scholarly journals The Role of Glial Cells in Regulating Feeding Behavior: Potential Relevance to Anorexia Nervosa

2021 ◽  
Vol 11 (1) ◽  
pp. 186
Author(s):  
Linda Frintrop ◽  
Stefanie Trinh ◽  
Jochen Seitz ◽  
Markus Kipp
Keyword(s):  
Anorexia Nervosa ◽  
Food Intake ◽  
Eating Behavior ◽  
Drug Targets ◽  
Cell Function ◽  
Brain Regions ◽  
Glia Cells ◽  
Brain Volume Loss ◽  
Complex Process ◽  
The Central Nervous System

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.

Naltrexone administered to central nucleus of amygdala or PVN: neural dissociation of diet and energy

2000 ◽  
Vol 279 (1) ◽  
pp. R86-R92 ◽  
Author(s):  
Michael J. Glass ◽  
Charles J. Billington ◽  
Allen S. Levine
Keyword(s):  
Food Intake ◽  
Food Consumption ◽  
Neural Circuitry ◽  
Brain Regions ◽  
Wide Distribution ◽  
Central Nucleus ◽  
Total Energy Consumption ◽  
Direct Stimulation ◽  
The Central Nervous System ◽  
Diet Intake

There is evidence that opioids may affect food consumption through mechanisms as diverse as reward or energy metabolism. However, these hypotheses are derived from studies employing peripheral or, more rarely, intracerebroventricular administration of drugs. Opioid receptors have a wide distribution in the central nervous system and include a number of regions implicated in food intake such as the hypothalamic paraventricular nucleus (PVN) and the central nucleus of the amygdala (ACe). It is not known whether local opioid receptor blockade in either of these regions will produce similar effects on food intake. To examine this issue, a chronic cannula was aimed at either the PVN or ACe of rats that were fed a choice of a high-fat and high-carbohydrate diet, which allows for the measurement of both preference and total energy consumption. Naltrexone influenced preferred and nonpreferred food consumption, depending on the site of administration. Consumption of both preferred and nonpreferred diets was suppressed after PVN naltrexone administration, whereas only preferred diet intake was reduced after ACe injection of naltrexone. The present evidence indicates that direct stimulation of different brain regions with naltrexone may be associated with diverse effects on diet selection, which may be accounted for by manipulation of specific functional neural circuitry.

scholarly journals Structural and functional changes in the central nervous system in the course of anorexia nervosa

2017 ◽  
Vol 18 (4) ◽  
pp. 321-330
Author(s):  
Michał Hys ◽  
Nikodem Skoczeń ◽  
Ewelina Soroka ◽  
Marcin Olajossy
Keyword(s):  
Central Nervous System ◽  
Eating Disorders ◽  
Nervous System ◽  
Anorexia Nervosa ◽  
White Matter ◽  
Food Intake ◽  
Brain Regions ◽  
Fiber Tractography ◽  
Functional Changes ◽  
The Brain

AbstractNew achievements within structural and functional imaging of central nervous system offer a basis for better understanding of the mechanisms underlying many mental disorders. In everyday clinical practice, we encounter many difficulties in the therapy of eating disorders. They are caused by a complex psychopathological picture, varied grounds of the problems experienced by patients, often poor motivation for active participation in the treatment process, difficulties in communication between patients and therapeutic staff, and various biological conditions of eating disorders. In this paper, the latest reports on new concepts and methods of diagnosis and treatment of anorexia nervosa have been analyzed. The selection of the analyzed publications was based on the criteria taking into account the time of publication, the size of research cohorts, as well as the experience of research teams in the field of nutritional disorders, confirmed by the number of works and their citations. The work aims to spread current information on anorexia nervosa neurobiology that would allow for determining the brain regions involved in the regulation of food intake, and consequently that may be a potential place where neurobiochemical processes responsible for eating disorders occur. In addition, using modern methods of structural imaging, the authors want to show some of the morphometric variations, particularly within white matter, occurring in patients suffering from anorexia nervosa, as well as those evaluated with magnetoencephalography of processes associated with the neuronal processing of information related to food intake. For example as regards anorexia nervosa, it was possible to localize the areas associated with eating disorders and broaden our knowledge about the changes in these areas that cause and accompany the illness. The described in this paper research studies using diffusion MRI fiber tractography showed the presence of changes in the white matter pathways of the brain, especially in the corpus callosum, which indicate a reduced content of myelin. These changes probably reflect malnutrition, and directly represent the effect of lipid deficiency. This leads to a weakening of the structure, and even cell death. In addition, there are more and more reports that show the normal volume of brain cells in patients with long-term remission of anorexia. It was also shown that in patients in remission stage there are functional changes within the amygdala in response to a task not related symptomatologically with anorexia nervosa. The appearing in the scientific literature data stating that in patients with anorexia nervosa there is a reduced density of GFAP + cells of the hippocampus and increased expression of vimentin and nestin, is also worth noting.

