Hormones In Rodents Research Articles

Role of estrogen in sex differences in memory, emotion and neuropsychiatric disorders.

Estrogen regulates a wide range of neuronal functions in the brain, such as dendritic spine formation, remodeling of synaptic plasticity, cognition, neurotransmission, and neurodevelopment. Estrogen interacts with intracellular estrogen receptors (ERs) and membrane-bound ERs to produce its effect via genomic and non-genomic pathways. Any alterations in these pathways affect the number, size, and shape of dendritic spines in neurons associated with psychiatric diseases. Increasing evidence suggests that estrogen fluctuation causes changes in dendritic spine density, morphology, and synapse numbers of excitatory and inhibitory neurons differently in males and females. In this review, we discuss the role of estrogen hormone in rodents and humans based on sex differences. First, we explain estrogen role in learning and memory and show that a high estrogen level alleviates the deficits in learning and memory. Secondly, we point out that estrogen produces a striking difference in emotional memories in men and women, which leads them to display sex-specific differences in underlying neuronal signaling. Lastly, we discuss that fluctuations in estrogen levels in men and women are related to neuropsychiatric disorders, including schizophrenia, autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), bipolar disorder (BPD), major depressive disorder (MDD), substance use disorder (SUD), and anxiety disorders.

Adiponectin affects ileal contractility of mouse preparations.

Adiponectin (ADPN) has been reported to induce inhibitory effects on gastric motor activity, which, being a source of peripheral satiety signals, would contribute to the central anorexigenic effects of the hormone in rodents. However, peripheral satiety signals can also originate from the small intestine. Since there are no data on the effects of ADPN in this gut region, the present study aimed to investigate whether ADPN affects murine ileal contractility. Immunofluorescence experiments and Western blot were also performed to reveal the expression of ADPN receptors. Mechanical responses of ileal preparations were recorded in vitro via force-displacement transducers. Preparations showed a tetrodotoxin- and atropine-insensitive spontaneous contractile activity. Electrical field stimulation (EFS) induced tetrodotoxin- and atropine-sensitive contractile responses. ADPN induced a decay of the basal tension and decreased the amplitude of either the spontaneous contractility or the EFS-induced excitatory responses. All ADPN effects were abolished by the nitric oxide (NO) synthesis inhibitor NG-nitro l-arginine. The expression of the ADPN receptor, AdipoR1, but not AdipoR2, was also revealed in enteric glial cells. The present results offer the first evidence that ADPN acts on ileal preparations. The hormone exerts inhibitory effects, likely involving AdipoR1 on enteric glial cells and NO. From a physiological point of view, it could be hypothesized that the depressant action of ADPN on ileal contractility represents an additional peripheral satiety signal which, as also described for the ileal brake, could contribute to the central anorexigenic effects of the hormone.NEW & NOTEWORTHY This study provides the first evidence that adiponectin (ADPN) is able to act on ileal preparations. Functional results demonstrate that the hormone, other than causing a slight decay of the basal tension, depresses the amplitude of both spontaneous contractility and neurally induced excitatory responses of the mouse ileum through the involvement of nitric oxide. The expression of the ADPN receptor AdipoR1 and its localization on glial cells was revealed by Western blot and immunofluorescence analysis.

SHORT-TERM EFFECT OF Naja naja SHED SKIN EXTRACT ON HISTOPATHOLOGY OF TESTIS, EPIDIDYMIS AND VAS DEFERENS OF SWISS ALBINO MICE

Ancient literature reveals that snake shed skin had been frequently used to treat several diseases like glaucoma, hernia, psoriasis, hemorrhoids, etc. Previously, it was reported that Naja naja shed skin extract causes temporary cessation of the estrous cycle and altered female reproductive hormones in rodents, and the probable bioactive molecule behind such alterations was also identified. Based on this information, the present study was designed to establish the effect of Naja naja shed skin extract on the male reproductive system of Swiss albino mice. The extract was prepared with physiological saline and was injected intraperitoneally in the male mice for 7 consecutive days @ 10 mg kg-1 body weight. The short-term histopathological studies were performed by Haematoxylin and Eosin staining and the sperm morphology was analyzed by using bright-field microscopy. The snake skin extract markedly changed the gross histological architecture of the seminiferous tubules including disorganization of germinal epithelial cells, accumulation of exfoliated cells in the lumen, tailless sperm in the epididymis, disorganized basal cells in vas deferens as well as marked alteration of sperm morphology. The present work with snake shed skin strongly indicates that it is not simply a biological waste, but it might be a treasure house of many bioactive compounds.

