Correlation between estrogens and serum adipocytokines in premenopausal and postmenopausal women

Hong, Soon Cheol; Yoo, Seung‐Min; Cho, Geum Joon; Kim, Tak; Hur, Jun Young; Park, Yong Kyun; Lee, Kyu Wan; Kim, Sun Haeng

doi:10.1097/gme.0b013e31802cddca

Cited by 83 publications

(63 citation statements)

References 41 publications

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“…Circulating leptin is higher in women than that in men (Hickey et al 1996), but there are also sex differences in leptin found in children (Hellström et al 2000). Leptin concentrations are positively correlated with serum E2 levels in pre-menopausal women; however, the increase in WAT mass in post-menopausal women also increases circulating leptin concentrations (Hong et al 2007). The aforementioned findings indicate that sex steroids and other sex-specific factors regulate leptin.…”

Section: Leptinmentioning

confidence: 64%

“…Such findings indicate a potential role for both E2 and gender in leptin action and regulation. The vast majority of evidence supports the premise that E2 increases leptin production and release from WAT, but that other factors besides E2 are related to the sexual dimorphism displayed by this adipokine (Machinal et al 1999, Hellström et al 2000, Hong et al 2007.…”

Section: Leptinmentioning

confidence: 81%

“…The aforementioned findings indicate that sex steroids and other sex-specific factors regulate leptin. Furthermore, leptin transcript expression is higher in the subcutaneous WAT of pre-menopausal women than that in post-menopausal women (Hong et al 2007), presumably due to the higher E2 concentrations found in younger women. Similar support for the role of E2 in leptin secretion comes from experiments with rodent models wherein OVX rats demonstrate a 25% decrease in Ob transcript levels in visceral WAT (Machinal et al 1999).…”

Section: Leptinmentioning

confidence: 96%

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The role of sex steroids in white adipose tissue adipocyte function

Newell-Fugate

2017

Reproduction

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Abstractwith the increasing knowledge that gender influences normal physiology, much biomedical research has begun to focus on the differential effects of sex on tissue function. Sexual dimorphism in mammals is due to the combined effects of both genetic and hormonal factors. Hormonal factors are mutable particularly in females in whom the estrous cycle dominates the hormonal milieu. Given the severity of the obesity epidemic and the fact that there are differences in the obesity rates in men and women, the role of sex in white adipose tissue function is being recognized as increasingly important. Although sex differences in white adipose tissue distribution are well established, the mechanisms affecting differential function of adipocytes within white adipose tissue in males and females remain largely understudied and poorly understood. One of the largest differences in the endocrine environment in males and females is the concentration of circulating androgens and estrogens. This review examines the effects of androgens and estrogens on lipolysis/lipogenesis, adipocyte differentiation, insulin sensitivity and adipokine production in adipocytes from white adipose tissue with a specific emphasis on the sexual dimorphism of adipocyte function in white adipose tissue during both health and disease.Reproduction (2017) 153 R133-R149

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Section: Leptinmentioning

confidence: 64%

Section: Leptinmentioning

confidence: 81%

Section: Leptinmentioning

confidence: 96%

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The role of sex steroids in white adipose tissue adipocyte function

Newell-Fugate

2017

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“…In this context, previous research by our group demonstrates that there is a sexual dimorphism in mitochondrial function and biogenesis in WAT, in that mitochondria of female rats are more functional than those of males, and this is accompanied by greater adiponectin expression (Amengual-Cladera et al 2012a,b). Although estrogens are known to modulate both mitochondrial biogenesis (Mattingly et al 2008) and adipokine secretion (Hong et al 2007), our previous studies in ovariectomized rats pointed out that 17-b estradiol (E 2 ) would not be the only factor responsible for the differences between males and females in WAT (Amengual-Cladera et al 2012c).…”

Section: Introductionmentioning

confidence: 99%

Opposite effects of 17-β estradiol and testosterone on mitochondrial biogenesis and adiponectin synthesis in white adipocytes

