AI Article Synopsis

  • Obesity is a major global health issue, characterized by excessive body fat that functions like an organ, disrupting metabolic processes and overall body function.
  • One key factor in obesity is low-grade inflammation, driven by pro-inflammatory substances released from fat tissue, which negatively affects insulin sensitivity and reproductive hormones.
  • The review highlights the complicated interactions between fat-derived hormones and immune responses, emphasizing the need for further research to develop targeted treatments for reproductive issues linked to obesity.

Article Abstract

Obesity, which leads to metabolic dysregulation and body function impairment, emerges as one of the pressing health challenges worldwide. Excessive body fat deposits comprise a dynamic and biologically active organ possessing its own endocrine function. One of the mechanisms underlying the pathophysiology of obesity is low-grade systemic inflammation mediated by pro-inflammatory factors such as free fatty acids, lipopolysaccharides, adipokines (including leptin, resistin and visfatin) and cytokines (TNF-α, IL-1β, Il-6), which are secreted by adipose tissue. Together with obesity-induced insulin resistance and hyperandrogenism, the exacerbated immune response has a negative impact on the hypothalamic-pituitary-gonadal axis at all levels and directly affects reproduction. In women, it results in disrupted ovarian function, irregular menstrual cycles and anovulation, contributing to infertility. This review focuses on the abnormal intracellular communication, altered gene expression and signaling pathways activated in obesity, underscoring its multifactorial character and consequences at a molecular level. Extensive presentation of the complex interplay between adipokines, cytokines, immune cells and neurons may serve as a foundation for future studies in search of potential sites for more targeted treatment of reproductive disorders related to obesity.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11395521PMC
http://dx.doi.org/10.3390/ijms25179391DOI Listing

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