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Cao J, Wang X, Chen J, Zhang N, Liu Z. The vagus nerve mediates the stomach-brain coherence in rats. Neuroimage 2022; 263:119628. [PMID: 36113737 PMCID: PMC10008817 DOI: 10.1016/j.neuroimage.2022.119628] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/19/2022] [Revised: 08/20/2022] [Accepted: 09/12/2022] [Indexed: 11/26/2022] Open
Abstract
Interactions between the brain and the stomach shape both cognitive and digestive functions. Recent human studies report spontaneous synchronization between brain activity and gastric slow waves in the resting state. However, this finding has not been replicated in any animal models. The neural pathways underlying this apparent stomach-brain synchrony is also unclear. Here, we performed functional magnetic resonance imaging while simultaneously recording body-surface gastric slow waves from anesthetized rats in the fasted vs. postprandial conditions and performed a bilateral cervical vagotomy to assess the role of the vagus nerve. The coherence between brain fMRI signals and gastric slow waves was found in a distributed "gastric network", including subcortical and cortical regions in the sensory, motor, and limbic systems. The stomach-brain coherence was largely reduced by the bilateral vagotomy and was different between the fasted and fed states. These findings suggest that the vagus nerve mediates the spontaneous coherence between brain activity and gastric slow waves, which is likely a signature of real-time stomach-brain interactions. However, its functional significance remains to be established.
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Affiliation(s)
- Jiayue Cao
- Department of Biomedical Engineering, University of Michigan, Ann Arbor, USA
| | - Xiaokai Wang
- Department of Biomedical Engineering, University of Michigan, Ann Arbor, USA
| | - Jiande Chen
- Division of Gastroenterology and Hepatology, University of Michigan, Ann Arbor, USA
| | - Nanyin Zhang
- Department of Biomedical Engineering, Huck Institutes of the life sciences, Pennsylvania State University, USA
| | - Zhongming Liu
- Department of Biomedical Engineering, University of Michigan, Ann Arbor, USA; Department of Electrical Engineering and Computer Science, University of Michigan, Ann Arbor, USA.
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2
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Kosugi K, Yoshida K, Suzuki T, Kobayashi K, Yoshida K, Mimura M, Tanaka KF. Activation of ventral CA1 hippocampal neurons projecting to the lateral septum during feeding. Hippocampus 2020; 31:294-304. [PMID: 33296119 PMCID: PMC7984357 DOI: 10.1002/hipo.23289] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/15/2020] [Revised: 11/24/2020] [Accepted: 11/27/2020] [Indexed: 01/20/2023]
Abstract
A number of studies have reported the involvement of the ventral hippocampus (vHip) and the lateral septum (LS) in negative emotional responses. Besides these well‐documented functions, they are also thought to control feeding behavior. In particular, optogenetic and pharmacogenetic interventions to LS‐projecting vHip neurons have demonstrated that the vHip→LS neural circuit exerts an inhibition on feeding behavior. However, there have been no reports of vHip neuronal activity during feeding. Here, we focused on LS‐projecting vCA1 neurons (vCA1→LS) and monitored their activity during feeding behaviors in mice. vCA1→LS neurons were retrogradely labeled with adeno‐associated virus carrying a ratiometric Ca2+ indicator and measured compound Ca2+ dynamics by fiber photometry. We first examined vCA1→LS activity in random food‐exploring behavior and found that vCA1→LS activation seemed to coincide with food intake; however, our ability to visually confirm this during freely moving behaviors was not sufficiently reliable. We next examined vCA1→LS activity in a goal‐directed, food‐seeking lever‐press task which temporally divided the mouse state into preparatory, effort, and consummatory phases. We observed vCA1→LS activation in the postprandial period during the consummatory phase. Such timing‐ and pathway‐specific activation was not observed from pan‐vCA1 neurons. In contrast, reward omission eliminated this activity, indicating that vCA1→LS activation is contingent on the food reward. Sated mice pressed the lever significantly fewer times but still ate food; however, vCA1→LS neurons were not activated, suggesting that vCA1→LS neurons did not respond to habitual behavior. Combined, these results suggest that gastrointestinal interoception rather than food‐intake motions or external sensations are likely to coincide with vCA1→LS activity. Accordingly, we propose that vCA1→LS neurons discriminate between matched or unmatched predictive bodily states in which incoming food will satisfy an appetite. We also demonstrate that vCA1→LS neurons are activated in aversive/anxious situations in an elevated plus maze and tail suspension test. Future behavioral tests utilizing anxious conflict and food intake may reconcile the multiple functions of vCA1→LS neurons.
