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Metabolites
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Obesity and Associated Comorbidities: Implications for Neural and Immune Regulation...
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Obesity and Associated Comorbidities: Implications for Neural and Immune Regulation of Energy Metabolism

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (1 March 2023) | Viewed by 13734

Special Issue Editors

Dr. Joana M. Gaspar

E-Mail Website
Guest Editor
Department of Biochemistry, Federal University of Santa Catarina, Florianópolis 88040-900, SC, Brazil
Interests: energy homeostasis; hypothalamus, neuroinflamation; obesity; metabolic diseases; neurodevelopmental diseases; mitochondrial dysfunction
Special Issues, Collections and Topics in MDPI journals
Dr. Natalia F. Mendes

E-Mail Website
Guest Editor
School of Medical Sciences, University of Campinas, Campinas 13083-970, SP, Brazil
Interests: glial cells; immunometabolism; neurogenesis; neuroinflammation; obesity; energy metabolism; metabolic disorders
Special Issues, Collections and Topics in MDPI journals
Dr. Silvia Ravera

E-Mail Website
Guest Editor
Department of Experimental Medicine, University of Genoa, 16132 Genova, Italy
Interests: neuronal energy metabolism; multiple sclerosis; peripheral neuropathies; cancer biology; biochemistry; cell biology; mitochondria biogenesis and dynamics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The brain modulates several aspects of metabolism, integrating metabolic inputs from the periphery through nutrients, gut-derived satiety signals and adiposity-related hormones. Highly coordinated interactions between the brain and peripheral metabolic organs are critical for the maintenance of energy, glucose and lipid homeostasis.

Defective crosstalk between the brain and peripheral organs contributes to the development of metabolic disorders, namely obesity and type 2 diabetes. This Special Issue highlights the brain’s regulation of energy metabolism. Specific areas include, but are not limited to, the identification of molecular mechanisms of hypothalamic regulation of food intake, energy expenditure and liver metabolism, the role of microbiota and the gut–brain axis in energy homeostasis, obesity-induced neuroinflammation and dysregulation of brain metabolism, and molecular targets for obesity treatment. Manuscripts dealing with other pertinent challenging issues are also highly encouraged.

Dr. Joana M. Gaspar
Dr. Natalia F. Mendes
Dr. Silvia Ravera
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. Metabolites is an international peer-reviewed open access monthly 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

  • brain metabolism
  • neuroinflammation
  • energy homeostasis
  • obesity
  • mitochondrial dysfunction
  • gut–brain axis
  • nutrient sensing
  • neurogenesis
  • glial cells

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Published Papers (4 papers)

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Research

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13 pages, 2240 KiB  
Article
Effects of APOE Genotype and Western Diet on Metabolic Phenotypes in Female Mice
by Amy Christensen and Christian J. Pike
Metabolites 2023, 13(2), 287; https://doi.org/10.3390/metabo13020287 - 16 Feb 2023
Cited by 1 | Viewed by 2253
Abstract
Western diets high in sugars and saturated fats have been reported to induce metabolic and inflammatory impairments that are associated with several age-related disorders, including Alzheimer’s disease (AD) and type 2 diabetes (T2D). The apolipoprotein E (APOE) genotype is associated with [...] Read more.
Western diets high in sugars and saturated fats have been reported to induce metabolic and inflammatory impairments that are associated with several age-related disorders, including Alzheimer’s disease (AD) and type 2 diabetes (T2D). The apolipoprotein E (APOE) genotype is associated with metabolic and inflammatory outcomes that contribute to risks for AD and T2D, with the APOE4 genotype increasing risks relative to the more common APOE3 allele. In this study, we investigated the impacts of the APOE genotype on systemic and neural effects of the Western diet. Female mice with knock-in of human APOE3 or APOE4 were exposed to control or Western diet for 13 weeks. In the control diet, we observed that APOE4 mice presented with impaired metabolic phenotypes, exhibiting greater adiposity, higher plasma leptin and insulin levels, and poorer glucose clearance than APOE3 mice. Behaviorally, APOE4 mice exhibited worse performance in a hippocampal-dependent learning task. In visceral adipose tissue, APOE4 mice exhibited generally higher expression levels of macrophage- and inflammation-related genes. The cerebral cortex showed a similar pattern, with higher expression of macrophage- and inflammation-related genes in APOE4 than APOE3 mice. Exposure to the Western diet yielded modest, statistically non-significant effects on most metabolic, behavioral, and gene expression measures in both APOE genotypes. Interestingly, the Western diet resulted in reduced gene expression of a few macrophage markers, specifically in APOE4 mice. The observed relative resistance to the Western diet suggests protective roles of both female sex and young adult age. Further, the data demonstrate that APOE4 is associated with deleterious systemic and neural phenotypes and an altered response to a metabolic stressor, findings relevant to the understanding of interactions between the APOE genotype and risks for metabolic disorders. Full article
(This article belongs to the Special Issue Obesity and Associated Comorbidities: Implications for Neural and Immune Regulation of Energy Metabolism)
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13 pages, 2290 KiB  
Article
Butin Mitigates Memory Impairment in Streptozotocin-Induced Diabetic Rats by Inhibiting Oxidative Stress and Inflammatory Responses
by Asma B. Omer, Mahmood Hassan Dalhat, Mohammad Kaleem Khan, Obaid Afzal, Abdulmalik S. A. Altamimi, Sami I. Alzarea, Waleed Hassan Almalki and Imran Kazmi
Metabolites 2022, 12(11), 1050; https://doi.org/10.3390/metabo12111050 - 1 Nov 2022
Cited by 8 | Viewed by 1985
Abstract
It has been reported from the previous literature that butin restores mitochondrial dysfunction by modulation of oxidative stress and glutamate-induced neurotoxicity in mouse hippocampus HT22 cells. Butin also possesses an anti-Huntington’s effect in rats. Considering the current background, this study was designed to [...] Read more.
It has been reported from the previous literature that butin restores mitochondrial dysfunction by modulation of oxidative stress and glutamate-induced neurotoxicity in mouse hippocampus HT22 cells. Butin also possesses an anti-Huntington’s effect in rats. Considering the current background, this study was designed to evaluate the neuroprotective effect of butin against memory loss caused by streptozotocin (STZ). STZ (40 mg/kg) was intraperitoneally injected into rats. Three days later, diabetic rats were identified and included in the study. A total of 30 rats (12 nondiabetic and 18 diabetics) were grouped as Group A (control-non-diabetic rats) and Group B (STZ diabetic control) were treated with 1 mL of sodium CMC (0.5% w/v). Group C (STZ+ butin 25) were treated with butin 25 mg/kg. Group D (STZ+ butin 50) and Group E (butin per se) were administered with butin 50 mg/kg. Each therapy was administered orally once each day for 15-day. The Morris water maze and the Y-maze behavioural tests were run throughout the experimental programme. Animals were put to death on day 15 and their brains were removed for biochemical assays (CAT, SOD, GSH, MDA, nitrite, acetylcholinesterase (AchE), IL-1, and mitochondrial enzyme complexes). Rats with neurobehavioral impairments brought on by STZ have less spontaneous movement, learning capacity, and memory. Additionally, STZ decreased endogenous antioxidants and increased pro-inflammatory cytokines, nitrite, MDA, and AchE. Neurobehavioral deficits and metabolic markers were dramatically improved by butin. Full article
(This article belongs to the Special Issue Obesity and Associated Comorbidities: Implications for Neural and Immune Regulation of Energy Metabolism)
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Review

