Regulation of leptin gene expression and secretion by steroid hormones

Brann, Darrell W.; Sevilla, Liesl De; Zamorano, Pedro; Mahesh, Virendra B.

doi:10.1016/s0039-128x(99)00049-5

Cited by 59 publications

(41 citation statements)

References 14 publications

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“…These data agree with a previous report (16), but differ from data presented in another study, which reports that estradiol treatment does not modify plasma leptin levels (17). The reason for this discrepancy may be related to the experimental protocols, duration of estradiol treatment and feeding status.…”

Section: Discussionsupporting

confidence: 82%

“…The reason for this discrepancy may be related to the experimental protocols, duration of estradiol treatment and feeding status. To reinforce the notion that estrogens affect leptin secretion, it has been shown that estradiol has a direct effect on white adipocytes, increasing the synthesis and secretion of leptin (16), as well as its mRNA expression (18). The presence of estrogen receptors in adipocytes (19) provides a possible mechanism by which estrogen may modulate food intake, increasing leptin release.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Estradiol-induced hypophagia is associated with the differential mRNA expression of hypothalamic neuropeptides

Silva

Castro

Amaral

et al. 2010

Braz J Med Biol Res

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Estradiol-induced hypophagia is associated with the differential mRNA expression of hypothalamic neuropeptides

Silva

Castro

Amaral

et al. 2010

Braz J Med Biol Res

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“…One possible contributor to increased leptin expression in visceral fat in GDM might be altered estrogen receptor subtypes expression ratio in adipose depots of GDM in response to rising estrogen level with advancing gestation (Sivan et al, 1998;Brann et al, 1999;Tanaka et al, 2001 andYi et al, 2008). Here we found similarly to Yi and colleagues (Yi et al, 2008) The second group of candidates possibly affecting leptin expression in visceral fat in pregnancy includes insulin and glucose (Boucher et al, 2005 andSalvatores et al, 2006).…”

mentioning

confidence: 99%

Expression of adipokines and estrogen receptors in adipose tissue and placenta of patients with gestational diabetes mellitus

Kleiblová

Dostálová

Bartlova

et al. 2010

Molecular and Cellular Endocrinology

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To cite this version:P. Kleiblova, I. Dostalova, M. Bartlova, Z. Lacinova, I. Ticha, et al.. Expression of adipokines and estrogen receptors in adipose tissue and placenta of patients with gestational diabetes mellitus. Molecular and Cellular Endocrinology, Elsevier, 2009, 314 (1) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Page 1 of 36A c c e p t e d M a n u s c r i p t A c c e p t e d M a n u s c r i p t 2 SUMMARYThe purpose of this study was to assess the expression profile of genes with potential role in the development of insulin resistance (adipokines, cytokines/chemokines, estrogen receptors) in subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT) and placenta of pregnant women with gestational diabetes mellitus (GDM) and age-matched women with physiological pregnancy at the time of Caesarean section. qRT-PCR was used for expression analysis of the studied genes. Leptin gene expression in VAT of GDM group was significantly higher relative to control group. Gene expressions of interleukin-6 and interleukin-8 were significantly increased, whereas the expressions of genes for estrogen receptors α and β were significantly reduced in SAT of GDM group relative to controls, respectively. We found no significant differences in the expression of any genes of interest (LEP, RETN, ADIPOR1, ADIPOR2, CD68, ERα, ERβ) in placentas of women with GDM relative to controls. We conclude that increased expression of leptin in visceral adipose depot together with increased expressions of proinflammatory cytokines and reduced expressions of estrogen receptors in subcutaneous fat may play a role in the etiopathogenesis of GDM.

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“…12,13 If these differences are replicated in vivo, variation in the total leptin signal may reflect the differential contribution made by different fat stores. Leptin gene expression and production is regulated by many physiological signals including insulin, 14,15 the sympathetic system, 16 growth hormone, 14 polyunsaturated fatty acids, 17 steroids, 18 thyroid hormones, 12 retinoic acid 13 and leptin itself. 19 Variations in levels of these regulatory factors may contribute to the variation in basal circulating leptin levels.…”

Section: Introductionmentioning

confidence: 99%

Plasma leptin levels are related to body composition, sex, insulin levels and the A55V polymorphism of the UCP2 gene

Rance¹,

Johnstone²,

Murison³

et al. 2007

Int J Obes

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Objective: Circulating leptin levels show a high degree of individual variability even after the main effect of body fatness is accounted for. We therefore wanted to determine the roles of variation in body composition, age, sex and polymorphisms of the UCP2 gene and promoter region on levels of circulating leptin. Subjects: One hundred and fifty Caucasian subjects, which represented a cross-section of the population from NE, Scotland, were recruited. Measurements: Body composition was measured using dual X-ray absorptiometry. Fasted circulating leptin, insulin, T3 and T4 levels were measured, and all individuals were genotyped for the UCP2 polymorphisms A55V, -866G4A and exon-8 ins/del. Results: The results indicate that circulating leptin was significantly related to sex and principle component (PC) scores representing overall adipose tissue mass and a second representing the contrast of central to peripheral bone mineral content. Residual leptin was associated with the A55V polymorphism (Po 0.001) explaining 11.3% of the residual variance. There was a marginal effect associated with exon-8 ins/del (P ¼ 0.045) explaining 4.4% of the residual variance in leptin. Log e transformed circulating fasting insulin was related to PC scores representing general adiposity and sex. Residual Log e insulin was associated with the A55V and exon-8 ins/del polymorphisms explaining 5.7% (P ¼ 0.015) and 5% (P ¼ 0.026) of the residual variation, respectively. The -866G4A polymorphism was not significantly associated with residual leptin or insulin. Leptin and insulin were significantly (P ¼ 0.007) correlated. Statistically removing the effect of insulin on leptin still showed association between leptin and A55V (P ¼ 0.002). Removing the effect of leptin on insulin, the A55V polymorphism was no longer significant (P ¼ 0.120). After accounting for the correlation between insulin and leptin, the exon-8 ins/del was no longer significant for residual leptin (P ¼ 0.119) or Log e insulin (P ¼ 0.252). Conclusion: These data suggest that the A55V polymorphism directly affected the levels of leptin but not via an effect on insulin.

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Regulation of leptin gene expression and secretion by steroid hormones

Cited by 59 publications

References 14 publications

Estradiol-induced hypophagia is associated with the differential mRNA expression of hypothalamic neuropeptides

Estradiol-induced hypophagia is associated with the differential mRNA expression of hypothalamic neuropeptides

Expression of adipokines and estrogen receptors in adipose tissue and placenta of patients with gestational diabetes mellitus

Plasma leptin levels are related to body composition, sex, insulin levels and the A55V polymorphism of the UCP2 gene

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