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Affiliation(s)
- Kenzo Kosugi
- Department of Neurosurgery, Keio University School of Medicine, Tokyo, Japan
| | - Keitaro Yoshida
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan
| | - Toru Suzuki
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan
| | - Kenta Kobayashi
- Section of Viral Vector Development, National Institute for Physiological Sciences, Okazaki, Japan
| | - Kazunari Yoshida
- Department of Neurosurgery, Keio University School of Medicine, Tokyo, Japan
| | - Masaru Mimura
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan
| | - Kenji F Tanaka
- Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan
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Gomes TR, Freitas ER, Watanabe PH, Sousa ADR, Ferreira ACS, Tavares LMDS. Cashew nut meal (Anacardium occidentale L.) in the feeding of growing rabbits. CIÊNCIA ANIMAL BRASILEIRA 2020. [DOI: 10.1590/1809-6891v21e-61927] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
Abstract
Abstract Two trials were conducted: (1) to determine the chemical composition, digestibility of nutrients and energy of cashew nut meal (CNM); and (2) to evaluate the effects of increasing its levels (0, 5, 10, 15, 20 and 25%) in diets for growing rabbits on performance, carcass characteristics and economic evaluation. The digestibility assay utilized 24 rabbits (55 days of age), distributed in a completely randomized design with two treatments and 12 repetitions, with one reference and another test feed composed of 70% basal diet and 30% CNM. The digestibility of dry matter, crude protein and gross energy from CNM were, respectively, 76.61, 61.71 and 56.53%. The digestible dry matter, digestible protein and digestible energy were, respectively, 74.28, 16.97 and 3,549 kcal/kg. The performance assay utilized 120 rabbits, with an average of 45 days of age and weight 1090 ± 151g, distributed in a completely randomized design with six treatments and 10 repetitions with two rabbits of the same sex per cage. The inclusion of CNM above 5% promoted a linear reduction in feed intake and improved feed conversion, without affecting weight gain and carcass characteristics to the 20% level of inclusion. There was also a linear reduction in feed cost per kilogram of weight gain and linear improvement in rates of economic efficiency and cost index up to 25% CNM inclusion. Based on these findings - and to not hurt performance - it is recommended to include up to 20% CNM in rabbits' diet.
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Suarez AN, Noble EE, Kanoski SE. Regulation of Memory Function by Feeding-Relevant Biological Systems: Following the Breadcrumbs to the Hippocampus. Front Mol Neurosci 2019; 12:101. [PMID: 31057368 PMCID: PMC6482164 DOI: 10.3389/fnmol.2019.00101] [Citation(s) in RCA: 30] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/14/2019] [Accepted: 04/03/2019] [Indexed: 12/15/2022] Open
Abstract
The hippocampus (HPC) controls fundamental learning and memory processes, including memory for visuospatial navigation (spatial memory) and flexible memory for facts and autobiographical events (declarative memory). Emerging evidence reveals that hippocampal-dependent memory function is regulated by various peripheral biological systems that are traditionally known for their roles in appetite and body weight regulation. Here, we argue that these effects are consistent with a framework that it is evolutionarily advantageous to encode and recall critical features surrounding feeding behavior, including the spatial location of a food source, social factors, post-absorptive processing, and other episodic elements of a meal. We review evidence that gut-to-brain communication from the vagus nerve and from feeding-relevant endocrine systems, including ghrelin, insulin, leptin, and glucagon-like peptide-1 (GLP-1), promote hippocampal-dependent spatial and declarative memory via neurotrophic and neurogenic mechanisms. The collective literature reviewed herein supports a model in which various stages of feeding behavior and hippocampal-dependent memory function are closely linked.
