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Cells
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Inter-organ Crosstalk in Energy Homeostasis
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Inter-organ Crosstalk in Energy Homeostasis

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 7289

Special Issue Editors

Prof. Dr. Claude Knauf

E-Mail Website
Guest Editor
Physiopathology of the Gut Brain Axis, Digestive Health Research Institute (IRSD), Inserm U1220, 31024 Toulouse, France
Interests: obesity; diabetes; gut–brain axis
Dr. Lionel Carneiro

E-Mail Website
Guest Editor
Research Group, Physiopathology of the Gut Brain Axis, Digestive Health Research Institute (IRSD), Inserm U1220, 31024 Toulouse, France
Interests: metabolism; neuroscience; gut-brain axis; obesity and diabetes
Special Issues, Collections and Topics in MDPI journals
Dr. Camille Allard

E-Mail Website
Guest Editor
Energy Balance and Obesity, Neurocentre Magendie, University of Bordeaux, U1215 Inserm, France
Interests: brain; metabolism; diabetes; obesity; glial cells; pancreatic islets

Special Issue Information

Dear Colleagues,

Metabolic disorders, including diabetes and obesity, are on the rise in modern societies despite research efforts to tackle what is now considered a pandemic. Energy homeostasis involves a wide range of mechanisms, tissues and organs. Interestingly, all these partners are interacting with each other to maintain energy balance in physiological conditions. The central nervous system plays a key role by being strongly involved in the coordination of all these mechanisms. The brain constantly receives various signals (nutrients, metabolites, hormones, neural inputs, etc.) from peripheral organs (gut, liver, pancreas, adipose tissue, etc.), providing information on the body energy status. In addition to the brain, the peripheral organs can also sense multiple circulating cues, neural cues, or both, which ultimately leads to metabolic adaptations. This complex communication is crucial: considerable evidence of disrupted crosstalk has been reported between the brain and the periphery, but also between peripheral organs themselves in the development and maintenance of metabolic diseases. Therefore, a harmonious inter-organ collaboration is determinant for maintaining energy balance.

In this Special Issue we aim to bring together a collection of recent data exploring the complex relationships between the central nervous system and peripheral organs for energy homeostasis regulation. Specific areas of interest include but are not limited to nutrient sensing, gut–brain axis, brain–periphery communication, inter-organ communication, obesity, diabetes and nutrition.

Prof. Dr. Claude Knauf
Dr. Lionel Carneiro
Dr. Camille Allard
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

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

  • energy homeostasis
  • brain–periphery
  • obesity
  • diabetes
  • nutrition
  • endocrinology

Published Papers (3 papers)