Capllonch-Amer¹,

Lladó²,

Proenza³

et al. 2014

Journal of Molecular Endocrinology

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Sexual dimorphism has been found in both mitochondrial functionality and adiponectin expression in white adipose tissue, with female rats presenting more functional mitochondria than males and greater adiponectin expression. However, little is known about the role of sex hormones in this dimorphism. The aim was to elucidate the role of sex hormones in mitochondrial biogenesis and dynamics and in adiponectin synthesis in white adipocytes, and also to provide new evidence of the link between these processes. 3T3-L1 preadipocytes were differentiated and treated either with 17-b estradiol (E 2 ; 10 nM), progesterone (Pg), testosterone (1 mM both), or a combination of Pg or testosterone with flutamide (FLT; 10 mM) or E 2 (1 mM). The markers of mitochondrial biogenesis and dynamics and adiponectin expression were analyzed. E 2 induced mitochondrial proliferation and differentiation in 3T3-L1, although testosterone showed opposite effects. Pg treatment stimulated proliferation but impaired differentiation. In concerns mitochondrial dynamics, these hormones promoted fusion over fission. FLT treatment indicated that Pg elicits its effects on mitochondrial dynamics through the androgen receptor. E 2 coadministration with testosterone or Pg reversed its effects. In conclusion, our results show that E 2 induces stimulation of mitochondrial biogenesis in white adipocytes in vitro, especially in situations that imply an impairment of mitochondrial function, whereas testosterone would have opposite effects. Moreover, testosterone and Pg alter mitochondrial dynamics by promoting fusion over fission, while E 2 stimulates both processes. All these alterations run in parallel with changes in adiponectin expression, thus suggesting the existence of a link between mitochondrial biogenesis and dynamics and adiponectin synthesis in white adipocytes.

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“…The following critical objectives need to be examined: 1) Do the adipokines exist in the extracellular space of normal and cancerous breast tissue in vivo?, and 2) What are the effects of sex steroids on adipokine levels in normal breast tissue in vivo? Estrogen correlated positively with serum leptin, but not serum adiponectin, in premenopausal healthy women according to report by Hong et al (254), but it was unclear if a correlation also exist in the tumor microenvironment. We therefore decided to investigate 40 women (Paper II) using the microdialysis technique.…”

Section: Cytokine Name Receptormentioning

confidence: 63%

Hormonal regulation of immune modulators in human breast tissue

Morad¹

2015

Linköping University Medical Dissertations

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Breast cancer is the most common form of cancer and the second leading cause of malignancy-associated death in women worldwide. Estrogens are the main sex hormones in women. They are essential for the development and function of normal breast mammary glands; however, prolonged exposure to estrogens increases the risk of breast cancer development and progression. Approximately two-thirds of all breast cancer patients are positive for estrogen receptor (ER), but only 50% of those cases can benefit from antiestrogen therapy. In this thesis we investigated the effects of estrogen, diet modification, and anti-estrogen drugs on several immune modulators in normal human breast tissue. We used the microdialysis technique to sample the immune modulators in situ in normal human breast tissue, in malignant breast tissue, and in tumor tissue from both the immune competent mice with murine breast cancer and immune deficient mice bearing human breast tumors. Furthermore, we also used ex vivo culture of normal breast tissue and in vitro cell culture of breast cancer cell lines. A combined cell culture (co-culture) of breast cancer cell lines, together with the primary mature adipocytes, was also used in this thesis. In Paper I and Paper II, our results suggested that estrogen exerted both proinflammatory and pro-tumorigenic effects in normal human breast tissue. Estradiol increased extracellular interleukin-1β (IL-1β) and leptin levels and decreased IL-1Ra and adiponectin levels in normal human breast tissue. In contrast, tamoxifen decreased IL-1β and leptin levels and increased IL-1Ra and adiponectin levels, shifting the environment towards an antiinflammatory and antitumorigenic state. Diet modification with flaxseed for 30 days also increased IL-1Ra levels, creating an anti-inflammatory environment in normal breast tissue. In the breast cancer tissue, we found that extracellular IL-1β levels and leptin levels were significantly higher, whereas adiponectin levels were significantly lower, compared with normal adjacent breast tissue, which suggested a more proinflammatory state. In the third paper, our in vivo investigation of normal breast tissue revealed significant correlations between vascular endothelial growth factor (VEGF) and leptin, IL-1β and leptin, and between VEGF and IL-1β. No correlations were found in the abdominal subcutaneous (s.c.) fat tissue. Our in vitro inhibition experiments suggested that VEGF was a potent regulator of leptin, but that leptin was not a potent regulator of VEGF. Co-culture per se altered the release of VEGF and leptin and enhanced the effects of estradiol, compared with monocultures of the included cell types. In conclusion, the results presented in this thesis will increase the overall understanding of the role of estrogens in breast cancer, which may be useful in future treatment studies

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Correlation between estrogens and serum adipocytokines in premenopausal and postmenopausal women

Abstract: Estrogen deficiency resulted in increased TNF-alpha levels. Serum leptin levels correlated positively with estrogen levels in premenopausal women. However, the increase in obesity in postmenopausal women increased leptin, which increases insulin resistance.

Cited by 83 publications

References 41 publications

The role of sex steroids in white adipose tissue adipocyte function

The role of sex steroids in white adipose tissue adipocyte function

Opposite effects of 17-β estradiol and testosterone on mitochondrial biogenesis and adiponectin synthesis in white adipocytes

Hormonal regulation of immune modulators in human breast tissue

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