.00380.2001.

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Intrauterine lung development, culminating in physiological pulmonary surfactant production by epithelial type II (TII) cells, is driven by fluid distension through unknown mechanisms. Differentiation of alveolar epithelial and mesenchymal cells is mediated by soluble factors like parathyroid hormone-related protein (PTHrP), a stretch-sensitive TII cell product. PTHrP stimulates pulmonary surfactant production by a paracrine feedback loop mediated by leptin, a soluble product of the mature lipofibroblast (LF). When LFs and TIIs are stretched in coculture, there is a fivefold increase in surfac
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47

Viengchareun, S., H. Bouzinba-Segard, J.-P. Laigneau, M.-C. Zennaro, P. A. Kelly, A. Bado, M. Lombès, and N. Binart. "Prolactin potentiates insulin-stimulated leptin expression and release from differentiated brown adipocytes." Journal of Molecular Endocrinology 33, no. 3 (December 2004): 679–91. http://dx.doi.org/10.1677/jme.1.01563.

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The pituitary hormone prolactin (PRL) exerts pleiotropic effects, which are mediated by a membrane receptor (PRLR) present in numerous cell types including adipocytes. Brown adipose tissue (BAT) expresses uncoupling proteins (UCPs), involved in thermogenesis, but also secretes leptin, a key hormone involved in the control of body weight. To investigate PRL effects on BAT, we used the T37i brown adipose cell line, and demonstrated that PRLRs are expressed as a function of cell differentiation. Addition of PRL leads to activation of the JAK/STAT and MAP kinase signaling pathways, demonstrating t
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48

Morton, Gregory J., Kevin D. Niswender, Christopher J. Rhodes, Martin G. Myers, James E. Blevins, Denis G. Baskin, and Michael W. Schwartz. "Arcuate Nucleus-Specific Leptin Receptor Gene Therapy Attenuates the Obesity Phenotype of Koletsky (fak/fak) Rats." Endocrinology 144, no. 5 (May 1, 2003): 2016–24. http://dx.doi.org/10.1210/en.2002-0115.

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Leptin signaling in the hypothalamic arcuate nucleus (ARC) is hypothesized to play an important role in energy homeostasis. To investigate whether leptin signaling limited to this brain area is sufficient to reduce food intake and body weight, we used adenoviral gene therapy to express the signaling isoform of the leptin receptor, leprb, in the ARC of leptin receptor-deficient Koletsky (fak/fak) rats. Successful expression of adenovirus containing leprb (Ad-leprb) selectively in the ARC was documented by in situ hybridization. Using real-time PCR, we further demonstrated that bilateral microin
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Zimmermann-Belsing, T., G. Brabant, JJ Holst, and U. Feldt-Rasmussen. "Circulating leptin and thyroid dysfunction." European Journal of Endocrinology 149, no. 4 (October 1, 2003): 257–71. http://dx.doi.org/10.1530/eje.0.1490257.

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The identification and sequencing of the ob gene and its product, leptin, in 1994 opened new insights in the study of the mechanisms controlling body weight and led to a surge of research activity. Since its discovery, leptin has been the subject of an enormous amount of work especially within the fields of nutrition, metabolism and endocrinology. Leptin is accepted as an adipose signal, and even though the underlying mechanisms are not fully clarified, leptin, in addition to the thyroid hormones, is believed to be involved in regulation during the switch from the fed to the starved state. It
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Arias-Alvarez, M., R. M. Garcia-Garcia, L. Revuelta, P. G. Rebollar, and P. L. Lorenzo. "238 EFFECTS OF LEPTIN SUPPLEMENTATION ON NUCLEAR AND CYTOPLASMIC IN VITRO MATURATION OF RABBIT OOCYTES." Reproduction, Fertility and Development 20, no. 1 (2008): 198. http://dx.doi.org/10.1071/rdv20n1ab238.

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Reproductive function is affected substantially by nutritional status. Leptin is a peptide secreted mainly by adipocytes that reflects the amount of body fat and acts as a modulator of oocyte quality. The aim of this study was to analyze, for the first time in the rabbit, the influence of leptin on meiotic and cytoplasmic maturation (cortical granule (CG) migration) of rabbit oocytes in vitro (IVM). Cumulus–oocyte complexes (COCs) were collected from 25 young New Zealand white female rabbits (<3 parturitions) in 3 replicates. COCs were aspirated from ovarian follicles >1 mm in size and w
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