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Affiliation(s)
| | | | - Scott E. Kanoski
- Human and Evolutionary Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, CA, United States
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5
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Hannapel R, Ramesh J, Ross A, LaLumiere RT, Roseberry AG, Parent MB. Postmeal Optogenetic Inhibition of Dorsal or Ventral Hippocampal Pyramidal Neurons Increases Future Intake. eNeuro 2019; 6:ENEURO.0457-18.2018. [PMID: 30693314 PMCID: PMC6348449 DOI: 10.1523/eneuro.0457-18.2018] [Citation(s) in RCA: 28] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/21/2018] [Accepted: 11/21/2018] [Indexed: 01/29/2023] Open
Abstract
Memory of a recently eaten meal can serve as a powerful mechanism for controlling future eating behavior because it provides a record of intake that likely outlasts most physiological signals generated by the meal. In support, impairing the encoding of a meal in humans increases the amount ingested at the next eating episode. However, the brain regions that mediate the inhibitory effects of memory on future intake are unknown. In the present study, we tested the hypothesis that dorsal hippocampal (dHC) and ventral hippocampal (vHC) glutamatergic pyramidal neurons play a critical role in the inhibition of energy intake during the postprandial period by optogenetically inhibiting these neurons at specific times relative to a meal. Male Sprague Dawley rats were given viral vectors containing CaMKIIα-eArchT3.0-eYFP or CaMKIIα-GFP and fiber optic probes into dHC of one hemisphere and vHC of the other. Compared to intake on a day in which illumination was not given, inhibition of dHC or vHC glutamatergic neurons after the end of a chow, sucrose, or saccharin meal accelerated the onset of the next meal and increased the amount consumed during that next meal when the neurons were no longer inhibited. Inhibition given during a meal did not affect the amount consumed during that meal or the next one but did hasten meal initiation. These data show that dHC and vHC glutamatergic neuronal activity during the postprandial period is critical for limiting subsequent ingestion and suggest that these neurons inhibit future intake by consolidating the memory of the preceding meal.
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Affiliation(s)
- Reilly Hannapel
- Neuroscience Institute, Georgia State University, Atlanta, GA 30303
| | - Janavi Ramesh
- Neuroscience Institute, Georgia State University, Atlanta, GA 30303
| | - Amy Ross
- Neuroscience Institute, Georgia State University, Atlanta, GA 30303
| | - Ryan T. LaLumiere
- Department of Psychological and Brain Sciences and Iowa Neuroscience Institute, University of Iowa, Iowa City, IA 52242
| | - Aaron G. Roseberry
- Neuroscience Institute, Georgia State University, Atlanta, GA 30303
- Department of Biology, Georgia State University, Atlanta, GA 30303
| | - Marise B. Parent
- Neuroscience Institute, Georgia State University, Atlanta, GA 30303
- Department of Psychology, Georgia State University, Atlanta, GA 30303
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6
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Barth BB, Shen X. Computational motility models of neurogastroenterology and neuromodulation. Brain Res 2018; 1693:174-179. [PMID: 29903620 PMCID: PMC6671680 DOI: 10.1016/j.brainres.2018.02.038] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/16/2017] [Revised: 01/18/2018] [Accepted: 02/24/2018] [Indexed: 01/15/2023]
Abstract
The success of neuromodulation therapies, particularly in the brain, spinal cord, and peripheral nerves, has been greatly aided by computational, biophysical models. However, treating gastrointestinal disorders with electrical stimulation has been much less explored, partly because the mode of action of such treatments is unclear, and selection of stimulation parameters is often empirical. Progress in gut neuromodulation is limited by the comparative lack of biophysical models capable of simulating neuromodulation of gastrointestinal function. Here, we review the recently developed biophysical models of electrically-active cells in the gastrointestinal system that contribute to motility. Biophysical models are replacing phenomenologically-defined models due to advancements in electrophysiological characterization of key players in the gut: enteric neurons, smooth muscle fibers, and interstitial cells of Cajal. In this review, we explore existing biophysically-defined cellular and network models that contribute to gastrointestinal motility. We focus on recent models that are laying the groundwork for modeling electrical stimulation of the gastrointestinal system. Developing models of gut neuromodulation will improve our mechanistic understanding of these treatments, leading to better parameterization, selectivity, and efficacy of neuromodulation to treat gastrointestinal disorders. Such models may have direct clinical translation to current neuromodulation therapies, such as sacral nerve stimulation.