A review of the effects of acute and chronic cannabinoid exposure on the stress response

While cannabis has been used for centuries for its stress-alleviating properties, the effects of acute and chronic cannabinoid exposure on responses to stress remain poorly understood. This review provides an overview of studies that measured stress-related endpoints following acute or chronic cannabinoid exposure in humans and animals. Acute cannabinoid exposure increases basal concentrations of stress hormones in rodents and humans and has dose-dependent effects on stress reactivity in humans and anxiety-like behavior in rodents. Chronic cannabis exposure is associated with dampened stress reactivity, a blunted cortisol awakening response (CAR), and flattened diurnal cortisol slope in humans. Sex differences in these effects remain underexamined, with limited evidence for sex differences in effects of cannabinoids on stress reactivity in rodents. Future research is needed to better understand sex differences in the effects of cannabis on the stress response, as well as downstream impacts on mental health and stress-related disorders.

Direct and Indirect Measurements of Sex Hormones in Rodents During Fear Conditioning.

Fear conditioning (FC) is a widely accepted tool for the assessment of learning and memory processes in rodents related to normal and dysregulated acquired fear. The study of sex differences in fear learning and memory is vast and currently increasing. Sex hormones have proven to be crucial for fear memory formation in males and females, and several methods have been developed to assess this hormonal state in rats and mice. Herein, we explain a routine FC and extinction protocol, together with the evaluation of sex hormonal state in male and female rodents. We explain three protocols for the evaluation of this hormonal state directly from blood samples extracted during the procedure or indirectly through histological verification of the estrous cycle for females or behavioral assessment of social hierarchies in males. Although females have typically been considered to present great variability in sex hormones, it is highlighted that sex hormone assessment in males is as variable as in females and equally important for fear memory formation. The readout of these protocols has had a great impact on different fields of fear learning and memory study and appears essential when studying FC. The proven interaction with drugs involved in the modulation of these processes makes sex hormone assessment during FC a valuable tool for the development of effective treatments for fear-related disorders in men and women. © 2021 Wiley Periodicals LLC. Basic Protocol 1: Fear conditioning and fear extinction Basic Protocol 2: Blood collection for direct measurement of sex hormone levels in fear conditioning Basic Protocol 3: Indirect measurement of sex hormones in females during fear conditioning Basic Protocol 4: Assessment of dominance status in males before a fear conditioning protocol Support Protocol: Construction of a confrontation tube.

Do corticosterone levels predict female depressive-like behavior in rodents?

Dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis is often linked to the neurobiology of depression, though the presence and type of this dysregulation is not a consistent finding. Meanwhile, significant sex differences exist regarding depression and the HPA axis. Animal models of depression simulate certain aspects of the human disease and aim to advance our knowledge regarding its neurobiology and discover new antidepressant treatments. Most animal models of depression induce a depressive-like phenotype taking advantage of stressful experimental conditions, that also increase corticosterone, the main stress hormone in rodents. In this review we present inconsistent results in male and female rodents regarding the interaction between the depressive-like behavioral phenotype and corticosterone. In commonly used models, the female depressive-like phenotype in rodents seems significantly less dependent on the stress hormone corticosterone, whereas the male behavioral response is more evident and associates with variations of corticosterone. Further research and clarification of this sex-dependent interaction will have significant ramifications on the improvement of the validity of animal models of depression.

