What is the Origin of FSHR Polymorphism?

The term is a combination of the acronym "FSHR" for the receptor, and "polymorphism," derived from the Greek poly- (many) and morphē (form), signifying multiple forms of a gene sequence within a population. This concept is fundamental to pharmacogenomics, recognizing that genetic differences influence an individual's response to endogenous hormones and exogenous fertility medications. It underscores the genetic basis for individual variability in reproductive endocrine function.

What is the Mechanism of FSHR Polymorphism?

The functional mechanism of an FSHR polymorphism is often a subtle change in the receptor's structure, which impacts its ligand binding affinity or signal transduction efficiency. For example, a less responsive receptor variant may require higher circulating levels of FSH to elicit the same biological response, such as follicle maturation or spermatogenesis. Understanding a patient's specific FSHR genotype can therefore inform the clinical decision-making process regarding the optimal dosing strategy for gonadotropin administration in assisted reproductive technologies.

FSHR Polymorphism

Meaning

FSHR Polymorphism refers to the common variations in the DNA sequence of the gene that encodes the Follicle-Stimulating Hormone Receptor (FSHR), a critical glycoprotein receptor found primarily on ovarian granulosa cells and testicular Sertoli cells. These genetic variations, or single nucleotide polymorphisms (SNPs), can alter the receptor’s sensitivity and responsiveness to circulating Follicle-Stimulating Hormone (FSH). Clinically, certain polymorphisms, such as the N680S variant, are associated with differing outcomes in fertility treatments and ovarian reserve assessment.