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Effect of synbiotic pomegranate juice on glycemic, sex hormone profile and anthropometric indices in PCOS: A randomized, triple blind, controlled trial.
Esmaeilinezhad, Z, Babajafari, S, Sohrabi, Z, Eskandari, MH, Amooee, S, Barati-Boldaji, R
Nutrition, metabolism, and cardiovascular diseases : NMCD. 2019;(2):201-208
Abstract
BACKGROUND AND AIMS Polycystic Ovarian Syndrome is a common reproductive, endocrine, and metabolic disease in women. Pomegranate juice, known as a rich source of phytochemicals with high antioxidant activity, enriched with probiotic may improve PCOS. METHODS AND RESULTS A randomized, controlled, triple-blinded, parallel trial study was performed in PCOS patients (n = 92). Three treatment groups (23 patients each) received 2 L of synbiotic pomegranate juice (SPJ), pomegranate juice (PJ), and synbiotic beverage (SB) weekly. The control group (23 patients) received 2 L of placebo beverage weekly. Primary outcome was any change in insulin resistance and secondary outcomes were fasting blood sugar (FBS), insulin sensitivity, testosterone, luteinizing hormone (LH), follicle stimulating hormone (FSH), body mass index (BMI), waist and hip circumference, from baseline to the end of the trial. At the end of the study, 86 patients were analyzed. There was significant change in insulin resistance in the SPJ and SB groups. Insulin sensitivity increased significantly in the SPJ and SB groups. Insulin also changed significantly in the SPJ and SB groups. BMI, weight and waist circumference decreased significantly in the SPJ and SB groups. Testosterone level also decreased significantly in the SPJ and SB groups. There was no significant change in FPG, LH and FSH in any of the groups. CONCLUSION SPJ in the form of a new beverage can improve insulin resistance, insulin, testosterone level, BMI, weight and waist circumference in PCOS. This trial was registered in Iranian Registry of Clinical Trials, with number: 25272.
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Sex differences, endogenous sex-hormone hormones, sex-hormone binding globulin, and exogenous disruptors in diabetes and related metabolic outcomes.
Liu, S, Sun, Q
Journal of diabetes. 2018;(6):428-441
Abstract
In assessing clinical and pathophysiological development of type 2 diabetes (T2D), the critical role of the sex steroids axis is underappreciated, particularly concerning the sex-specific relationships with many relevant cardiometabolic outcomes. In this issue of the Journal of Diabetes, we provide a comprehensive overview of these significant associations of germline variants in the genes governing the sex steroid pathways, plasma levels of steroid hormones, and sex hormone-binding globulin (SHBG) with T2D risk that have been observed in many clinical and high-quality large prospective cohorts of men and women across ethnic populations. Together, this body of evidence indicates that sex steroids and SHBG should be routinely incorporated into clinical characterization of T2D patients, particularly in screening prediabetic patients, such as those with metabolic syndrome, using plasma levels of SHBG. Given that several germline mutations in the SHBG gene have also been directly related to both plasma concentrations of SHBG and clinical manifestation of T2D, targeting signals in the sex steroid axis, particularly SHBG, may have significant utility in the prediction and treatment of T2D. Further, many of the environmental endocrine disrupting chemicals may exert their potential adverse effects on cardiometabolic outcomes via either estrogenic or androgenic signaling pathways, highlighting the importance of using the sex steroids and SHBG as important biochemical markers in both clinical and population studies in studying sex-specific mechanisms in the pathogenesis of T2D and its complications, as well as the need to equitably allocate resources in studying both men and women.
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Chromium supplementation does not improve weight loss or metabolic and hormonal variables in patients with polycystic ovary syndrome: A systematic review.
