Abstract

Eating behavior is controlled by hypothalamic circuits in which agouti-related peptide-expressing neurons when activated in the arcuate nucleus, promote food intake while pro-opiomelanocortin-producing neurons promote satiety. The respective neurotransmitters signal to other parts of the hypothalamus such as the paraventricular nucleus as well as several extra-hypothalamic brain regions to orchestrate eating behavior. This complex process of food intake may be influenced by glia cells, in particular astrocytes and microglia. Recent studies showed that GFAP+ astrocyte cell density is reduced in the central nervous system of an experimental anorexia nervosa model. Anorexia nervosa is an eating disorder that causes, among the well-known somatic symptoms, brain volume loss which was associated with neuropsychological deficits while the underlying pathophysiology is unknown. In this review article, we summarize the findings of glia cells in anorexia nervosa animal models and try to deduce which role glia cells might play in the pathophysiology of eating disorders, including anorexia nervosa. A better understanding of glia cell function in the regulation of food intake and eating behavior might lead to the identification of new drug targets.

Highlights

  • Academic Editors: Andrea Phillipou and Giacomo ManciniReceived: 17 November 2021Accepted: 25 December 2021Published: 30 December 2021Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.In the central nervous system (CNS) exist billions of cells with various functions, molecular structures, and morphologies

  • We address the influence of astrocytes in food intake processes because these cells are subject to change in the activity-based anorexia (ABA) animal model [35,36]

  • The brain volume reduction in the ABA model is linked to a reduction in GFAP+ cell density

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Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. In the central nervous system (CNS) exist billions of cells with various functions, molecular structures, and morphologies. These cells build up complex circuits to fulfill a specific task in the human body, i.e., eating behavior. The circuits are not limited to neuronal cells, glia cells play an important element in these pathways. Recent studies showed that glia cells are active and important regulators in food intake behavior and are, potential drug targets for metabolic disorders. We summarize in this review the neuronal circuits of eating behavior in the hypothalamus, the role of glia cells in this process, and the potential influence of glia cells for eating disorders with a specific focus on anorexia nervosa (AN)

Neuronal Control of Appetite in the Hypothalamus
Orexigenic
A illustration of food intake regulation in the ARC when AgRP
Astrocyte Pathology
Disturbed Gliotransmission as a Regulator of Feeding Behavior
Astrocytes in Behavioral Disorders
Astrocytes as Targets of Peripheral Food Intake Signals
Microglia Pathology
10. Neuroinflammation in Eating Disorders and the Role of Microglia
12. Glia Cell Pathology in AN
Effects
13. Pathways of Food Intake in ABA
Findings
14. Conclusions and Outlook
Full Text
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