Figure 1.

HFDs can lead to the accumulation of adipose tissue and an increase in the systemic release of adipokines. The interaction between PCOS and abdominal obesity may result in a vicious cycle (as indicated by the black arrows in the diagram) in which excess androgens promote visceral adiposity. This, in turn, may promote excess androgens of ovarian and/or adrenal origin via various mediators, including autocrine, paracrine, and endocrine pathways, or indirectly through the induction of insulin resistance and hyperinsulinemia. Moreover, elevated levels of adipokines can impair the GnRH pulse by overstimulating kisspeptin neurons, which can have an impact on the release of FSH and LH gonadotropins from the pituitary gland and the secretion of E2 and P4 hormones from the ovaries. Finally, high levels of insulin, which are a characteristic feature of HFDs, can increase the amplitude of the GnRH pulse in the hypothalamus, leading to an increase in LH secretion from the pituitary gland. List of abbreviations included in the figure: follicle stimulating hormone (FSH); luteinizing hormone (LH); polycystic ovary syndrome (PCOS). Image created with BioRender.com.