Elevated Corticosterone Level Due To Chronic Stress on Hb-Egf Expression as a Marker of Endometrial Receptivity Disorder in Rattus norvegicus

Endometrial receptivity is a physiological state in which the endometrium obtains an adhesive phenotype that allows embryo implantation and have a role in the problem of implantation failure. Endometrial receptivity disorders can be caused by interference with the Hypothalamus-Pituitary-Gonad (HPG) axis due to the activation of the Hypothalamus-Pituitary-Adrenal (HPA) axis by stress. HB-EGF is a biomarker of endometrial receptivity that plays a role in the decidualization of endometrial stromal cells to reach the receptive state and initiation of implantation. Corticosterone is the dominant glucocorticoid hormone in rodents, as is cortisol in humans. High corticosterone due to chronic stress triggers disruption of homeostasis in the endometrium by resulting in decreased levels of HB-EGF. This study aims to find out the effect of increased corticosterone levels due to chronic stress on HB-EGF expression in endometrium Rattus norvegicus. This research has obtained ethical eligibility from the Research Ethics Commission of the Faculty of Medicine Airlangga University. The samples on this study were 34 rat (Rattus norvegicus) which were divided into 2 groups, the control group and the stress treatment group using the Chronic Unpredictable Mild Stress (CUMS) method. Corticosterone level were obtain from blood serum detected via ELISA and HB EGF expression was obtained from endometrial in diestrus phase was evaluated by immunohistochemical methods. Corticosterone levels in the stress treatment group were higher (72.84 ± 64.03) than in the control group (23.29 ± 8.42). HB-EGF expression in the stress treatment group was lower (82.06 ± 5.91) than in the control group (118.76 ± 13.20). Statistical tests showed significant differences in HB-EGF expression in endometrium Rattus norvegicus p = 0,000 (p <0.05). Elevated level of corticosterone can decrease HB-EGF expression in endometrium Rattus norvegicus.

A Neurodevelopmental Model of Combined Pyrethroid and Chronic Stress Exposure.

Attention-deficit hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders of childhood and previous studies indicate the dopamine system plays a major role in ADHD pathogenesis. Two environmental exposures independently associated with dopaminergic dysfunction and ADHD risk include exposure to deltamethrin, a pyrethroid insecticide, and chronic stress. We hypothesized that combined neurodevelopmental exposure to both deltamethrin and corticosterone (CORT), the major stress hormone in rodents, would result in additive changes within the dopamine system. To study this, we developed a novel dual exposure paradigm and exposed pregnant C57BL/6 dams to 3 mg/kg deltamethrin through gestation and weaning, and their offspring to 25 μg/mL CORT dissolved in the drinking water through adulthood. Midbrain RNA expression as well as striatal and cortical protein expression of key dopaminergic components were investigated, in addition to ADHD-like behavioral tasks and electrochemical dopamine dynamics via fast-scan cyclic voltammetry. Given the well-described sexual dimorphism of ADHD, males and females were assessed separately. Males exposed to deltamethrin had significantly decreased midbrain Pitx3 expression, decreased cortical tyrosine hydroxylase (TH) expression, increased activity in the Y maze, and increased dopamine uptake rate in the dorsal striatum. These effects did not occur in males exposed to CORT only, or in males exposed to both deltamethrin and CORT, suggesting that CORT may attenuate these effects. Additionally, deltamethrin- and CORT-exposed females did not display these dopaminergic features, which indicates these changes are sex-specific. Our results show dopaminergic changes from the RNA through the functional level. Moreover, these data illustrate the importance of testing multiple environmental exposures together to better understand how combined exposures that occur in certain vulnerable populations could affect similar neurodevelopmental systems, as well as the importance of studying sex differences of these alterations.