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34 pages, 1476 KiB  
Review
Mechanisms of Maternal Diet-Induced Obesity Affecting the Offspring Brain and Development of Affective Disorders
by Daniel E. Radford-Smith and Daniel C. Anthony
Metabolites 2023, 13(3), 455; https://doi.org/10.3390/metabo13030455 - 20 Mar 2023
Cited by 12 | Viewed by 4071
Abstract
Depression and metabolic disease are common disorders that share a bidirectional relationship and continue to increase in prevalence. Maternal diet and maternal behaviour both profoundly influence the developmental trajectory of offspring during the perinatal period. At an epidemiological level, both maternal depression and [...] Read more.
Depression and metabolic disease are common disorders that share a bidirectional relationship and continue to increase in prevalence. Maternal diet and maternal behaviour both profoundly influence the developmental trajectory of offspring during the perinatal period. At an epidemiological level, both maternal depression and obesity during pregnancy have been shown to increase the risk of neuropsychiatric disease in the subsequent generation. Considerable progress has been made to understand the mechanisms by which maternal obesity disrupts the developing offspring gut–brain axis, priming offspring for the development of affective disorders. This review outlines such mechanisms in detail, including altered maternal care, the maternal microbiome, inflammation, breast milk composition, and maternal and placental metabolites. Subsequently, offspring may be prone to developing gut–brain interaction disorders with concomitant changes to brain energy metabolism, neurotransmission, and behaviour, alongside gut dysbiosis. The gut microbiome may act as a key modifiable, and therefore treatable, feature of the relationship between maternal obesity and the offspring brain function. Further studies examining the relationship between maternal nutrition, the maternal microbiome and metabolites, and offspring neurodevelopment are warranted to identify novel therapeutic targets. Full article
(This article belongs to the Special Issue Obesity and Associated Comorbidities: Implications for Neural and Immune Regulation of Energy Metabolism)
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16 pages, 995 KiB  
Review
Obesity-Induced Brain Neuroinflammatory and Mitochondrial Changes
by Luisa O. Schmitt and Joana M. Gaspar
Metabolites 2023, 13(1), 86; https://doi.org/10.3390/metabo13010086 - 5 Jan 2023
Cited by 32 | Viewed by 4477
Abstract
Obesity is defined as abnormal and excessive fat accumulation, and it is a risk factor for developing metabolic and neurodegenerative diseases and cognitive deficits. Obesity is caused by an imbalance in energy homeostasis resulting from increased caloric intake associated with a sedentary lifestyle. [...] Read more.
Obesity is defined as abnormal and excessive fat accumulation, and it is a risk factor for developing metabolic and neurodegenerative diseases and cognitive deficits. Obesity is caused by an imbalance in energy homeostasis resulting from increased caloric intake associated with a sedentary lifestyle. However, the entire physiopathology linking obesity with neurodegeneration and cognitive decline has not yet been elucidated. During the progression of obesity, adipose tissue undergoes immune, metabolic, and functional changes that induce chronic low-grade inflammation. It has been proposed that inflammatory processes may participate in both the peripheral disorders and brain disorders associated with obesity, including the development of cognitive deficits. In addition, mitochondrial dysfunction is related to inflammation and oxidative stress, causing cellular oxidative damage. Preclinical and clinical studies of obesity and metabolic disorders have demonstrated mitochondrial brain dysfunction. Since neuronal cells have a high energy demand and mitochondria play an important role in maintaining a constant energy supply, impairments in mitochondrial activity lead to neuronal damage and dysfunction and, consequently, to neurotoxicity. In this review, we highlight the effect of obesity and high-fat diet consumption on brain neuroinflammation and mitochondrial changes as a link between metabolic dysfunction and cognitive decline. Full article
(This article belongs to the Special Issue Obesity and Associated Comorbidities: Implications for Neural and Immune Regulation of Energy Metabolism)
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