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Affiliation(s)
- Bradley B Barth
- Department of Biomedical Engineering, Duke University, Room 2141, CIEMAS, 101 Science Drive, Durham, NC, USA.
| | - Xiling Shen
- Department of Biomedical Engineering, Duke University, Room 2167, CIEMAS, 101 Science Drive, Durham, NC, USA.
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7
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Abstract
Research and clinical experience with vagotomy have confirmed that damage to the central nervous system severely affects physiological movement in the gastrointestinal system. The aim of this study was to investigate the effects of synchronized dual-pulse gastric electrical stimulation (SGES) on the apoptosis of enteric neurons and the possible pathways involved in these effects in vagotomized rats. For this purpose, Male Sprague-Dawley (SD) rats were randomized into a control group, an early subdiaphragmatic vagotomized group (ESDV group), an early subdiaphragmatic vagotomized group with short-term SGES (ESDV + SSGES group), a terminal subdiaphragmatic vagotomized group (TSDV group) and a terminal subdiaphragmatic vagotomized group with long-term SGES (TSDV + LSGES group). The expression levels of connexin 43 (Cx43), glial cell line-derived neurotrophic factor (GDNF), p-Akt, pan-Akt and PGP9.5 were assessed by RT-qPCR, western blot analysis and immunofluorescence staining. Apoptosis was determined by terminal-deoxynucleoitidyl transferase-mediated nick-end labeling (TUNEL) assay. We found that Cx43 expression was decreased in the ESDV and TSDV groups, but was significantly upregulated in the SSGES and LSGES groups. In addition, the GDNF and PGP9.5 expression levels were significantly decreased in the ESDV group compared with the control and TSDV groups and were upregulated in both the SSGES and LSGES groups. The LSGES group exhibited a clear increase in p-Akt expression compared with the TSDV group. Fewer TUNEL-positive cells were observed in the SSGES and LSGES groups than in the ESDV and TSDV groups. More TUNEL-positive cells were found in the stomach of rats subjected to subdiaphragmatic vagotomy. On the whole, our data indicate that SGES improved enteric neuronal survival, possibly through GDNF and the phosphatidylinositol 3-kinase (PI3K)/Akt pathways.
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Affiliation(s)
- Nian Wang
- Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China
| | - Kun Li
- Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China
| | - Shuangning Song
- Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China
| | - Jie Chen
- Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China
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8
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Parent MB. Cognitive control of meal onset and meal size: Role of dorsal hippocampal-dependent episodic memory. Physiol Behav 2016; 162:112-9. [PMID: 27083124 DOI: 10.1016/j.physbeh.2016.03.036] [Citation(s) in RCA: 18] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/05/2016] [Revised: 03/28/2016] [Accepted: 03/30/2016] [Indexed: 12/17/2022]
Abstract
There is a large gap in our understanding of how top-down cognitive processes, such as memory, influence energy intake. Similarly, there is limited knowledge regarding how the brain controls the timing of meals and meal frequency. Understanding how cognition influences ingestive behavior and how the brain controls meal frequency will provide a more complete explanation of the neural mechanisms that regulate energy intake and may also increase our knowledge of the factors that contribute to diet-induced obesity. We hypothesize that dorsal hippocampal neurons, which are critical for memory of personal experiences (i.e., episodic memory), form a memory of a meal, inhibit meal onset during the period following a meal, and limit the amount ingested at the next meal. In support, we describe evidence from human research suggesting that episodic memory of a meal inhibits intake and review data from human and non-human animals showing that impaired hippocampal function is associated with increased intake. We then describe evidence from our laboratory showing that inactivation of dorsal hippocampal neurons decreases the interval between sucrose meals and increases intake at the next meal. We also describe our evidence suggesting that sweet orosensation is sufficient to induce synaptic plasticity in dorsal hippocampal neurons and raise the possibility that impaired dorsal hippocampal function and episodic memory deficits contribute to the development and/or maintenance of diet-induced obesity. Finally, we raise some critical questions that need to be addressed in future research.