Transcriptome profiles of corticosterone-induced cytotoxicity reveals the involvement of neurite growth-related genes in depression

Corticosterone (CORT), the main HPA-axis glucocorticoid hormone in rodents, is involved in the regulation of animal stress responses. However, the neural mechanisms underlying the effects of corticosteroids on depression are yet to be elucidated. We found that fluoxetine reversed neurite growth inhibition induced by CORT in PC12 cells, a widely used model system for neurobiological and neurotoxicological studies. Transcriptome profiling showed that 1,609 genes were up-regulated, whereas 1,764 genes were down-regulated significantly in the CORT group in comparison with the Control group. Of them, the expression of 589 DEGs was reversed after fluoxetine treatment, and genes related to cell morphogenesis, neurite growth, and immune function were involved in the neuroprotective effect of fluoxetine against CORT. Furthermore, expression of neurite growth-related genes, such as such as Calpain 2 (Capn2), vesicle-associated membrane protein 7 (Vamp7) and C-type natriuretic peptide (Cnp), altered in a brain region- or treatment-specific manner in the animal models of depression. Therefore, the interaction between stress, glucocorticoids, and neurite growth inhibition may be a candidate pathophysiology underlying major depressive disorder (MDD), and the identification of Capn2, Vamp7 and Cnp might provide insight into treatment of MDD.

Chronic mild corticosterone exposure during adolescence enhances behaviors and upregulates neuroplasticity-related proteins in rat hippocampus

Adolescence is a critical period with ongoing maturational processes in stress-sensitive systems. It remains unknown how adolescent individuals would be affected by chronic exposure to corticosterone (the major stress hormone in rodents, CORT) at the doses that are usually not detrimental in adults. In this study, male Sprague-Dawley rats were injected with CORT (5 mg/kg) or vehicle for 21 days during adolescence (postnatal day (PND) 29–49) or adulthood (PND 71–91) and then subjected to behavioral testing or sacrifice for neurobiological analyses. Shortly after treatment cessation, different from CORT-treated adults showing increased anxiety-like behaviors, CORT-treated adolescents exhibited enhanced prepulse inhibition and spatial learning. They also showed increased expression of hippocampal neuroplasticity-related proteins, including BDNF, nectin3, and AMPA receptor subunits. These effects became undetectable after a four-week washout period when CORT-treated adolescents exhibited improved reversal learning. Together, these findings demonstrate that chronic CORT exposure at the dose of 5 mg/kg endows adolescent individuals with enhanced cognitive capacities, possibly supported by increased hippocampal neuroplasticity. This study also highlights mild elevation of CORT levels during adolescence as a potential approach of promoting adaptive behaviors.

Measuring corticosterone concentrations over a physiological dynamic range in female rats

Accurate assessment of plasma corticosterone, the primary stress hormone in rodents, is an essential part of characterizing the stress response in experimental animals. To this end, both enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA) remain widely used. However, considerable assay-specific variability exists among commercially available corticosterone assays due to differing assay principles, detection methods, range, and sensitivity. While technical comparisons of commercially available corticosterone assays have previously been conducted, the ability to detect acute stress-induced endocrine changes has not been compared among these methods to date. Using the forced swim test, a commonly utilized behavioral paradigm in rodents as a physiologically-relevant acute stress challenge, we compared four commercial corticosterone assays – three ELISA kits and one RIA kit – in their ability to detect corticosterone across a dynamic range of both baseline and acute swim stress-driven concentrations. While all methods yielded results that were consistent at measuring relative differences between samples, only two of the four assays evaluated detected a statistically significant increase in corticosterone in rats exposed to acute swim stress compared to rats at baseline. The ELISA kit from Enzo Life Sciences demonstrated the greatest percent increase in plasma corticosterone from baseline to acute stress conditions. The RIA kit from MP Biomedicals also detected a significant corticosterone increase and yielded higher concentrations of corticosterone both at baseline and in the acute stress condition relative to the other three assays. We conclude that choice of assay can impact interpretation of data due to differences in efficacy across a dynamic range of physiological concentrations of corticosterone.

Control of (pre)-analytical aspects in immunoassay measurements of metabolic hormones in rodents.

