Figure 3.

Schematic representation of the putative mechanisms linking low SHBG with the development NAFLD and PCOS. Increased hepatic de no lipogenesis inhibits SHBG synthesis through downregulating HNF-4α, leading to increasing androgen bioavailability and disrupting negative feedback relationship of hypothalamic–pituitary–ovarian axis, subsequently resulting in higher levels of LH and lower levels of FSH in most women with PCOS. Higher LH levels seem to cause hyperandrogenemia by exuberating androgens secretion from follicular theca cells, whereas lower FSH levels lead to anovulation. System insulin resistance associated with inflammatory cytokines directly induces granulosa cells apoptosis, leading to arrested follicular maturation, contribute to anovulation and multiple cystic follicles (CF) formation in PCOS.