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Affiliation(s)
- Marise B Parent
- Neuroscience Institute, Department of Psychology, Georgia State University, PO Box 5030, Atlanta, GA 30303-5030, United States.
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9
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Ji X, Li D, Li H. Preparation and application of a novel molecularly imprinted solid-phase microextraction monolith for selective enrichment of cholecystokinin neuropeptides in human cerebrospinal fluid. Biomed Chromatogr 2015; 29:1280-9. [DOI: 10.1002/bmc.3418] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/08/2014] [Revised: 11/15/2014] [Accepted: 11/28/2014] [Indexed: 11/10/2022]
Affiliation(s)
- Xiang Ji
- College of Chemistry and Molecular Sciences; Wuhan University; Wuhan 430072 China
| | - Dan Li
- College of Chemistry and Molecular Sciences; Wuhan University; Wuhan 430072 China
| | - Hua Li
- College of Chemistry and Molecular Sciences; Wuhan University; Wuhan 430072 China
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10
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Xu L, Li Z, Guo F. Curcumin improves expression of ghrelin through attenuating oxidative stress in gastric tissues of streptozotocin-induced diabetic gastroparesis rats. Eur J Pharmacol 2013; 718:219-25. [DOI: 10.1016/j.ejphar.2013.08.030] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/31/2013] [Revised: 08/14/2013] [Accepted: 08/30/2013] [Indexed: 12/14/2022]
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Panickar KS. Effects of dietary polyphenols on neuroregulatory factors and pathways that mediate food intake and energy regulation in obesity. Mol Nutr Food Res 2012; 57:34-47. [DOI: 10.1002/mnfr.201200431] [Citation(s) in RCA: 73] [Impact Index Per Article: 5.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/05/2012] [Revised: 08/08/2012] [Accepted: 08/22/2012] [Indexed: 12/20/2022]
Affiliation(s)
- Kiran S. Panickar
- Department of Pediatrics; University of Maryland School of Medicine; Baltimore MD USA
- Diet, Genomics, & Immunology Laboratory; Beltsville Human Nutrition Research Center; Agricultural Research Service; United States Department of Agriculture; Beltsville MD USA
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12
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Mizrahi M, Ben Ya'acov A, Ilan Y. Gastric stimulation for weight loss. World J Gastroenterol 2012; 18:2309-19. [PMID: 22654422 PMCID: PMC3353365 DOI: 10.3748/wjg.v18.i19.2309] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/11/2011] [Revised: 09/02/2011] [Accepted: 04/28/2012] [Indexed: 02/06/2023] Open
Abstract
The prevalence of obesity is growing to epidemic proportions, and there is clearly a need for minimally invasive therapies with few adverse effects that allow for sustained weight loss. Behavior and lifestyle therapy are safe treatments for obesity in the short term, but the durability of the weight loss is limited. Although promising obesity drugs are in development, the currently available drugs lack efficacy or have unacceptable side effects. Surgery leads to long-term weight loss, but it is associated with morbidity and mortality. Gastric electrical stimulation (GES) has received increasing attention as a potential tool for treating obesity and gastrointestinal dysmotility disorders. GES is a promising, minimally invasive, safe, and effective method for treating obesity. External gastric pacing is aimed at alteration of the motility of the gastrointestinal tract in a way that will alter absorption due to alteration of transit time. In addition, data from animal models and preliminary data from human trials suggest a role for the gut-brain axis in the mechanism of GES. This may involve alteration of secretion of hormones associated with hunger or satiety. Patient selection for gastric stimulation therapy seems to be an important determinant of the treatment’s outcome. Here, we review the current status, potential mechanisms of action, and possible future applications of gastric stimulation for obesity.
