Comparison of oral estrogens and estrogens plus androgen on bone mineral density, menopausal symptoms, and lipid-lipoprotein profiles in surgical menopause

Nb, Watts; Notelovitz, Morris; Mc, Timmons; Wa, Addison; Wiita, Brinda; Lj, Downey

doi:10.1016/0029-7844(94)00448-m

Cited by 251 publications

(98 citation statements)

References 33 publications

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“…Experimental data suggest direct effects of testosterone on body composition, lipid levels and glucose metabolism. We postulate that increased androgenicity contributes to the accumulation of visceral fat and impairment of glucose metabolism, creating a vicious circle, whereby the increase in insulin and fat tissue in turn promote the production of 123 Surgical T Transdermal (patch) 300 mg per day 24 weeksBraunstein et al 124 Surgical T Transdermal (patch) 150/300/450 mg per day 24 weeksSimon et al 125 Surgical T Transdermal (patch) 300 mg per day 24 weeksDavis et al 126 Surgical T Transdermal (patch) 300 mg per day 24 weeksShifren et al 120 Natural T Transdermal (patch) 300 mg per day 24 weeksNathorst-Boost et al 127 Natural T Transdermal (gel) 10 mg per day 3 monthsBurger et al 128 Natural/surgical T Implant 50 mg Â 1 6 weeks -Davis et al 122 Natural/surgical T Implant 50 mg per 3 months 24 months k fat mass Farish et al 129 Surgical T Implant 100 mg Â 1 6 monthsHickok et al 130 -MT Oral 1.25 mg per day 6 months k HDL-C Watts et al 131 Surgical MT Oral 2.5 mg per day 24 months k HDL-C, triglycerides Basaria et al 132 Natural/surgical MT Oral 2.5 mg per day 16 weeks k HDL-C, triglycerides m fibrinogen Dobs et al 133 Natural/surgical MT Oral 2.5 mg per day 16 weeks k HDL-C, triglycerides, fat mass Lobo et al 134 Natural/surgical MT Oral 1.25 mg per day 16 weeks k HDL-C, triglycerides Warnock et al 135 Surgical MT Oral 1.25 mg per day 8 weeks k HDL-C, triglycerides Leao et al 136 Surgical MT Oral 1.25 mg per day 12 months k HDL-C m visceral fat mass Barrett-Connor et al 137 Surgical MT Oral 1.25 mg per day 24 months k HDL-C, triglycerides Raisz et al 138 Natural/surgical MT Oral 2.5 mg per day 9 weeks k HDL-C, triglycerides Penotti et al 139 Natural TU Oral 40 mg per day 8 months k HDL-C, m pulsatile index (PI)…”

Section: Discussionmentioning

confidence: 99%

Testosterone, SHBG and cardiovascular health in postmenopausal women

Brand

Schouw

2010

Int J Impot Res

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Cardiovascular disease (CVD) affects men and women differently with women having a lower incidence and later onset of disease. Research has recently refocused interest on the cardiovascular role of androgens. The purpose of this review is to summarize the evidence available on the association between testosterone and cardiovascular health in postmenopausal women. Published studies relating testosterone and sex hormone-binding globulin (SHBG) to CVD and its risk factors were reviewed. Studies included in this review suggest that increased androgenicity, characterized by high testosterone and low SHBG levels, is associated with an adverse CVD risk factor profile in postmenopausal women. However, evidence for an association with cardiovascular events is lacking and it is uncertain whether the observed associations with endogenous testosterone have clinical implications regarding the use of postmenopausal testosterone therapy. Large-scale, longitudinal studies relating testosterone and SHBG levels to cardiovascular risk factors and endpoints are needed to determine the temporal relationship between androgenicity and cardiovascular risk and to ascertain the long-term efficacy and safety of testosterone therapy in postmenopausal women.

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Section: Discussionmentioning

confidence: 99%

Testosterone, SHBG and cardiovascular health in postmenopausal women

Brand

Schouw

2010

Int J Impot Res

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“…Nevertheless, we have observed distinct and stage-specific expression profiles for the sex steroid receptors, so that, at least at the level of regulation of expression, differences between the receptors exists. Thus, complex regulation in osteoblasts at distinct stages of differentiation may partially underlie the improved outcome of patients receiving both estrogen and androgen hormones (Watts et al 1995, Raisz et al 1996, Barrett-Connor 1998. Increased understanding of sex steroid receptor regulation may also aid in the understanding of the pathogenesis of age-related bone loss in both males and females.…”

Section: Figurementioning

confidence: 99%

“…dihydrotestosterone) is effective at ameliorating this loss. Interestingly, recent evidence suggests that combination therapy with both estrogen and androgenic steroids is more effective than estrogen replacement in women (Watts et al 1995, Raisz et al 1996, Rosenberg et al 1997, Barrett-Connor 1998. In ovariectomized animals, replacement with nonaromatizable androgens yields beneficial effects that are clearly distinct from those observed with estrogen replacement (Coxam et al 1996).…”

Section: Introductionmentioning

confidence: 99%

Osteoblast differentiation influences androgen and estrogen receptor-alpha and -beta expression