The measurement of circulating hormones by immunoassay remains a cornerstone in preclinical endocrine research. For scientists conducting and interpreting immunoassay measurements of rodent samples, the paramount aim usually is to obtain reliable and meaningful measurement data in order to draw conclusions on biological processes. However, the biological variability between samples is not the only variable affecting the readout of an immunoassay measurement and a considerable amount of unwanted or unintended variability can be quickly introduced during the pre-analytical and analytical phase. This review aims to increase the awareness for the factors ‘pre-analytical’ and ‘analytical’ variability particularly in the context of immunoassay measurement of circulating metabolic hormones in rodent samples. In addition, guidance is provided how to gain control over these variables and how to avoid common pitfalls associated with sample collection, processing, storage and measurement. Furthermore, recommendations are given on how to perform a basic validation of novel single and multiplex immunoassays for the measurement of metabolic hormones in rodents. Finally, practical examples from immunoassay measurements of plasma insulin in mice address the factors ‘sampling site and inhalation anesthesia’ as frequent sources of introducing an unwanted variability during the pre-analytical phase. The knowledge about the influence of both types of variability on the immunoassay measurement of circulating hormones as well as strategies to control these variables are crucial, on the one hand, for planning and realization of metabolic rodent studies and, on the other hand, for the generation and interpretation of meaningful immunoassay data from rodent samples.

Docosahexaenoic acid (DHA) prevents corticosterone-induced changes in astrocyte morphology and function.

The many functions of astrocytes, such as glutamate recycling and morphological plasticity, enable them to stabilize synapses environment and protect neurons. Little is known about how they adapt to glucocorticoid-induced stress, and even less about the influence of dietary factors. We previously showed that omega-3 polyunsaturated fatty acids (ω3PUFA), dietary fats which alleviate stress responses, influence the way astroglia regulate glutamatergic synapses. We have explored the role of docosahexaenoic acid (DHA), the main ω3PUFA, in the astroglial responses to corticosterone, the main stress hormone in rodents to determine whether ω3PUFA help astrocytes resist stress. Cultured rat astrocytes were enriched in DHA or arachidonic acid (AA, the main ω6PUFA) and given 100nM corticosterone for several days. Corticosterone stimulated astrocyte glutamate recycling by increasing glutamate uptake and glutamine synthetase (GS), and altered the astrocyte cytoskeleton. DHA-enriched astrocytes no longer responded to the action of corticosterone on glutamate uptake, had decreased GS, and the cytoskeletal effect of corticosterone was delayed, while AA-enriched cells were unaffected. The DHA-dependent anti-corticosterone effect was related to fewer glucocorticoid receptors, while corticosterone increased DHA incorporation into astrocyte membranes. Thus, DHA helps astrocytes resist the influence of corticosterone, so perhaps promoting a sustainable response by the stressed brain. We show that corticosterone increases the glutamate recycling capacity of rat cortical astrocytes in culture, and alters their morphology, which may be detrimental in the long term. Increasing the membrane incorporation of docosahexaenoic acid (DHA), the main omega-3 in brain, reduces the amount of glucocorticoid receptors (GR) and prevents the effects of corticosterone. This may help the astrocytes maintain a functional phenotype in chronic stress situations.

Effectiveness of different corticosterone administration methods to elevate corticosterone serum levels, induce depressive-like behavior, and affect neurogenesis levels in female rats

High levels of chronic stress or stress hormones are associated with depressive-like behavior in animal models. However, slight elevations in corticosterone (CORT) – the major stress hormone in rodents – have also been associated with improved performances, albeit in a sex-dependent manner. Some of the discrepancies in the literature regarding the effects of high CORT levels may be due to different administrations methods. The current study aims to compare the effects of ∼40mg/kg given either via subcutaneous injection, through an implanted pellet, or in the drinking water, for ∼21days on CORT serum levels, depressive-like behavior in the forced swim test (FST), and neurogenesis levels in the dentate gyrus (DG) in adult female rats. We found that animals exposed to the daily injections showed elevated CORT levels throughout the administration period, while the pellet animals showed only a transient increase, and drinking water animals revealed no elevation in CORT in serum. In addition, only the injection group exhibited higher levels of immobility in the FST. Interestingly, animals receiving CORT via injection or drinking water had lower numbers of doublecortin-positive cells in the ventral DG one week after the last CORT administration compared to animals implanted with a CORT pellet. These results will contribute to the growing literature on the effects of chronic CORT exposure and may help to clarify some of the discrepancies among previous studies, particularly in females.