scholarly journals Forebrain melanocortin signaling enhances the hindbrain satiety response to CCK-8

2009 ◽  
Vol 296 (3) ◽  
pp. R476-R484 ◽  
Author(s):  
James E. Blevins ◽  
Gregory J. Morton ◽  
Diana L. Williams ◽  
David W. Caldwell ◽  
Lloyd S. Bastian ◽  
...  
Keyword(s):  
Food Intake ◽  
Nucleus Tractus Solitarius ◽  
Brain Regions ◽  
Pcr Analysis ◽  
Satiety Response ◽  
Cholera Toxin Subunit B ◽  
The Central Nervous System ◽  
Regulate Food Intake ◽  
Melanocortin Signaling ◽  
Laser Capture

Melanocortin 4 receptors (MC4R) are hypothesized to mediate the central nervous system actions of leptin to enhance the satiety effects of cholecystokinin (CCK). To further elucidate this mechanism, we confirmed that peripheral administration of CCK-8 is less effective in producing this effect in MC4R-deficient mice (MC4R−/−). Whereas intraperitoneal (ip) CCK-8 at 0.75 nmol/kg lean body mass (lbm) suppressed food intake in wild-type mice, CCK-8 doses of 7.5 nmol/kg lbm were required to attenuate food intake in MC4R−/− mice. To determine whether melanocortin signaling in the hypothalamic paraventricular nucleus (PVN) participates in regulating this CCK satiety response, we administered the MC3/MC4R antagonist, SHU9119, into the PVN of rats before ip CCK-8 administration. PVN administration of SHU9119 attenuated the ability of CCK-8 to reduce 30-min food intake by 20%. To determine whether MC4R are expressed by PVN neurons that project directly to hindbrain nuclei involved in the satiety response to ip CCK-8, the retrograde tracer fluorescent cholera toxin subunit B was injected into the nucleus tractus solitarius (NTS) of the hindbrain. After 4 days, labeled PVN neurons were collected by laser capture microdissection and found to express MC4R mRNA by quantitative RT-PCR analysis. These data provide evidence for a neuroanatomical link between hypothalamic melanocortin signaling in the PVN and NTS neurons that regulate food intake. These findings highlight the contribution of melanocortin signaling in the PVN toward regulating the satiety effects of CCK-8 while acknowledging that melanocortin-dependent pathways in other brain regions and/or melanocortin-independent mechanisms are also important in this mechanism.

scholarly journals Immediate and Prolonged Patterns of Agouti-Related Peptide-(83–132)-Induced c-Fos Activation in Hypothalamic and Extrahypothalamic Sites*

Endocrinology ◽  
2001 ◽  
Vol 142 (3) ◽  
pp. 1050-1056 ◽  
Author(s):  
Mary M. Hagan ◽  
Stephen C. Benoit ◽  
Paul A. Rushing ◽  
Laurel M. Pritchard ◽  
Stephen C. Woods ◽  
...  
Keyword(s):  
Food Intake ◽  
Single Injection ◽  
Brain Regions ◽  
Lateral Septum ◽  
Short Term ◽  
Related Peptide ◽  
Sustained Effect ◽  
Orexigenic Peptide ◽  
The Central Nervous System

Abstract Several lines of evidence substantiate the important role of the central nervous system melanocortin 3- and 4-receptor (MC3/4-R) system in the control of food intake and energy balance. Agouti-related peptide (AgRP), an endogenous antagonist of these receptors, produces a robust and unique pattern of increased food intake that lasts up to 7 days after a single injection. Little is known about brain regions that may mediate this powerful effect of AgRP on food intake. To this end we compared c-Fos-like immunoreactivity (c-FLI) in several brain sites of rats injected intracerebroventricularly with 1 nmol AgRP-(83–132) 2 and 24 h before death and compared c-FLI patterns to those induced by another potent orexigenic peptide, neuropeptide Y (NPY). Although both NPY and AgRP induced c-FLI in hypothalamic areas, AgRP also produced increased c-FLI in the accumbens shell and lateral septum. Although NPY elicited no changes in c-FLI 24 h after administration, AgRP induced c-FLI in the accumbens shell, nucleus of the solitary tract, central amygdala, and lateral hypothalamus. These results indicate that an NPY-like hypothalamic circuit mediates the short-term effects of AgRP, but that the unique sustained effect of AgRP on food intake involves a complex circuit of key extrahypothalamic reward and feeding regulatory nuclei.

