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Cells
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Neural Mechanisms of Eating Disorders and Obesity
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Neural Mechanisms of Eating Disorders and Obesity

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (20 November 2024) | Viewed by 2648

Special Issue Editor

Dr. Xiaobing Zhang

E-Mail Website
Guest Editor
Department of Psychology, Florida State University, Tallahassee, FL 30304, USA
Interests: neural circuits of feeding motivation and food intake; neural plasticity in obesity and eating disorders

Special Issue Information

Dear Colleagues,

Food intake is an innated behavior that is controlled by the brain through sensing peripheral metabolic signals and environmental food cues. However, both diet components such as those high in fat and a stressful environment can cause neural plasticity of central feeding circuits that leads to eating disorders and obesity. In addition, the diet and environmental factors target central emotion and motivation pathways to change the motivation for food reward. Therefore, it is critically important to know how these diet and environmental factors evoke neural plasticity in central pathways for feeding and motivation to develop eating disorders and obesity.

This Special Issue will focus on novel neural circuits and neural plasticity in developing obesity and eating disorders; sex differences in obesity and eating disorders; gut–brain communication for normal and dysfunctional energy sensing; neuropeptide and hormones in controlling food intake, obesity, and eating disorders; and pharmacological mechanisms for eating regulation and obesity control.

Dr. Xiaobing Zhang
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • food intake
  • food reward
  • feeding motivation
  • eating disorders
  • obesity
  • neural circuits
  • neural plasticity
  • binge-eating disorder
  • anorexic disorder
  • high-fat diet
  • stress

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Published Papers (2 papers)

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Research

15 pages, 3102 KiB  
Article
Intermittent Overconsumption of High Fat Diet Promotes Microglial Reactivity in the Hypothalamus and Hindbrain of Female Rats
by Alexis A. Campanile and Lisa A. Eckel
Cells 2025, 14(3), 233; https://doi.org/10.3390/cells14030233 - 6 Feb 2025
Viewed by 556
Abstract
Elevated proinflammatory cytokines were reported in binge eating spectrum disorders characterized by intermittent overconsumption during periods of otherwise normal or restricted food intake. It is unknown whether binge eating promotes neuroinflammation, similar to that observed following chronic overconsumption of a high fat diet [...] Read more.
Elevated proinflammatory cytokines were reported in binge eating spectrum disorders characterized by intermittent overconsumption during periods of otherwise normal or restricted food intake. It is unknown whether binge eating promotes neuroinflammation, similar to that observed following chronic overconsumption of a high fat diet (HFD) in rodents. Here, we used a rodent model of binge-like eating to test the hypothesis that intermittent overconsumption of HFD promotes microglial reactivity in brain areas that control food intake. To promote overconsumption, one group of rats received chow plus intermittent access to HFD (INT). Control groups received either chow only (CHOW) or chow plus continuous access to HFD (CONT). Following behavioral testing, brains were processed to visualize ionized calcium-binding adaptor molecule 1 (Iba1), a microglial marker. INT rats consumed more calories than the control rats on days when the HFD was available, and fewer calories than the control rats on days when they only had access to chow. Despite consuming fewer total calories and 50% fewer fat calories, lean INT rats developed a pattern of microglial reactivity in feeding-relevant brain areas similar to obese CONT rats. We conclude that intermittent overconsumption of HFD, without diet-induced weight gain, promotes microglial reactivity in brain regions that control feeding. Full article
(This article belongs to the Special Issue Neural Mechanisms of Eating Disorders and Obesity)
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26 pages, 9444 KiB  
Article
SIK2 Controls the Homeostatic Character of the POMC Secretome Acutely in Response to Pharmacological ER Stress Induction
by Mehmet Soner Türküner, Ayşe Yazıcı and Ferruh Özcan
Cells 2024, 13(18), 1565; https://doi.org/10.3390/cells13181565 - 17 Sep 2024
Viewed by 1580
Abstract
The neuronal etiology of obesity is centered around a diet-induced inflammatory state in the arcuate nucleus of the hypothalamus, which impairs the functionality of pro-opiomelanocortine neurons (POMCs) responsible for whole-body energy homeostasis and feeding behavior. Intriguingly, systemic salt inducible kinase 2 (SIK2) knockout [...] Read more.
The neuronal etiology of obesity is centered around a diet-induced inflammatory state in the arcuate nucleus of the hypothalamus, which impairs the functionality of pro-opiomelanocortine neurons (POMCs) responsible for whole-body energy homeostasis and feeding behavior. Intriguingly, systemic salt inducible kinase 2 (SIK2) knockout mice demonstrated reduced food intake and energy expenditure along with modestly dysregulated metabolic parameters, suggesting a causal link between the absence of SIK2 activity in POMCs and the observed phenotype. To test this hypothesis, we conducted a comparative secretomics study from POMC neurons following pharmacologically induced endoplasmic reticulum (ER) stress induction, a hallmark of metabolic inflammation and POMC dysregulation in diet-induced obese (DIO) mice. Our data provide significant in vitro evidence for the POMC-specific SIK2 activity in controlling energy metabolism and feeding in DIO mice by regulating the nature of the related POMC secretome. Our data also suggest that under physiological stress conditions, SIK2 may act as a gatekeeper for the secreted inflammatory factors and signaling molecules critical for cellular survival and energy homeostasis. On the other hand, in the absence of SIK2, the gate opens, leading to a surge of inflammatory cytokines and apoptotic cues concomitant with the dysregulation of POMC neurons. Full article
(This article belongs to the Special Issue Neural Mechanisms of Eating Disorders and Obesity)
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