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Research

19 pages, 3778 KiB  
Article
High-Fat Diet Modulates the Excitability of Neurons within the Brain–Liver Pathway
by Adrien J. R. Molinas, Lucie D. Desmoulins, Roslyn K. Davis, Hong Gao, Ryousuke Satou, Andrei V. Derbenev and Andrea Zsombok
Cells 2023, 12(8), 1194; https://doi.org/10.3390/cells12081194 - 20 Apr 2023
Cited by 3 | Viewed by 1397
Abstract
Stimulation of hepatic sympathetic nerves increases glucose production and glycogenolysis. Activity of pre-sympathetic neurons in the paraventricular nucleus (PVN) of the hypothalamus and in the ventrolateral and ventromedial medulla (VLM/VMM) largely influence the sympathetic output. Increased activity of the sympathetic nervous system (SNS) [...] Read more.
Stimulation of hepatic sympathetic nerves increases glucose production and glycogenolysis. Activity of pre-sympathetic neurons in the paraventricular nucleus (PVN) of the hypothalamus and in the ventrolateral and ventromedial medulla (VLM/VMM) largely influence the sympathetic output. Increased activity of the sympathetic nervous system (SNS) plays a role in the development and progression of metabolic diseases; however, despite the importance of the central circuits, the excitability of pre-sympathetic liver-related neurons remains to be determined. Here, we tested the hypothesis that the activity of liver-related neurons in the PVN and VLM/VMM is altered in diet-induced obese mice, as well as their response to insulin. Patch-clamp recordings were conducted from liver-related PVN neurons, VLM-projecting PVN neurons, and pre-sympathetic liver-related neurons in the ventral brainstem. Our data demonstrate that the excitability of liver-related PVN neurons increased in high-fat diet (HFD)-fed mice compared to mice fed with control diet. Insulin receptor expression was detected in a population of liver-related neurons, and insulin suppressed the firing activity of liver-related PVN and pre-sympathetic VLM/VMM neurons in HFD mice; however, it did not affect VLM-projecting liver-related PVN neurons. These findings further suggest that HFD alters the excitability of pre-autonomic neurons as well as their response to insulin. Full article
(This article belongs to the Special Issue Inter-organ Crosstalk in Energy Homeostasis)
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21 pages, 6824 KiB  
Article
Intermittent Fasting Resolves Dyslipidemia and Atherogenesis in Apolipoprotein E-Deficient Mice in a Diet-Dependent Manner, Irrespective of Sex
by Jules Mérian, Lamia Ghezali, Charlotte Trenteseaux, Thibaut Duparc, Diane Beuzelin, Vanessa Bouguetoch, Guillaume Combes, Nabil Sioufi, Laurent O. Martinez and Souad Najib
Cells 2023, 12(4), 533; https://doi.org/10.3390/cells12040533 - 07 Feb 2023
Cited by 2 | Viewed by 2822
Abstract
In humans and animal models, intermittent fasting (IF) interventions promote body weight loss, improve metabolic health, and are thought to lower cardiovascular disease risk. However, there is a paucity of reports on the relevance of such nutritional interventions in the context of dyslipidemia [...] Read more.
In humans and animal models, intermittent fasting (IF) interventions promote body weight loss, improve metabolic health, and are thought to lower cardiovascular disease risk. However, there is a paucity of reports on the relevance of such nutritional interventions in the context of dyslipidemia and atherosclerotic cardiovascular diseases. The present study assessed the metabolic and atheroprotective effects of intermittent fasting intervention (IF) in atherosclerosis-prone apolipoprotein E-deficient (Apoe-/-) mice. Groups of male and female Apoe-/- mice were fed a regular (chow) or atherogenic (high-fat, high-cholesterol, HFCD) diet for 4 months, either ad libitum or in an alternate-day fasting manner. The results show that IF intervention improved glucose and lipid metabolism independently of sex. However, IF only decreased body weight gain in males fed chow diet and differentially modulated adipose tissue parameters and liver steatosis in a diet composition-dependent manner. Finally, IF prevented spontaneous aortic atherosclerotic lesion formation in mice fed chow diet, irrespective of sex, but failed to reduce HFCD-diet-induced atherosclerosis. Overall, the current work indicates that IF interventions can efficiently improve glucose homeostasis and treat atherogenic dyslipidemia, but a degree of caution is warranted with regard to the individual sex and the composition of the dietary regimen. Full article
(This article belongs to the Special Issue Inter-organ Crosstalk in Energy Homeostasis)
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19 pages, 7543 KiB  
Article
Homocysteine Metabolism Pathway Is Involved in the Control of Glucose Homeostasis: A Cystathionine Beta Synthase Deficiency Study in Mouse
by Céline Cruciani-Guglielmacci, Kelly Meneyrol, Jessica Denom, Nadim Kassis, Latif Rachdi, Fatna Makaci, Stéphanie Migrenne-Li, Fabrice Daubigney, Eleni Georgiadou, Raphaël G. Denis, Ana Rodriguez Sanchez-Archidona, Jean-Louis Paul, Bernard Thorens, Guy A. Rutter, Christophe Magnan, Hervé Le Stunff and Nathalie Janel
Cells 2022, 11(11), 1737; https://doi.org/10.3390/cells11111737 - 25 May 2022
Cited by 5 | Viewed by 2288
Abstract
Cystathionine beta synthase (CBS) catalyzes the first step of the transsulfuration pathway from homocysteine to cystathionine, and its deficiency leads to hyperhomocysteinemia (HHcy) in humans and rodents. To date, scarce information is available about the HHcy effect on insulin secretion, and the link [...] Read more.
Cystathionine beta synthase (CBS) catalyzes the first step of the transsulfuration pathway from homocysteine to cystathionine, and its deficiency leads to hyperhomocysteinemia (HHcy) in humans and rodents. To date, scarce information is available about the HHcy effect on insulin secretion, and the link between CBS activity and the setting of type 2 diabetes is still unknown. We aimed to decipher the consequences of an inborn defect in CBS on glucose homeostasis in mice. We used a mouse model heterozygous for CBS (CBS+/−) that presented a mild HHcy. Other groups were supplemented with methionine in drinking water to increase the mild to intermediate HHcy, and were submitted to a high-fat diet (HFD). We measured the food intake, body weight gain, body composition, glucose homeostasis, plasma homocysteine level, and CBS activity. We evidenced a defect in the stimulated insulin secretion in CBS+/− mice with mild and intermediate HHcy, while mice with intermediate HHcy under HFD presented an improvement in insulin sensitivity that compensated for the decreased insulin secretion and permitted them to maintain a glucose tolerance similar to the CBS+/+ mice. Islets isolated from CBS+/− mice maintained their ability to respond to the elevated glucose levels, and we showed that a lower parasympathetic tone could, at least in part, be responsible for the insulin secretion defect. Our results emphasize the important role of Hcy metabolic enzymes in insulin secretion and overall glucose homeostasis. Full article
(This article belongs to the Special Issue Inter-organ Crosstalk in Energy Homeostasis)
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