scholarly journals Cybernetic principles in the systematic concept of hypothalamic feeding control

2006 ◽  
Vol 154 (2) ◽  
pp. 167-173 ◽  
Author(s):  
Oliver Fricke ◽  
Gerd Lehmkuhl ◽  
Donald W Pfaff
Keyword(s):  
Anorexia Nervosa ◽  
Food Intake ◽  
20Th Century ◽  
Eating Behavior ◽  
Large Field ◽  
Biological Mechanisms ◽  
Hypothalamic Control ◽  
Biological Concepts ◽  
Hypothalamic Function ◽  
Feeding Control

Research on biological mechanisms of eating behavior and related disorders, such as obesity and anorexia nervosa, has become a large field of research in the last 15 years. With the discovery of peptides related to hypothalamic control of food intake (e.g. leptin and ghrelin) the search for the biological ‘master key’ of feeding control was renewed. As a result, mid-20th century biological concepts based on systematic and cybernetic thoughts fell into oblivion. This review highlights discoveries of hypothalamic-controlled feeding and eating behavior with a cybernetic and systematic perspective. Interestingly, older ideas of hypothalamic function offer possibilities for the incorporation of new molecular discoveries into systematic concepts of feeding behavior.

Central Histamine, the H3-Receptor and Obesity Therapy

2019 ◽  
Vol 18 (7) ◽  
pp. 516-522
Author(s):  
Néstor F. Díaz ◽  
Héctor Flores-Herrera ◽  
Guadalupe García-López ◽  
Anayansi Molina-Hernández
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Animal Studies ◽  
Energy Homeostasis ◽  
Receptor Activation ◽  
Receptor Ligands ◽  
Histaminergic System ◽  
H3 Receptor ◽  
Weight One ◽  
The Central Nervous System

The brain histaminergic system plays a pivotal role in energy homeostasis, through H1- receptor activation, it increases the hypothalamic release of histamine that decreases food intake and reduces body weight. One way to increase the release of hypothalamic histamine is through the use of antagonist/inverse agonist for the H3-receptor. Histamine H3-receptors are auto-receptors and heteroreceptors located on the presynaptic membranes and cell soma of neurons, where they negatively regulate the synthesis and release of histamine and other neurotransmitters in the central nervous system. Although several compounds acting as H3-receptor antagonist/inverse agonists have been developed, conflicting results have been reported and only one has been tested as anti-obesity in humans. Animal studies revealed the opposite effect in food intake, energy expeditor, and body weight, depending on the drug, spice, and route of administration, among others. The present review will explore the state of art on the effects of H3-receptor ligands on appetite and body-weight, going through the following: a brief overview of the circuit involved in the control of food intake and energy homeostasis, the participation of the histaminergic system in food intake and body weight, and the H3-receptor as a potential therapeutic target for obesity.

scholarly journals The Gut–Brain Axis and Its Role in Controlling Eating Behavior in Intestinal Inflammation

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 981
Author(s):  
Gordon William Moran ◽  
Gita Thapaliya
Keyword(s):  
Food Intake ◽  
Eating Behavior ◽  
Emotional Eating ◽  
Intestinal Inflammation ◽  
Cognitive Factors ◽  
Anxiety And Depression ◽  
Gut Peptides ◽  
Future Health ◽  
Inflammatory Bowel ◽  
Inflammatory Burden

Malnutrition represents a major problem in the clinical management of the inflammatory bowel disease (IBD). Presently, our understanding of the cross-link between eating behavior and intestinal inflammation is still in its infancy. Crohn’s disease patients with active disease exhibit strong hedonic desires for food and emotional eating patterns possibly to ameliorate feelings of low mood, anxiety, and depression. Impulsivity traits seen in IBD patients may predispose them to palatable food intake as an immediate reward rather than concerns for future health. The upregulation of enteroendocrine cells (EEC) peptide response to food intake has been described in ileal inflammation, which may lead to alterations in gut–brain signaling with implications for appetite and eating behavior. In summary, a complex interplay of gut peptides, psychological, cognitive factors, disease-related symptoms, and inflammatory burden may ultimately govern eating behavior in intestinal inflammation.

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