The ratio of estrogen receptor α to estrogen receptor β in adipose tissue is associated with leptin production and obesity

Shin, Jung Hoon; Hur, Jun Young; Seo, Hong Seog; Jeong, Yu A.; Lee, Jae Kwan; Oh, Min Jeong; Kim, Tak; Saw, Ho Suk; Kim, Sun Haeng

doi:10.1016/j.steroids.2007.03.013

Cited by 49 publications

(49 citation statements)

References 29 publications

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“…Using mouse mammary epithelial cells, Helguero et al (2005) showed that activation of ERb opposes ERa-induced proliferation and increases apoptosis. Other studies have focused on the ratio of the ERa to ERb expression (Shin et al 2007, Yi et al 2008 and showed that the ratio of ERa to ERb expression in adipocytes is an important potential regulatory factor in leptin expression. As discussed above, the reported ability of ERb to antagonize ERa activity adds complexity to the interpretation of this experiment; therefore, the functions of the two subtypes in ATDC5 cell were to be defined in this study.…”

Section: Discussionmentioning

confidence: 99%

Estrogen stimulates leptin receptor expression in ATDC5 cells via the estrogen receptor and extracellular signal-regulated kinase pathways

Wang

Li²,

Jiang³

et al. 2012

Journal of Endocrinology

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Regulation of the physiological processes of endochondral bone formation during long bone growth is controlled by various factors including the hormones estrogen and leptin. The effects of estrogen are mediated not only through the direct activity of estrogen receptors (ERs) but also through cross talk with other signaling systems implicated in chondrogenesis. The receptors of both estrogen and leptin (OBR (LEPR)) are detectable in growth plate chondrocytes of all zones. In this study, the expression of mRNA and protein of OBR in chondrogenic ATDC5 cells and the effect of 17b-estradiol (E 2 ) stimulation were assessed using quantitative PCR and western blotting. We have found that the mRNA of Obr was dynamically expressed during the differentiation of ATDC5 cells over 21 days. Application of E 2 (10 K7 M) at day 14 for 48 h significantly upregulated OBR mRNA and protein levels (P!0 . 05). The upregulation of Obr mRNA by E 2 was shown to take place in a concentration-dependent manner, with a concentration of 10 K7 M E 2 having the greatest effect. Furthermore, we have confirmed that E 2 affected the phosphorylation of ERK1/2 (MAPK1/MAPK3) in a time-dependent manner where a maximal fourfold change was observed at 10 min following application of E 2 . Finally, pretreatment of the cells with either U0126 (ERK1/2 inhibitor) or ICI 182 780 (ER antagonist) blocked the upregulation of OBR by E 2 and prevented the E 2 -induced phosphorylation of ERK. These data demonstrate, for the first time, the existence of cross talk between estrogen and OBR in the regulation of bone growth whereby estrogen regulates the expression of Obr in growth plate chondrocytes via ERs and the activation of ERK1/2 signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Estrogen stimulates leptin receptor expression in ATDC5 cells via the estrogen receptor and extracellular signal-regulated kinase pathways

Wang

Li²,

Jiang³

et al. 2012

Journal of Endocrinology

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“…Higher ER-α expression in adipose tissue was observed among obese postmenopausal women [14] . The ratio of ER-α to ER-β in adipose tissue was associated with obesity in both pre-and postmenopausal women [15] . Male ER-α knockout mice have previously been reported to develop obesity after sexual maturity [16,17] .…”

Section: Introductionmentioning

confidence: 99%

Association analysis of genetic polymorphisms and potential interaction of the osteocalcin (BGP) and ER-α genes with body mass index (BMI) in premenopausal Chinese women

Xiao

Luo

et al. 2010

Acta Pharmacol Sin

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Aim: To investigate whether estrogen receptor α (ER-α) PvuII and osteocalcin (also known as bone Gla protein, or BGP) HindIII genetic polymorphisms and their potential interactions are associated with body mass index (BMI) variation. Methods: Data on BMI and ER-α PvuII and BGP HindIII genotypes were obtained from 328 healthy premenopausal Chinese women in east China. The study subjects were unrelated, at least 21 years old (mean age of 33.2±5.9 years), and had an average BMI of 21.58±2.59. All subjects were genotyped at the ER-α PvuII and BGP HindIII loci using polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP). Results: The BGP HindIII genotypes were significantly associated with BMI (P=0.003). Carriers of the HH and Hh genotypes had approximately 2.73% and 1.27% higher BMI than those of the hh genotype, respectively. In contrast, the ER-α PvuII polymorphism was not significantly associated with BMI (P=0.454). In addition, there was no evidence of potential interactions between the ER-α and BGP genes in our subjects (P≥0.013). Conclusion:The HindIII polymorphism of the BGP gene, but not the PvuII polymorphism of the ER-α gene or their potential interaction, was associated with BMI in premenopausal Chinese women.