Maleki, V, Izadi, A, Farsad-Naeimi, A, Alizadeh, M
Nutrition research (New York, N.Y.). 2018;:1-10
Abstract
Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in women of reproductive age, and recently, chromium was discussed as an adjuvant way to manage it. Herein, a systematic review was conducted which centered on the effects of chromium on ovarian physiology with a focus on body mass index, as well as hormonal and metabolic dysfunctions in women suffering from PCOS. This review was performed using the guidelines from Preferred Reporting Items for Systematic Reviews. Clinical trials investigating chromium in women with PCOS with outcome measures related to metabolic and hormonal status were included. The search was conducted using PubMed, Scopus, and Google Scholar databases for clinical trials in the English language from the inception of the resources until May 2017 with the terms: chromium, chromium picolinate, CrP, polycystic ovary syndrome, PCOS, and sclerocystic ovary syndrome. The search resulted in 89 articles, and after inclusion and exclusion criteria were applied, 6 articles were selected for analysis. Two studies that evaluated the effect of chromium on body weight or body mass index reported no effect. Another study reported the beneficial effect of chromium on weight reduction. It seems that the effect of chromium in the reduction of blood glucose is insignificant, and results are inconsistent in relation to dyslipidemia. With regard to the effects of chromium on concentrations of sex hormones, a longer duration of treatment is needed to produce significant changes. The articles reviewed demonstrated that chromium supplementation has limited effects on weight reduction, glucose control, lipid profile, and hormonal disturbance of women with PCOS; however, more studies are needed due to the clinical changes observed in patients with PCOS after chromium supplementation.
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An integrated mechanism of pediatric pseudotumor cerebri syndrome: evidence of bioenergetic and hormonal regulation of cerebrospinal fluid dynamics.
Sheldon, CA, Kwon, YJ, Liu, GT, McCormack, SE
Pediatric research. 2015;(2):282-9
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Abstract
Pseudotumor cerebri syndrome (PTCS) is defined by the presence of elevated intracranial pressure (ICP) in the setting of normal brain parenchyma and cerebrospinal fluid (CSF). Headache, vision changes, and papilledema are common presenting features. Up to 10% of appropriately treated patients may experience permanent visual loss. The mechanism(s) underlying PTCS is unknown. PTCS occurs in association with a variety of conditions, including kidney disease, obesity, and adrenal insufficiency, suggesting endocrine and/or metabolic derangements may occur. Recent studies suggest that fluid and electrolyte balance in renal epithelia is regulated by a complex interaction of metabolic and hormonal factors; these cells share many of the same features as the choroid plexus cells in the central nervous system (CNS) responsible for regulation of CSF dynamics. Thus, we posit that similar factors may influence CSF dynamics in both types of fluid-sensitive tissues. Specifically, we hypothesize that, in patients with PTCS, mitochondrial metabolites (glutamate, succinate) and steroid hormones (cortisol, aldosterone) regulate CSF production and/or absorption. In this integrated mechanism review, we consider the clinical and molecular evidence for each metabolite and hormone in turn. We illustrate how related intracellular signaling cascades may converge in the choroid plexus, drawing on evidence from functionally similar tissues.
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"Getting from here to there"--mechanisms and limitations to the activation of the androgen receptor in castration-resistant prostate cancer.
Sharifi, N, McPhaul, MJ, Auchus, RJ
Journal of investigative medicine : the official publication of the American Federation for Clinical Research. 2010;(8):938-44
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Abstract
Despite the clinical regression that typifies the initial response of advanced prostate cancer to gonadal testosterone depletion, tumors eventually progress. However, evidence supports the concept that signaling via the androgen receptor (AR) is important in progression to castration-resistant prostate cancer (CRPC).Steroid hormones are synthesized from cholesterol in a series of tightly regulated steps involving the cleavage of carbon-carbon bonds, the introduction of functional groups derived from activated molecular oxygen, and the oxidation and reduction of carbon-carbon and carbon-oxygen bonds. In the adrenal cortex and gonads, steroidogenesis is tightly regulated, very efficient, and highly directional. In contrast, steroid metabolism in peripheral tissues is characterized by competing enzymes and pathways, low efficiency, and great variability. Many steps are mechanistically and functionally irreversible, but some are not, and the repertoire of specific enzymes, intracellular redox state, and access to hormone precursors all contribute to steroid flux and accumulation.The investigation of steroid metabolizing enzymes in CRPC often assumes that the pathways and the patterns of metabolism mirror those defined in the adrenals and the gonads and validated by human deficiency syndromes. Unfortunately, several potential pathways using different enzymes might contribute substantially to androgen synthesis in CRPC. Finally, a number of mechanisms have been reported by which the AR is activated independent of ligand. Recent observations have suggested that AR forms with constitutive activity occur in CRPC, stimulating transcription without a requirement for ligand. This overview outlines a broad view of how the mechanisms by which the AR may be activated, whether by alternate pathways of androgen synthesis or the production of alternate forms of the AR, with an emphasis on what aspects must be accounted for when using model systems to explore the biology of human prostate cancer.