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13
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Gallas S, Fetissov SO. Ghrelin, appetite and gastric electrical stimulation. Peptides 2011; 32:2283-9. [PMID: 21672567 DOI: 10.1016/j.peptides.2011.05.027] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/13/2011] [Revised: 05/26/2011] [Accepted: 05/27/2011] [Indexed: 12/18/2022]
Abstract
Ghrelin is a peptide hormone produced mainly by the stomach and has widespread physiological functions including increase in appetite. The stimulation of the ghrelin system represents a potential therapeutic approach in various disorders characterized by deficient ghrelin signaling or by low appetite. This stimulation may be achieved via pharmacological targeting of the ghrelin receptor with synthetic ghrelin or ghrelin mimetics or via increased endogenous ghrelin production. Recently, it was demonstrated that gastric electrical stimulation (GES) with Enterra parameters results in increased ghrelin production in rats. Furthermore, recent data revealed putative role of ghrelin-reactive immunoglobulins in the modulation of the ghrelin signaling which can be also stimulated by GES. Here, we review the links between GES and ghrelin in existing GES experimental and clinical applications for treatment of gastroparesis, functional dyspepsia or obesity and discuss if GES can be proposed as a non-pharmacological approach to improve ghrelin secretion in several pathological conditions characterized by low appetite, such as anorexia nervosa or anorexia-cachexia syndrome.
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Affiliation(s)
- Syrine Gallas
- Digestive System & Nutrition Laboratory, ADEN EA4311, Rouen University, IFR23, Rouen 76183, France
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14
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Min DK, Tuor UI, Chelikani PK. Gastric distention induced functional magnetic resonance signal changes in the rodent brain. Neuroscience 2011; 179:151-8. [PMID: 21284950 DOI: 10.1016/j.neuroscience.2011.01.051] [Citation(s) in RCA: 45] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/26/2010] [Revised: 01/14/2011] [Accepted: 01/23/2011] [Indexed: 12/29/2022]
Abstract
Investigating the localization of gastric sensation within the brain is important for understanding the neural correlates of satiety. Previous rodent studies have identified the brain-stem and hypothalamus as key mediators of gastric distention-induced satiation. Although, recent blood oxygen level-dependent functional magnetic resonance imaging (BOLD fMRI) studies in humans have identified a role for higher cortico-limbic structures in mediating the satiation effects of gastric distention, the role of these regions in rodents remains to be characterized. We determined the effects of gastric distention on global spatio-temporal BOLD fMRI signal changes in the rodent brain. Brain images were acquired with a high resolution 9.4 T magnet during gastric distention with continuous monitoring of blood pressure in adult male Sprague Dawley rats (n=8-10). Distention of the stomach with an intragastric balloon, at rates which mimicked the rate of consumption and emptying of a mixed nutrient liquid meal, resulted in robust reduction in food intake and increase in blood pressure. Gastric distention increased BOLD fMRI activity within homeostatic regions such as the hypothalamus and nucleus tractus solitarius, as well as non homeostatic regions including the hippocampus, amygdala, thalamus, cerebellum and the cortex (cingulate, insular, motor and sensory cortices). Further, the increase in BOLD fMRI activity following distention was strongly correlated to an increase in blood pressure. These results indicate that gastric distention, mimicking the rate of intake and emptying of a liquid meal, increases BOLD fMRI activity in both homeostatic and non homeostatic brain circuits which regulate food intake, and that these BOLD fMRI signal changes may in part be attributable to transient increases in blood pressure.
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Affiliation(s)
- D K Min
- Gastrointestinal Research Group, Department of Production Animal Health, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada
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15
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Panickar K, Bhathena S. Control of Fatty Acid Intake and the Role of Essential Fatty Acids in Cognitive Function and Neurological Disorders. Front Neurosci 2009. [DOI: 10.1201/9781420067767-c18] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/11/2022] Open
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16
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Xu L, Sun X, Tang M, Chen JDZ. Involvement of the Hippocampus and Neuronal Nitric Oxide Synapse in the Gastric Electrical Stimulation Therapy for Obesity. Obes Surg 2008; 19:475-83. [DOI: 10.1007/s11695-008-9579-7] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/08/2008] [Accepted: 05/19/2008] [Indexed: 11/27/2022]
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