Melanin-concentrating hormone (MCH) is a 19-amino acid cyclic peptide that is specifically produced in the lateral hypothalamic area, a region of the brain responsible for various essential physiological functions such as nutrient detection, food consumption, sleep-wake patterns, memory consolidation, and reproduction. Among these functions, the regulation of metabolism is particularly noteworthy. MCH plays a crucial role in managing energy equilibrium and glucose levels by influencing food intake, peripheral lipid metabolism, energy expenditure, physical activity, and thermogenesis in brown adipose tissue. Nevertheless, the control of energy balance by MCH is a multifaceted process that entails interactions with numerous neuroendocrine systems. This study aims to outline the current understanding of how MCH interacts with various hormonal factors. Additionally, we discuss the potential application of melanin-concentrating hormone receptor antagonists in treating metabolic issues stemming from exposure to phthalates, which can impact gender-related physiological functions.
The skin, a self-regulating protective barrier organ, is empowered with sensory and computing capabilities to counteract the environmental stressors to maintain and restore disrupted cutaneous homeostasis. These complex functions are coordinated by a cutaneous neuro-endocrine system that also communicates in a bidirectional fashion with the central nervous, endocrine, and immune systems, all acting in concert to control body homeostasis. Although UV energy has played an important role in the origin and evolution of life, UV absorption by the skin not only triggers mechanisms that defend skin integrity and regulate global homeostasis but also induces skin pathology (e.g., cancer, aging, autoimmune responses).
The outcomes described stem from the conversion of UV electromagnetic energy into chemical, hormonal, and neural signals, depending on the specific chromophores and tissue areas exposed to different UV wavelengths. UV radiation can enhance local neuroendocrine pathways, with UVB being more effective than UVA. This local stimulation can trigger the release of various substances like cytokines, corticotropin-releasing hormone, urocortins, proopiomelanocortin-peptides, and enkephalins into the bloodstream, leading to systemic effects such as activating the central hypothalamic-pituitary-adrenal axis, producing opioid-like effects, and inducing immunosuppression, regardless of vitamin D production. Exposure of the eyes and skin to UV can elicit similar responses, with UVB specifically activating certain brain regions for rapid stimulatory effects. As a result, UV exposure can impact the brain and central neuroendocrine system to help regulate the body's balance. This presents various therapeutic opportunities for UV radiation, including the treatment of autoimmune disorders, mood disorders, addiction, and obesity.
UV energy triggers skin-protective responses against stress, coordinated by the cutaneous-neuroendocrine system, and activates central neuroendocrine system pathways that regulate global homeostasis.
It is increasingly challenging to avoid being exposed to synthetic endocrine disrupting chemicals (EDCs) and environmental toxins. This continuous rise in exposure is believed to be a contributing factor to the simultaneous decline in human fertility observed over the past five decades. However, there is ongoing debate regarding the existence of associations, as conflicting research findings are frequently reported across all major EDC categories. The main objective of this comprehensive study was to identify and analyze robust evidence from peer-reviewed sources concerning the impact of environmentally relevant concentrations of EDCs on the fertility of adult men and women during the crucial periconception period, focusing on reproductive hormone levels, gamete and embryo characteristics, as well as the time it takes to achieve pregnancy in the general population. Additionally, the study aimed to determine whether individuals or couples diagnosed with subfertility have higher levels of EDCs or toxicants.
Finally, it aimed to pinpoint areas where data is lacking, hindering the identification of strong associations. Out of the more than 1480 known EDCs, significant evidence suggests a negative link between exposure to phthalates, PCBs, PBDEs, pyrethroids, organochloride pesticides, and male fertility and fecundity. There is only moderate evidence of a negative association between BPA, PCBs, organochloride pesticides, and female fertility and fecundity. Studies on women were fewer compared to men, with knowledge gaps apparent for both genders across all major EDC categories, as well as a scarcity of female fertility research following exposure to parabens, triclosans, dioxins, PFAS, organophosphates, and pyrethroids. Generally, individuals or couples experiencing subfertility show higher concentrations of EDCs, indicating a positive correlation between EDC exposure and subfertility. The question that remains unanswered is why individuals identified as having African or Eumelanated ancestry do not exhibit high levels of subfertility despite similar exposure to EDCs.
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