The Deep Correlation between Energy Metabolism and Reproduction: A View on the Effects of Nutrition for Women Fertility

Abstract

In female mammals, mechanisms have been developed, throughout evolution, to integrate environmental, nutritional and hormonal cues in order to guarantee reproduction in favorable energetic conditions and to inhibit it in case of food scarcity. This metabolic strategy could be an advantage in nutritionally poor environments, but nowadays is affecting women's health. The unlimited availability of nutrients, in association with reduced energy expenditure, leads to alterations in many metabolic pathways and to impairments in the finely tuned inter-relation between energy metabolism and reproduction, thereby affecting female fertility. Many energetic states could influence female reproductive health being under- and over-weight, obesity and strenuous physical activity are all conditions that alter the profiles of specific hormones, such as insulin and adipokines, thus impairing women fertility. Furthermore, specific classes of nutrients might affect female fertility by acting on particular signaling pathways. Dietary fatty acids, carbohydrates, proteins and food-associated components (such as endocrine disruptors) have per se physiological activities and their unbalanced intake, both in quantitative and qualitative terms, might impair metabolic homeostasis and fertility in premenopausal women. Even though we are far from identifying a "fertility diet", lifestyle and dietary interventions might represent a promising and invaluable strategy to manage infertility in premenopausal women.

Keywords: energy metabolism; fertility; nutrients; reproduction; women.

Figure 1

Number of publications reporting the association between female infertility and obesity. The great increase in number of reports appeared per year since 1980 reveals that the interest in the topic has increased during the last decades. Data were obtained using WOS (Web of Science).

Figure 2

Effects of insulin, leptin and adiponectin on the regulation of hypothalamic pituitary gonadal axis (HPG) and steroidogenesis under physiological and obesity-associated conditions. Under physiological conditions (left) the signaling pathways of insulin, leptin and adiponectin are able to sense the nutritional status, and, jointly with sex hormones sustain ovarian activity and reproduction. In obesity (right), the increased levels of insulin and leptin lead to insulin and leptin resistance that, together with the reduced adiponectin levels, contribute to a dysregulation of both the HPG axis and ovarian steroidogenesis, by further worsening the endocrine milieu (impaired E2 and P4 synthesis, increased T synthesis and free levels due to reduced SHBG synthesis) and impairing ovarian function and fertility success rate. In the figure the dotted lines represent impaired regulations. E2 = 17β-estradiol; P4 = progesterone; T = testosterone.