This study was conducted to evaluate body weight and composition during oral contraception with 30 microg ethinylestradiol plus 3 mg drospirenone (30EE+DRSP) in women affected by premenstrual syndrome (PMS) with somatic symptoms related to water retention.
This prospective study was performed using multifrequency bioelectrical impedance analysis in 18 normally cycling PMS patients (mean age, 28.8 years) evaluated at baseline, during the luteal phase of the menstrual cycle and after 3 and 6 cycles of 30EE+DRSP. Total body water (TBW), intracellular water (ICW), extracellular water (ECW), fat mass and fat-free mass were evaluated. Body weight, waist-to-hip ratio and blood pressure were also determined at each visit. Basal values were compared with those measured in 31 healthy females without PMS (controls).
PMS patients have higher levels of TBW and ICW than controls. After 6 months of 30EE+DRSP, TBW and ECW were significantly lower than before treatment. No significant variations in ICW or in the other parameters were observed.
In women with PMS, 30EE+DRSP reduces the concentrations in TBW and ECW. This effect is likely due to the antimineralocorticoid activity of DRSP. Whether these changes may account for the improvement of premenstrual fluid-related symptoms reported with this formulation is discussed.
"When chronic exposition occurs, it has been proposed that BPA interferes with fluid transport through the paracellular pathway, an important function of the colon that participates, together with the renal system, in the whole body fluid homeostasis and also maintains mucosal hydration (Masyuk et al. 2002; Geibel 2005). A permanent decrease in paracellular permeability induced by BPA may contribute to body fluid retention, a disorder commonly observed in high estrogenic states, as experienced by oral contraceptive users or in postmenopausal women with hormone replacement therapy (Oelkers 1996; Fruzzetti et al. 2007). In tissues such as the colon, where ERb is the predominantly expressed ER, a potent tissue response to low doses of BPA may be related to a better coupling of ERb with its coactivators (SRC-1e, TIF2 and TRAP220) in the presence of xenoestrogens, leading to transcriptional activity on reporter genes estimated to be 500 times greater for the BPA-ERb complex, in comparison to a binding to ERa (Routledge et al. 2000; Welshons et al. 2006; Swedenborg et al. 2009). "
[Show abstract][Hide abstract] ABSTRACT: From animal studies, a consensus exists that the synthetic estrogen bisphenol A (BPA), a plastic monomer widely used in the
food-packaging industry, is able to disrupt endocrine signalling pathways during development, with persisting effects later
in life. Although the fetal and then the adult gut expresses functional estrogen receptors (ERs), the endocrine impact of
BPA on the intestinal barrier function remains largely unexplored. The intestinal epithelium and mucosal immune cells provide
a first line of defence designed to restrict the passage of harmful substances from the lumen. Intestinal permeability is
high at birth, permitting lumen-to-mucosa exchanges involved in the maturation process of the gut immune system. As a barrier
to the external environment, gut epithelium is renewed constantly during life. Renewal of gut epithelial cells occurs in less
than ~96h, starting from fetal stage, and is dependent on controlled cell stimulation and proliferation by various signalling
pathways. Lessons learned from ER-deficient mice underline the importance of estrogen signalling in growth, organization and
maintenance of a normal epithelial barrier. In rats, BPA was recently shown to interact with ERs in the adult gut by mimicking
the estradiol-mediated decrease of epithelial permeability through genomic pathways. This effect also occurs in neonates when
low doses of BPA (5μg/kg BW/day: tenfold below the tolerable daily intake for humans) are orally administered to pregnant
and then lactating rats. A perinatal exposure to BPA also reduces epithelial cell proliferation in the colon of neonates,
while the overall decrease of intestinal permeability remains apparent in adulthood only in female offspring. As a consequence,
adult females perinatally exposed to BPA have been shown to develop severe inflammatory responses in a rat model of inflammatory
bowel disease, demonstrating enhanced expression and production of T-Helper 1 cytokines in inflamed areas. In mice, a mother-to-infant
transport of maternal BPA is consistent with the ability of the chemical to reach the fetus through the placental barrier:
BPA is present in the amniotic fluid and accumulates in the maturing gut. Although BPA, once absorbed by maternal gut, is
rapidly deactivated by first pass conjugation in the liver, recent studies emphasize that BPA at low, environmentally relevant
levels can transfer across the human placenta, mainly in an estrogen-active, unconjugated form. It is now thought that BPA
ingested by dams has repercussions on the education of the immune system by reducing intestinal permeability from fetal stages
and promotes severe inflammatory response later in life.
"lso found to be oestrous cycle - dependent ( O ' Mahony & Harvey , 2008 ) . These authors postulated that the anti - secretory effect of oestradiol may enhance salt and water retention in females , as commonly observed in oral contraceptive users with high oestrogen dosage , or during natural periods of elevated plasma oestrogen ( Oelkers , 1996 ; Fruzzetti et al . 2007 ) . Because water molecules can be driven passively by paracellular flux additional to the transcellular pathway ( Masyuk et al . 2002 ) , our data support the"
[Show abstract][Hide abstract] ABSTRACT: Oestradiol modulates paracellular permeability and tight junction (TJ) function in endothelia and reproductive tissues, but whether the ovarian hormones and cycle affect the paracellular pathway in the intestinal epithelium remains unclear. Oestrogen receptors (ERs) are expressed in intestinal epithelial cells, and oestradiol regulates epithelium formation. We examined the effects of oestrous cycle stage, oestradiol benzoate (EB), and progesterone (P) on colonic paracellular permeability (CPP) in the female rat, and whether EB affects expression of the TJ proteins in the rat colon and the human colon cell line Caco-2. In cyclic rats, CPP was determined through lumen-to-blood (51)Cr-labelled EDTA clearance, and in Ussing chambers for dextran permeability. CPP was also examined in ovariectomized (OVX) rats treated with P or EB, with and without the ER antagonist ICI 182,780, or with the selective agonists for ER beta (propyl pyrazole triol; PPT) or ER beta (diarylpropionitrile; DPN). In oestrus rats, CPP was reduced (P < 0.01) relative to dioestrus. In OVX rats, EB dose-dependently decreased CPP, an effect mimicked by DPN and blocked by ICI 182,780, whereas P had no effect. Oestradiol increased occludin mRNA and protein in the colon (P < 0.05), but not zona occludens (ZO)-1. Further, EB and DPN enhanced occludin and junctional adhesion molecule (JAM)-A expression in Caco-2 cells without change in ZO-1, an effect blocked by ICI 182,780. These data show that oestrogen reinforces intestinal epithelial barrier through ER beta-mediated up-regulation of the transmembrane proteins occludin and JAM-A determining paracellular spaces. These findings highlight the importance of the ER beta pathway in the control of colonic paracellular transport and mucosal homeostasis.
The Journal of Physiology 05/2009; 587(Pt 13):3317-28. DOI:10.1113/jphysiol.2009.169300 · 5.04 Impact Factor
"The research on the impact of oral contraceptives on water retention and body weight during the menstrual cycle is mixed. Fruzzetti et al. (2007) administered an oral contraceptive (OC) containing ethinylestradiol and drospirenone (DRSP) to eighteen women with premenstrual syndrome (PMS). Thirty women not experiencing PMS were used as the control group. "
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.