Wiren

Evans²,

Xw³

2002

Journal of Endocrinology

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Significant levels of estrogen and androgens circulate in men and women, and both play an important role in bone metabolism. While it is well established that either estrogen or androgen replacement therapy is effective at ameliorating bone loss associated with hypogonadism, recent evidence nevertheless suggests that estrogen and androgens have distinct molecular actions on the skeleton. In this study, we have employed normal rat calvarial osteoblast cultures to characterize relative expression profiles of estrogen (ER and ER ) and androgen receptors (AR) during osteoblast differentiation. Normal osteoblast cultures can proceed through in vitro differentiation with distinct stages of proliferation, matrix maturation and mineralization in the appropriate differentiation medium containing ascorbic acid. Expression profiles of AR, ER and ER in primary cultures during osteoblast differentiation were characterized both by semi-quantitative relative RT-PCR and by Western analysis. In cultures induced to differentiate by growth in the presence of ascorbic acid, the expression profile for each receptor was unique during the course of differentiation. ER levels were elevated during matrix maturation and then declined during mineralization. ER expression was relatively constant throughout differentiation, exhibiting more constitutive expression. In contrast, AR levels were lowest during proliferation, and then increased throughout differentiation with highest levels in the most mature mineralizing cultures. Since steroid hormone action is generally mediated by specific cognate receptors, these results suggest that androgen actions may target cells during the mineralization stage of osteoblast differentiation, while estrogen action through either receptor isoform is more likely to affect osteoblasts earlier during matrix maturation. Interestingly, sex steroid receptor expression profiles did not exhibit the same patterns of regulation if osteoblast cultures were grown without ascorbic acid in medium that did not support extracellular matrix deposition. Thus, sex steroids may distinctly influence skeletal health by differential modulation of function during osteoblast differentiation.

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“…Although women produce less androgen hormone than men and metabolize a higher proportion of their androgen to oestrogen, direct androgen activity mediated via the AR influences development of the female phenotype and is important for the healthy functioning of multiple organs in women, including the ovaries (Lebbe & Woodruff 2013, O'Reilly et al 2014, Sen et al 2014, uterus (Wood et al 2009, Cloke & Christian 2012, bone (Watts et al 1995), muscle (Smith et al 2014), adipose tissue (Barbosa-Desongles et al 2013, Chazenbalk et al 2013, and brain (Shifren 2002, Lobo et al 2003, Ryan et al 2009, Zarrouf et al 2009). However, less is known about the mechanisms of AR signalling in female tissues compared with either AR signalling in male target tissues (e.g.…”

Section: Introductionmentioning

confidence: 99%

Bringing androgens up a NOTCH in breast cancer

Tarulli

Butler

Tilley

et al. 2014

Endocrine-Related Cancer

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While it has been known for decades that androgen hormones influence normal breast development and breast carcinogenesis, the underlying mechanisms have only been recently elucidated. To date, most studies have focused on androgen action in breast cancer cell lines, yet these studies represent artificial systems that often do not faithfully replicate/ recapitulate the cellular, molecular and hormonal environments of breast tumours in vivo. It is critical to have a better understanding of how androgens act in the normal mammary gland as well as in in vivo systems that maintain a relevant tumour microenvironment to gain insights into the role of androgens in the modulation of breast cancer development. This in turn will facilitate application of androgen-modulation therapy in breast cancer. This is particularly relevant as current clinical trials focus on inhibiting androgen action as breast cancer therapy but, depending on the steroid receptor profile of the tumour, certain individuals may be better served by selectively stimulating androgen action. Androgen receptor (AR) protein is primarily expressed by the hormone-sensing compartment of normal breast epithelium, commonly referred to as oestrogen receptor alpha (ERa (ESR1))-positive breast epithelial cells, which also express progesterone receptors (PRs) and prolactin receptors and exert powerful developmental influences on adjacent breast epithelial cells. Recent lineage-tracing studies, particularly those focussed on NOTCH signalling, and genetic analysis of cancer risk in the normal breast highlight how signalling via the hormone-sensing compartment can influence normal breast development and breast cancer susceptibility. This provides an impetus to focus on the relationship between androgens, AR and NOTCH signalling and the crosstalk between ERa and PR signalling in the hormone-sensing component of breast epithelium in order to unravel the mechanisms behind the ability of androgens to modulate breast cancer initiation and growth.

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Comparison of oral estrogens and estrogens plus androgen on bone mineral density, menopausal symptoms, and lipid-lipoprotein profiles in surgical menopause

Abstract: Oral estrogen-androgen increased vertebral bone mineral density compared with pre-treatment values and relieved somatic symptoms. Safety indices, including lipoprotein levels, indicated that the combination was well tolerated over the 2 years of treatment.

Cited by 251 publications

References 33 publications

Testosterone, SHBG and cardiovascular health in postmenopausal women

Testosterone, SHBG and cardiovascular health in postmenopausal women

Osteoblast differentiation influences androgen and estrogen receptor-alpha and -beta expression

Bringing androgens up a NOTCH in breast cancer

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