Although an association between the metabolic syndrome and hyperandrogenism has been suggested in women with polycystic ovarian syndrome, few studies have investigated this relationship in postmenopausal women. We measured estradiol, testosterone, and sex hormone-binding globulin (SHBG) and calculated the free androgen index (FAI) in 212 postmenopausal women not using hormone therapy in the Women's Health Study. A modified definition of the metabolic syndrome (3 or more of the following: abdominal obesity, hypertriglyceridemia, low high-density lipoprotein, elevated blood pressure, and abnormal glucose metabolism) from the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults was used. Women with the metabolic syndrome had higher mean levels of estradiol, testosterone, and FAI values and lower SHBG levels. Higher FAI and lower SHBG were associated with all components of the metabolic syndrome. After adjustment for BMI and other factors, women in the highest tertile of FAI had an odds ratio of 12.6 (95% confidence interval, 3.8-41.6) for the metabolic syndrome, whereas those in the lowest SHBG tertile had an odds ratio of 7.3 (95% confidence interval, 2.7-19.8). When stratified by body mass index, the associations with high FAI and low SHBG remained significant even in women with body mass index less than 26.7 kg/m2. An androgenic hormone profile is associated with both the individual components of the metabolic syndrome and clustering of metabolic abnormalities in postmenopausal women.
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http://dx.doi.org/10.1016/j.metabol.2006.06.017 | DOI Listing |
Elife
January 2025
The University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, United Kingdom.
encodes three regulatory subunits of class IA phosphoinositide 3-kinase (PI3K), each associating with any of three catalytic subunits, namely p110α, p110β, or p110δ. Constitutional mutations cause diseases with a genotype-phenotype relationship not yet fully explained: heterozygous loss-of-function mutations cause SHORT syndrome, featuring insulin resistance and short stature attributed to reduced p110α function, while heterozygous activating mutations cause immunodeficiency, attributed to p110δ activation and known as APDS2. Surprisingly, APDS2 patients do not show features of p110α hyperactivation, but do commonly have SHORT syndrome-like features, suggesting p110α hypofunction.
View Article and Find Full Text PDFActa Obstet Gynecol Scand
January 2025
Department of Biomedical Sciences, Humanitas University, Milan, Italy.
Introduction: Recurrent pregnancy loss (RPL), defined as two or more consecutive pregnancy losses before 24 weeks of gestation, affects up to 1%-2% of couples. Aim of this retrospective cohort study was to report the main causes and pregnancy outcomes of a cohort of women with RPL and the efficacy of a personalized work-up and treatment in terms of live birth rate.
Material And Methods: Women with primary (pRPL) and secondary (sRPL) RPL underwent a complete work-up and personalized therapeutic management.
Front Endocrinol (Lausanne)
January 2025
Department of Precision and Regenerative Medicine and Ionian Area (DiMePRe-J), University of Bari Aldo Moro, Bari, Italy.
Indian J Clin Biochem
January 2025
Department of Biochemistry, Velammal Medical College Hospital and Research Institute, Madurai, Tamil Nadu 632002 India.
Unlabelled: Non-alcoholic fatty liver disease (NAFLD) is one of the major causes of chronic liver disease worldwide. There are conflicting reports on the association of serum ferritin levels and its utility in discriminating various stages of liver fibrosis in patients with NAFLD. This study is done to address the conflicts by analysing the National Health and Nutritional Examination Survey 2017-2020 (NHANES 2017-2020) data.
View Article and Find Full Text PDFMol Genet Metab Rep
March 2025
Department of Biochemistry, JSS Medical College and Hospital, JSS-AHER, Mysuru 570015, India.
Mitochondrial DNA (mtDNA) variants considerably affect diabetes mellitus by disturbing mitochondrial function, energy metabolism, oxidative stress response, and even insulin secretion. The m.3243 A > G variants is associated with maternally inherited diabetes and deafness (MIDD), where early onset diabetes and hearing loss are prominent features.
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