Abstract
The developing and adult brain is a target organ for the vast majority of hormones produced by the body, which are able to cross the blood–brain barrier and bind to their specific receptors on neurons and glial cells. Hormones ensure proper communication between the brain and the body by activating adaptive mechanisms necessary to withstand and react to changes in internal and external conditions by regulating neuronal and synaptic plasticity, neurogenesis and metabolic activity of the brain. The influence of hormones on energy metabolism and mitochondrial function in the brain has gained much attention since mitochondrial dysfunctions are observed in many different pathological conditions of the central nervous system. Moreover, excess or deficiency of hormones is associated with cell damage and loss of function in mitochondria. This review aims to expound on the impact of hormones (GLP-1, insulin, thyroid hormones, glucocorticoids) on metabolic processes in the brain with special emphasis on oxidative phosphorylation dysregulation, which may contribute to the formation of pathological changes. Since the brain concentrations of sex hormones and neurosteroids decrease with age as well as in neurodegenerative diseases, in parallel with the occurrence of mitochondrial dysfunction and the weakening of cognitive functions, their beneficial effects on oxidative phosphorylation and expression of antioxidant enzymes are also discussed.
Highlights
Maintenance of body homeostasis depends on proper communication between various organs and cells in a living organism, and this communication is in large part achieved by two different yet complementary systems, namely, the nervous system and the endocrine system
In response to stimuli from higher brain centers, hypothalamic neuroendocrine neurons release neurohormones into the hypophysial portal blood to act on cells of the anterior pituitary gland to induce the production of pituitary hormones, which are transported via the bloodstream to effector endocrine glands such as the thyroid, adrenal glands and gonads or, as in the case of growth hormone or prolactin, act directly on target cells
It is currently not possible to determine the role of steroids synthesized locally in the brain as compared to those derived from the periphery and there is no existing data, which may distinguish their influence on mitochondrial function
Summary
Maintenance of body homeostasis depends on proper communication between various organs and cells in a living organism, and this communication is in large part achieved by two different yet complementary systems, namely, the nervous system and the endocrine system. AAV-induced knockdown of liver IGF-1 gene expression in male mice at the fifth month of age over time resulted in a significant decrease in cortical ATP levels and a reduction in mitochondrial OXPHOS coupling capacity in the hippocampus, which was further associated with an increase in the levels of oxidative stress markers, as well as impairments in hippocampal-dependent spatial acquisition and learning It is noteworthy, that in the same experiments, deficiency in circulating IGF-1 levels did not influence or resulted in opposite effects on mitochondrial respiration in some of the peripheral tissues, since it increased lipid peroxidation in adipocytes and reduced adipose mass, which seem to illustrate well the tissue-dependent pleiotropic action of IGF-1 and differences between its peripheral and central effects [29]. As shown in an in vitro study conducted on a BV-2 microglial cell line, activation of GLP-1R and glucose-dependent insulinotropic polypeptide receptor (GIPR) reduced apoptotic cell death, increased the synthesis of neurotrophic factors and alleviated oxidative stress by inhibiting the accumulation of ROS and the release of nitric oxide (NO), as well as by upregulating the expression of antioxidative enzymes such as GPx1 and SOD1 [55]
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