Effects of in vivo estrogen treatment on adipose tissue metabolism and nuclear estrogen receptor binding in isolated rat adipocytes

Pedersen, Steen; Børglum, Jens; Møller‐Pedersen, Torben; Richelsen, Bjørn

doi:10.1016/0303-7207(92)90120-u

Cited by 74 publications

(45 citation statements)

References 31 publications

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“…The relative roles of GH and IGF-I on other aspects of adipocyte differentiation and fat metabolism are far from clear (Richelsen 1997). E 2 also has pronounced effects on fat distribution and metabolism (Pedersen et al 1992, Westerveld et al 1995 which may or may not be related to those of GH and/or IGF-I.…”

Section: Discussionmentioning

confidence: 99%

The effect of GH on estrogen receptor expression in the rat mammary gland

Feldman

Ruan²,

Tappin³

et al. 1999

Journal of Endocrinology

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Both GH and insulin-like growth factor I (IGF-I) synergize with estrogen to induce normal mammary gland development. However, the nature of this synergy has not been explored. To gain insight into the mechanism of these interactions we have examined the effects of these substances on the estrogen receptor (ER). ER levels in the mammary gland cytosols from hypophysectomized and oophorectomized rats, were measured using two assay systems: a dextran-coated charcoal procedure to measure binding to radiolabeled steroid, and an immunologic assay employing a specific antibody to the receptor. In both assays, levels of ER were at or near baseline detection (1-2 ng/mg protein). Treating animals with either bovine or human GH significantly increased ER activity (P<0·001), whereas prolactin (PRL) and/or estradiol treatment had no effect. That this increase was at the level of transcription was demonstrated by reverse transcriptase/ polymerase chain reaction. Following a single injection of GH (50 µg), a substantial increase in ER mRNA was observed by 10 h, with levels returning to baseline within 24 h; a concomitant increase in ER itself was also observed at the 10 h time point. The effect of GH appeared to occur mainly in the mammary stroma, because there were no differences in GH stimulation of ER between gland-free and gland containing mammary fat pads. Furthermore, analysis of mammary gland ER by immunocytochemistry demonstrated that while ER was present in the epithelial cells of non-treated animals, only GH treated animals had ER clearly visible in both glandular and fat cells of the tissue. In contrast, treating animals with des(1-3)-IGF-I did not result in reproducible increases in ER, nor in the staining of fat cell nuclei for ER. These data demonstrate a specific GH effect on the ER in the mammary fat cell.

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Section: Discussionmentioning

confidence: 99%

The effect of GH on estrogen receptor expression in the rat mammary gland

Feldman

Ruan²,

Tappin³

et al. 1999

Journal of Endocrinology

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“…As for the mechanism of action of estrogen, Pedersen et al (26) reported that IR binding was increased in adipocytes from rodents treated with estrogen. In that case, IR binding seemed to be due to an increased number of IRs (26).…”

Section: Estrogen Signaling Enhances Tolerance To Oxidative Stress Inmentioning

confidence: 99%

Estrogen, Insulin, and Dietary Signals Cooperatively Regulate Longevity Signals to Enhance Resistance to Oxidative Stress in Mice

Baba

Shimizu

Suzuki

et al. 2005

Journal of Biological Chemistry

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To investigate the biological significance of a longevity mutation found in daf-2 of Caenorhabditis elegans, we generated a homologous murine model by replacing Pro-1195 of insulin receptors with Leu using a targeted knock-in strategy. Homozygous mice died in the neonatal stage from diabetic ketoacidosis, whereas heterozygous mice showed the suppressed kinase activity of the insulin receptor but grew normally without spontaneously developing diabetes during adulthood. We examined heterozygous insulin receptor mutant mice for longevity phenotypes. Under 80% oxygen, mutant female mice survived 33.3% longer than wild-type female mice, whereas mutant male mice survived 18.2% longer than wild-type male mice. These results suggested that mutant mice acquired more resistance to oxidative stress, but the benefit of the longevity mutation was more pronounced in females than males. Manganese superoxide dismutase activity in mutant mice was significantly upregulated, suggesting that the suppressed insulin signaling leads to an enhanced antioxidant defense. To analyze the molecular basis of the gender difference, we administered estrogen to mutant mice. It was found that the survival of mice under 80% oxygen was extended when they were administered estradiol. In contrast, mutant and wild-type female mice showed shortened survivals when their ovaries were removed. The influence of estrogen is remarkable in mutant mice compared with wild-type mice, suggesting that estrogen modulates insulin signaling in mutant mice. Furthermore, we showed additional extension of survival under oxidative conditions when their diet was restricted. Collectively, we show that three distinct signals; insulin, estrogen, and dietary signals work in independent and cooperative ways to enhance the resistance to oxidative stress in mice.

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“…Both estrogen receptor a and b are found in the hypothalamus of the brain, and mice deficient in estrogen receptor-a develop a marked increase in adipose tissue mass, 5 consistent with a role for estrogen in the central regulation of body weight. It is possible that estradiol may regulate body weight by enhancing glucose uptake into the brain 21 or by increasing insulin receptor number, 22 processes that may influence recognition of the fed state. 23,24 There is also some evidence that ovariectomy increases hypothalamic neuropeptide Y (NPY) expression 25 and decreases hypothalamic corticotropin-releasing hormone (CRH) immunoreactivity, 26 both of which would promote hyperphagia.…”

Section: Introductionmentioning

confidence: 99%

Estrogen deficiency causes central leptin insensitivity and increased hypothalamic neuropeptide Y

et al. 2001

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OBJECTIVE: Altered fat distribution is a consequence of menopause, but the mechanisms responsible are unknown. Estrogen insufficiency in humans can be modeled using ovariectomized rats. We have shown that increased adiposity in these rats is due to reduced physical activity and transient hyperphagia, and can be reversed with 17b-estradiol treatment. The aims of this study were to examine whether this altered energy balance is associated with circulating leptin insufficiency, central leptin insensitivity, decreased hypothalamic leptin receptor (Ob-Rb) expression, and=or increased hypothalamic neuropeptide Y (NPY). METHODS: Plasma leptin levels, adipose tissue ob gene expression, energy balance responses to i.c.v. leptin, hypothalamic ObRb expression and NPY concentration in five separate hypothalamic regions were measured in adult female rats after either ovariectomy or sham operations. RESULTS: Obesity was not associated with hypoleptinemia or decreased ob gene expression in ovariectomized rats; however, it was associated with insensitivity to central leptin administration. Food intake was less suppressed and spontaneous physical activity was less stimulated by leptin. This was not due to decreased hypothalamic Ob-Rb expression. NPY concentration in the paraventricular nucleus of the hypothalamus was elevated in the ovariectomized rats, consistent with leptin insensitivity; however this effect was transient and disappeared as body fat and leptin levels increased further and hyperphagia normalized. CONCLUSION: Impaired central leptin sensitivity and overproduction of NPY may contribute to excess fat accumulation caused by estrogen deficiency.

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Effects of in vivo estrogen treatment on adipose tissue metabolism and nuclear estrogen receptor binding in isolated rat adipocytes

Cited by 74 publications

References 31 publications

The effect of GH on estrogen receptor expression in the rat mammary gland

The effect of GH on estrogen receptor expression in the rat mammary gland

Estrogen, Insulin, and Dietary Signals Cooperatively Regulate Longevity Signals to Enhance Resistance to Oxidative Stress in Mice

Estrogen deficiency causes central leptin insensitivity and increased hypothalamic neuropeptide Y

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