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“…The ratio ER/ER seems to be associated with obesity as well as with the serum level and the production of leptin in omental adipose tissue in women (Shin et al, 2007). In the brain, the disruption of the ER in the ventromedial nucleus of the hypothalamus leads to weight gain, increased visceral adiposity, hyperphagia, hyperglycaemia and impaired energy expenditure in female mice (Musatov et al, 2007).…”

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confidence: 99%

The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes

Nadal

Alonso-Magdalena

Soriano

et al. 2009

Molecular and Cellular Endocrinology

263

187

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. The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes. Molecular and Cellular Endocrinology, Elsevier, 2009, 304 (1-2) Please cite this article as: Nadal, A., Alonso-Magdalena, P., Soriano, S., Quesada, I., Ropero, A.B., The pancreatic ␤-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes, Molecular and Cellular Endocrinology (2008), doi:10.1016/j.mce.2009 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. THE PANCREATIC -CELL AS A TARGET OF ESTROGENS AND XENOESTROGENS: IMPLICATIONS FOR BLOOD GLUCOSE HOMEOSTASIS AND DIABETESAngel Rosen & Spiegelman, 2006;Fritsche et al., 2008). During the fasting state, insulin remains at low levels because plasma glucose concentration is low. In this situation, the levels of the counter-regulatory hormones, glucagon, adrenaline and corticosteroids are increased to promote hepatic glucose production. In contrast, insulin, the only hormone in the body able to decrease blood glucose levels, is increased during the fed state. Insulin decreases blood glucose by promoting adipocyte and muscle glucose uptake, as well as by preventing the liver from producing glucose by suppressing glycogenolysis and gluconeogenesis (Fritsche et al., 2008). neurotransmitters, hormones and nutrients, among which glucose is the most important.Normally, in response to short glucose stimulation, insulin biosynthesis is regulated by the increased translation of the preproinsulin transcript. After a prolonged glucose exposure, however, it is regulated via the insulin gene transcription (Orland et al., 1985;Permutt & Rotwein, 1983;Poitout et al., 2006). Both transcriptional and translational regulation of insulin biosynthesis is essential to maintain the intracellular stores of insulin on a long term basis.The secretory response of -cells depends on their electrical activity. This consists of oscillations of the membrane potential that range from electrically silent periods to depolarised plateaus on which Ca 2+ -action potentials originate (Rorsman et al., 2000).The classical stimulus-secretion coupling that drives insulin release involves the closure of K ATP channels by increasing the intracellular ATP/ADP ratio (Ashcroft et al., 1984) and diadenosine polyphosphates concentration (DPs) (Ripoll et al., 1996) oscillatory pattern is originated (Nadal et al., 1999;Santos et al., 1991;Valdeolmillos et al., 1989), which triggers a pulsatile insulin secretion (Barbosa et al., 1998;Gilon et al., 1993;Dyachok et al., 2008). Estrogens, estrogen receptors and blood glucose homeostasisT...

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The ratio of estrogen receptor α to estrogen receptor β in adipose tissue is associated with leptin production and obesity

Cited by 49 publications

References 29 publications

Estrogen stimulates leptin receptor expression in ATDC5 cells via the estrogen receptor and extracellular signal-regulated kinase pathways

Estrogen stimulates leptin receptor expression in ATDC5 cells via the estrogen receptor and extracellular signal-regulated kinase pathways

Association analysis of genetic polymorphisms and potential interaction of the osteocalcin (BGP) and ER-α genes with body mass index (BMI) in premenopausal Chinese women

The pancreatic β-cell as a target of estrogens and xenoestrogens: Implications for blood glucose homeostasis and diabetes

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