Diet, alcohol and reproduction-lessons from animal models

Metabolic stressors (e.g. under- or overnurition, alcohol) acting in the mother’s womb as well as in adulthood influence reproductive functions governed by the hypothalamic-pituitary-gonadal (HPG) axis. Studies link the intrauterine environment with later obesity, diabetes and polycystic ovarian syndrome. Data presenting reproductive dysfunctions associated with diet and alcohol will be discussed. Animal models of inadequate nutrition and alcohol exposure will be presented. Females prenatally exposed to alcohol (PAE) have delayed puberty, alterations in hormonal profile (estradiol, progesterone, prolactin, luteinizing hormone), irregular estrus cycles. Changes in hormonal profile (e.g. decrease in secretion of testosterone and luteinizing hormone) were also reported in PAE males. Inadequate diet may also leads to reproductive abnormalities (e.g. altered levels of sex steroids, hypogonadotropic hypogonadism, premature child birth or infertility) observed in obese and diabetic patients. In a variety of obese and diabetics animal models imbalance in hormonal profile was also confirmed.  Kisspeptins, coded by KiSS 1 gene, acting via GPR54 (KISS1 R) receptor, are important in regulation of the HPG axis. Kisspeptin acts together with neurokinin B (NKB) and dynorphin, which are co-express in KNDy neurons in the arcuate nucleus of the hypothalamus (ARC). Importantly, in the ARC integration of metabolic and reproductive functions occurs. Abnormalities observed in animal models of PAE, obesity and diabetes may be related to kisspeptin system. Moreover, in animal models of high fat diet-induced obesity and steptozotocin-induced diabetes dysregulations in hormonal profile and alterations in KNDy neurons were reported. Potential therapeutic intervention to improve reproductive functions in obese and diabetic patients will be presented. Supported by NCN grant 2011/01/B/NZ4/04992.