Diet-Induced Hypothalamic Inflammation, Phoenixin, and Subsequent Precocious Puberty.

Georgios Valsamakis,Evangelia Charmandari,Angeliki Arapaki,Dimitris Balafoutas,Nikolaos F Vlahos

doi:10.3390/nu13103460

Georgios Valsamakis, Evangelia Charmandari + Show 3 more

Open Access

https://doi.org/10.3390/nu13103460

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Journal: Nutrients	Publication Date: Sep 29, 2021
Citations: 15	License type: CC BY 4.0

Affiliation: National and Kapodistrian University of Athens

Abstract

Recent studies have shown a rise in precocious puberty, especially in girls. At the same time, childhood obesity due to overnutrition and energy imbalance is rising too. Nutrition and fertility are currently facing major challenges in our societies, and are interconnected. Studies have shown that high-fat and/or high-glycaemic-index diet can cause hypothalamic inflammation and microglial activation. Molecular and animal studies reveal that microglial activation seems to produce and activate prostaglandins, neurotrophic factors activating GnRH (gonadotropin-releasing hormone expressing neurons), thus initiating precocious puberty. GnRH neurons’ mechanisms of excitability are not well understood. In this review, we study the phenomenon of the rise of precocious puberty, we examine the physiology of GnRH neurons, and we review the recent literature regarding the pathophysiological mechanisms that connect diet-induced hypothalamic inflammation and diet-induced phoenixin regulation with precocious puberty.

Highlights

Puberty is the process of physical changes through which a child’s body matures into an adult body capable of sexual reproduction, and is marked by maturation of the genital organs, development of sexual characteristics, acceleration of growth, changes in affect and, in females, the occurrence of menarche [1]
Gonadotropin-releasing hormone (GnRH) is normally released from the hypothalamus in order to activate the pituitary gland for secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) [23] gonadotropin-releasing hormone (GnRH)-expressing neurons are located in various regions of the hypothalamus, such as the medial septum, the organum vasculosum and the rostral preoptic area, forming a neural network close to other central regulators
Potential mechanisms show that the above diet induces low-grade inflammation in the hypothalamus, and that the subsequent microglial activation mediates prostaglandins and neurotrophic factors to GnRH cells, activating precocious puberty

Summary

Introduction

Puberty is the process of physical changes through which a child’s body matures into an adult body capable of sexual reproduction, and is marked by maturation of the genital organs, development of sexual characteristics, acceleration of growth, changes in affect and, in females, the occurrence of menarche [1] It is caused by the activation and increased secretion of gonadotropin-releasing hormone (GnRH) by the hypothalamus, which in turn activates the gonads to produce hormones [2]. Gonadotropin-releasing hormone (GnRH) is normally released from the hypothalamus in order to activate the pituitary gland for secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) [23] GnRH-expressing neurons are located in various regions of the hypothalamus, such as the medial septum, the organum vasculosum and the rostral preoptic area, forming a neural network close to other central regulators This position lets the GnRH network be affected by various neuroendocrine and metabolic signals [24]. The aim of this review is to explore how a high-glycaemic-index diet and/or a high-fat diet could have an association with precocious puberty in either girls or boys

Physiology of Puberty

Precocious Puberty

Potential Mechanisms of Diet-Induced Precocious Pubarche

Findings

Conclusions