Hormones are the mediators of multiple metabolic, reproductive and developmental processes in our body. In addition, hormonal secretion depends on an intricate feedback loop that includes the participation of the hypothalamic-pituitary-gonadal (HPG) axis. The interaction between the HPG axis hormones is crucial for reproductive health. Any disturbance in this process might result in reproductive dysfunction. Nowadays, obesity contributes to the systemic dysfunction of the HPG axis, affecting the hypothalamic hormonal secretion resulting in reproductive dysfunction. How can a metabolic disease such as obesity affect hypothalamic function? Neuroinflammation and the combination of obesity-induced changes create a detrimental state that impacts the HPG axis function.
Metabolic function, adipose tissue, and lean body mass are the needed stimuli to promote puberty and reproductive function by the HPG axis. The cascade reaction starts in the hypothalamus and the secretion of GnRH by a unique population of neurons (around 1000 to 2000). Furthermore, GnRH is secreted in a pulsatile manner into the hypophyseal portal circulation leading to the binding of its receptor in the anterior pituitary. In turn, the anterior pituitary synthesizes and secretes LH and FSH, which stimulate steroidogenesis and gametogenesis in the gonads.
The interaction between food intake and energy expenditure and the HPG axis function could be explained by the hypothalamic neurons involved in these processes. Adipose tissue sends long-term signals to the primary brain stem and the hypothalamus. Indeed, as adipose tissue serves as an endocrine organ, its leptin secretion is necessary for the initiation of puberty. On the other hand, a leaner constitution and decreased fat deposits may reduce LH secretion frequency and delay gonadotropic development. In conclusion, this implies a tight connection between metabolic signals, pubertal maturation, and reproductive health mainly modulated by the hypothalamus, with the stimuli promoted by the adipose tissue.
Nowadays, 30% of the adult population classifies as obese, meaning that their BMI is over 30 kg/m2. Obesity affects multiple homeostatic processes in the human body, including reproductive function, and it is associated with a higher risk of cardiovascular disease, cerebral ischemia, and type II diabetes.
Obesity affects men’s and women’s reproductive functions by altering LH levels and lower testosterone concentration. However, this mechanism affects each gender differently. For instance, obesity’s effect on LH level in men reduces sperm number and quality, lowers sperm concentration, and a decreasing number of spermatozoa. As a result, in vitro studies have reported lower fertilization rates when the male partner is obese. On mice models, obese rats had decreased sperm production and a higher sperm DNA fragmentation rate.
In women, the reduction of infertility can also be associated with lower levels of LH. Nevertheless, women’s health is heavily affected by obesity and may include early puberty, pregnancy complications, infertility, menstrual irregularities, and spontaneous abortions.
Testosterone levels are crucial mediators for muscle strength, but it is also essential for men’s reproductive health. The obesity pandemic not only affects our body composition but it inhibits our reproductive health. The signals acquired by our hypothalamus from our adipose tissue affect the synthesis and release of GnRH, ultimately affecting the whole hormonal cascade. If we ever want to improve our reproductive health and hormonal balance, we need to start by reducing fat mass and increasing lean body mass. – Ana Paola Rodríguez Arciniega, MS
Lainez, N. M., & Coss, D. (2019). Obesity, Neuroinflammation, and Reproductive Function. Endocrinology, 160(11), 2719–2736. doi.org/10.1210/en.2019-00487
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