Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Neuroendocrine Effects on the Risk of Metabolic Syndrome in Children

Version 1 : Received: 24 May 2023 / Approved: 30 May 2023 / Online: 30 May 2023 (02:27:15 CEST)

A peer-reviewed article of this Preprint also exists.

Scorrano, G.; La Bella, S.; Matricardi, S.; Chiarelli, F.; Giannini, C. Neuroendocrine Effects on the Risk of Metabolic Syndrome in Children. Metabolites 2023, 13, 810. Scorrano, G.; La Bella, S.; Matricardi, S.; Chiarelli, F.; Giannini, C. Neuroendocrine Effects on the Risk of Metabolic Syndrome in Children. Metabolites 2023, 13, 810.

Abstract

Endocrine and nervous systems reciprocally interact to manage physiological individual functions and homeostasis. The nervous system modulates hormone release through the hypothalamus, the main cerebrally specialized structure of the neuroendocrine system. Indeed, it is involved in various metabolic processes, administering hormone and neuropeptide release at different levels. This complex activity is affected by neurons of various cerebral areas, environmental factors, peripheral organs, and mediators through feedback mechanisms. Therefore, neuroendocrine pathways have a key role in metabolic homeostasis control, and their abnormalities have been associated with the development of Metabolic Syndrome (MetS) in children. The impaired functioning of genes, hormones, and neuropeptides of various neuroendocrine pathways involved in several metabolic processes has been related to an increased risk of dyslipidaemia, visceral obesity, insulin resistance, type 2 diabetes mellitus, and hypertension. This review examines the neuroendocrine effects on the risk of MetS in children, identifying and underlying the several conditions associated with neuroendocrine pathway disruption. Neuroendocrine systems should be considered in the complex pathophysiology of MetS, and, when genetic or epigenetic mutations in "hot" pathways occur, they could be studied for new potential target therapies in severe and drug-resistant paediatric forms of MetS.

Keywords

Metabolic syndrome; obesity; neuroendocrine systems; stress response; genetic polymorphisms

Subject

Medicine and Pharmacology, Endocrinology and Metabolism

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