Molecular Mechanisms of Action of BPA.

Bisphenol A (BPA) exposure has been associated with serious endocrine-disrupting effects in humans and wildlife. Toxicological and epidemiological studies evidenced that BPA increases body mass index and disrupts normal cardiovascular physiology by interfering with endogenous hormones in rodents, nonhuman primates, and cell culture test systems. The BPA concentration derived from these experiments were used by government regulatory agencies to determine the safe exposure levels of BPA in humans. However, accumulating literature in vivo and in vitro indicate that at concentrations lower than that reported in toxicological studies, BPA could elicit a different endocrine-disrupting capacity. To further complicate this picture, BPA effects rely on several and diverse mechanisms that converge upon endocrine and reproductive systems. If all or just few of these mechanisms concur to the endocrine-disrupting potential of low doses of BPA is at present still unclear. Thus, taking into account that the incidence and/or prevalence of health problems associated with endocrine disruption have increased worldwide, the goal of the present review is to give an overview of the many mechanisms of BPA action in order to decipher whether different mechanisms are at the root of the effect of low dose of BPA on endocrine system.

Production of corticosteroid hormones in vitro by adrenals in rats with streptozotocin-induced diabetes.

We studied baseline and ACTH-stimulated in vitro production of corticosteroids by rat adrenals. Production of the basic corticosteroids pregnenolone (early precursor in corticosteroid synthesis), progesterone (intermediate precursor in synthesis of gluco- and mineralocorticoid hormones), and corticosterone (major glucocorticoid hormone in rodents) in animals with streptozotocin-induced diabetes was enhanced by 1.8-2.0 times in comparison with the control animals. Addition of ACTH to the incubation medium stimulated pregnenolone production by the adrenals equally in the control and experimental (diabetic) groups, while the increase in corticosterone production was less pronounced in the experimental group. Stimulation of corticosterone production in response to ACTH after saturation of the incubation medium with pregnenolone was also less pronounced in diabetic rats.

Inhibitory effects of forced swim stress and corticosterone on the acquisition but not expression of morphine-induced conditioned place preference: Involvement of glucocorticoid receptor in the basolateral amygdala

Addiction is a common chronic psychiatric disease which represents a global problem and stress has an important role to increase drug addiction and relapse. In the present study, we investigated the effects of physical stress and exogenous corticosterone on the acquisition and expression of morphine-induced conditioned place preference (CPP). Also, we tried to find out the role of glucocorticoid receptors (GRs) of basolateral amygdala (BLA) in this regard. In the CPP paradigm, conditioning score and locomotion activity were recorded by Ethovision software. Male adult rats received forced swim stress (FSS) as a physical stress or corticosterone (10mg/kg; ip) as a dominant stress hormone in rodents, 10min before morphine injection (5mg/kg; sc) during three conditioning days (acquisition) or just prior to CPP test in the post-conditioning day (expression). In FSS procedure, animals were forced to swim for 6min in cylinder filled with water (24–27°C). To evaluate the role of glucocorticoid receptors in the BLA, different doses of mifepristone (RU38486) as a GR antagonist were injected into the BLA (0.3, 3 and 30ng/side) during 3-day conditioning phase before FSS or injection of corticosterone in morphine-CPP paradigm. The results showed that FSS and corticosterone reduce the acquisition but not expression of morphine-induced CPP. Moreover, blockade of GRs in the BLA could diminish the inhibitory effects of FSS or corticosterone on the acquisition of morphine-induced CPP. It seems that stress exerts its effect on reward pathway via glucocorticoid receptors in the BLA.

