Inflammatory bowel disease (IBD), characterized by chronic inflammation of the gastrointestinal tract, is a global health care problem. Compelling evidence shows sex differences regarding the prevalence, pathophysiology, clinical presentation, and treatment outcome of IBD. Sex hormones, including estrogen, progesterone, and androgen, have been proposed to have a role in the pathogenesis of sexual dimorphism in IBD. Clinical and experimental data support the modulatory effects of sex hormones on various clinical characteristics of the disease, including intestinal barrier dysfunction and mucosal immune activation. Additionally, the potential role of sex hormones in the modulation of gut microbiota is attracting increasing attention. Here, we discuss the sex dimorphic disease profile and address the potential mechanisms involved in the sex-specific pathogenesis of IBD. Improved understanding of these sex differences in the clinic could improve the knowledge of patients with IBD with heterogeneous disease profiles.
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http://dx.doi.org/10.1093/ibd/izac094 | DOI Listing |
Background: Differential diagnosis of hypogonadotropic hypogonadism (HH) and constitutional delay of puberty (CDP) is extremely important since with the latter puberty begins and completes without any medical intervention and in the case of HH puberty does not occur or is incomplete. Failure to start treatment on time leads to medical and psychosocial maladjustment of the patient.
Aim: Development of a method for differential diagnosis of hypogonadotropic hypogonadism and constitutional delay of puberty in boys 13.
We have previously identified that infection induces a unique form of myeloid training that protects male but not female mice from high fat diet induced disease. Here we demonstrate that ovarian derived hormones account for this sex specific difference. Ovariectomy of females prior to infection permits metabolic reprogramming of the myeloid lineage, with BMDM exhibiting carbon source flexibility for cellular respiration, and mice protected from systemic metabolic disease.
View Article and Find Full Text PDFInt J Prev Med
December 2024
Gastrointestitional Cancer Research Center, Non-Communicable Disease Institute, Mazandaran University of Medical Sciences, Sari, Iran.
Background: The present study is a systematic review and meta-analysis aiming to investigate the effects of alcohol consumption on male sex hormones in humans.
Methods: We conducted searches on PubMed, Scopus, Science Direct, and Google Scholar from June 2020 to June 2022. We included observational studies (cohorts, case-controls, and cross-sectional studies) comparing FSH, LH, or testosterone levels in alcohol consumers versus non-consumers.
Mol Nutr Food Res
January 2025
Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Cardiovascular diseases (CVDs) are the leading cause of death globally. Decrease in female sex hormones during menopause increases the risk of cardiovascular disease, mainly ischemic heart disease (IHD). Quercetin, a flavonoid, has beneficial properties in CVDs due to its antioxidant, anti-inflammatory, and anti-apoptotic effects.
View Article and Find Full Text PDFEndocrinology
January 2025
Cardiopulmonary Immunotoxicology Branch, Public Health and Integrated Toxicology Division, Center for Public Health and Environmental Assessment, U.S. Environmental Protection Agency, Research Triangle Park, NC.
Maternal exposure to ozone during implantation results in reduced fetal weight gain in rats. Offspring from ozone-exposed dams demonstrate sexually dimorphic risks to high-fat diet feeding in adolescence. To better understand the adolescent hepatic metabolic landscape following fetal growth restriction, RNA sequencing was performed to characterize the effects of ozone-induced fetal growth restriction on male and female offspring.
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