Hormonal and Neuroendocrine Regulation of Energy Balance

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Background

Alteration in adequate energy balance maintenance results in serious disturbances such as obesity and its related metabolic disorders. In Mammals, energy balance is homeostatically controlled through hormonal and neuroendocrine systems which cooperation is based on cross-talk between central and peripheral signals. The hypothalamus as well as peripheral hormones among which those from the gastrointestinal tract, adipokines from adipose tissue, thyroid hormones and estrogens play a crucial role in energy homeostasis.
Unraveling the physiological, cellular and molecular mechanisms through which hormonal and neuroendocrine systems regulate energy balance has been a long-standing challenge in biology and is now more necessary when considering the world-wide increasing prevalence of obesity. Indeed, recognizing and understanding the biochemical and nutrient signaling pathways contributing to the nervous and endocrine integration of physiological mechanisms involved in the normal and/or abnormal regulation of energy balance is fundamental also to the development of new, effective, and targeted treatments for obesity.
Recent studies have highlighted the role of hypothalamic pro-opiomelanocortin-expressing neurons in the regulation of energy homeostasis by controlling energy expenditure and food intake. This is accomplished through a precise balance of production and degradation of α-melanocyte-stimulating hormone, an anorexigenic neuropeptide which is degraded to an inactive form unable to inhibit food intake by the key enzyme prolyl carboxypeptidase (PRCP), thus suggesting that pharmacologic approaches targeting PRCP may provide a novel and effective option for the management of obesity and its associated metabolic disorders. Indeed, efforts have been made to generate potent, brain-penetrant PRCP inhibitors. Estrogens have been demonstrated to regulate metabolism and estrogen receptors (ERs) are found in nuclear, cytoplasmic and membrane sites on neurons as well as glia, and have recently received increasing attention for their potentially important involvement in the CNS regulation of systemic metabolism and energy balance.
Weight loss due to negative energy balance is a goal for obese subjects not always reachable by dietary caloric restriction or increased physical activity. Lipid-lowering therapies have been suggested to have potential benefits, however, the establishment of comprehensive therapeutic strategies is still awaited. Recently, it has been reported that thyroid hormone (TH)- derivatives such as 3,5-diiodothyronine, 3-iodothyronamine and analogues like GC-1 possess interesting biological activities without deleterious effects (specifically at the cardiac level), opening new perspectives in thyroid physiology and TH derivatives usage as anti-obesity therapies.
Moreover, several studies, focusing on the interaction between thyroid hormone (TH), the autonomic nervous system and the liver, revealed an important role for the hypothalamus in the differential effects of TH on autonomic outflow to peripheral organs controlling energy balance. Recent reports suggest miRNAs are involved in important biological processes, including adipocyte differentiation and function, sugar and lipid metabolism, thus playing a role in energy homeostatsis.
This research topic aims to give a comprehensive and integrate view of the factors involved in the endocrine and neuroendocrine signaling in energy balance regulation to highlight their involvement into physiological processes and regulatory systems as well as their perturbation during pathological processes. All interested researchers are welcome to submit original and review articles as well as perspectives covering this topic.

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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