A guide for measurement of circulating metabolic hormones in rodents: Pitfalls during the pre-analytical phase

Researchers analyse hormones to draw conclusions from changes in hormone concentrations observed under specific physiological conditions and to elucidate mechanisms underlying their biological variability. It is, however, frequently overlooked that also circumstances occurring after collection of biological samples can significantly affect the hormone concentrations measured, owing to analytical and pre-analytical variability. Whereas the awareness for such potential confounders is increasing in human laboratory medicine, there is sometimes limited consensus about the control of these factors in rodent studies. In this guide, we demonstrate how such factors can affect reliability and consequent interpretation of the data from immunoassay measurements of circulating metabolic hormones in rodent studies. We also compare the knowledge about such factors in rodent studies to recent recommendations established for biomarker studies in humans and give specific practical recommendations for the control of pre-analytical conditions in metabolic studies in rodents.

Plasma Active Ghrelin Level in Patients with Type 2 Diabetes Mellitus and its Interrelationship with Insulin resistance, Hypertension, Dyslipidemia and Obesity


 
 
 
 BACKGROUND: Ghrelin is a multi-functional gut-derived peptide hormone. Administered ghrelin has shown an increase in appetite and food intake and also stimulate the secretion of the growth hormone in rodents as well as in humans. Ghrelin is the strongest orexigenic hormone.
 OBJECTIVE: The aim of the study was to estimate plasma active Ghrelin levels in type – II diabetes mellitus patients and establish its relation to Insulin Resistance, Hypertension, Dyslipidemia and Obesity.
 MATERIALS & METHODS: A total of 81 patients were enrolled in the study out of then 50 were the cases and 31 were controls.
 RESULTS: A significant negative correlation was found between Fasting plasma active ghrelin levels and systolic blood pressure (r = -0.71, p <0.02), diastolic blood pressure (r = -0.64, p <0.02) , obesity (r = -0.71, p <0.001), fasting insulin levels (r = -0.40, p <0.01), insulin resistance (r = -0.32, p <0.01).A deeper understanding on this interesting pleiotropic hormone could be anticipated to open new insights into the metabolic pathways causing a predisposition for obesity and its co-morbidities. JMS 2011;14(2):56-60
 
 
 

Maternal bisphenol A (BPA) decreases attractiveness of male offspring

Are you having little luck in the search for your soulmate? When you finally meet a woman does she seem disinterested? What could it be? Your breath? Your clothes? Findings from a new study (1) suggest it may be your mother's dietary exposure to bisphenol A (BPA). In the study published in PNAS, Jasarevic′ et al. (1) find that maternal BPA exposure impairs spatial ability, decreases exploratory behavior, and reduces attractiveness of male deer mice progeny. These traits are sexually dimorphic and are subjected to sexual selection because they are essential characteristics needed to find mates and reproduce in male deer mice (and other polygynous species) (2). Male deer mice, much like male meadow voles, traverse large territories during the breeding season to gain access to dispersed females (3). Female meadow voles prefer male meadow voles with better spatial ability, and male meadow voles with better spatial ability visit more female nest boxes (4, 5). Thus, home range size and spatial ability favor males in most polygynous species. Intriguingly, these sexually dimorphic traits also manifest in the hippocampus, an area important for spatial memory. Males have a larger hippocampus and greater levels of adult hippocampal neurogenesis than females during the breeding season (6, 7). The expression of sexually dimorphic spatial ability depends on both early (pre- or perinatal) and adult levels of sex hormones in rodents (3). The report by Jasarevic′ et al. (1) shows that these sexually dimorphic traits, spatial ability and exploratory behavior, in addition to attractiveness, are affected by maternal dietary exposure to the environmental endocrine disrupter BPA. Specifically, the authors show that maternal consumption of low levels of dietary BPA renders male offspring at a disadvantage for mating, not only because of poorer spatial navigation and greater anxiety-like behavior but also because they are less attractive to female conspecifics. These findings are significant as coupled with other studies, it seems that maternal dietary consumption of low levels of BPA may affect the fecundity of adult offspring through a number of mediating factors.