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Periphery-Brain Interactions and Leptin in the Regulation of Whole-Body Energy...
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Periphery-Brain Interactions and Leptin in the Regulation of Whole-Body Energy Metabolism

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (5 January 2022) | Viewed by 19789

Special Issue Editors

Dr. Mohammed Khair Hankir

E-Mail Website
Guest Editor
Department of Experimental Surgery, University Hospital Würzburg, 97080 Würzburg, Germany
Interests: bariatric surgery; gut-brain communication; adipose tissue thermogenesis; intestinal barrier; obesity; diabetes
Dr. Michael Bruneau Jr.

E-Mail Website
Guest Editor
Department of Health Sciences, Drexel University, Philadelphia, PA, USA
Interests: Physical activity and exercise testing and prescription; cardiovascular, metabolic and renal disease; gut hormones; special populations; systematic review and meta-analysis

Special Issue Information

Dear Colleagues,

Since the seminal discovery of the adipokine leptin in 1994, our understanding of the molecular, cellular and systems bases of whole-body energy metabolism regulation has grown tremendously. However, the incidence of obesity and its comorbidities such as type 2 diabetes and fatty liver disease continue to soar globally. In order to discover innovative ways of combating this pandemic, further progress clearly still needs to be made.

We now know that peripheral tissues bi-directionally communicate with the central nervous system through various signalling molecules to regulate whole-body energy metabolism. As a recently characterized example, leptin communicates with a chemically defined network of hypothalamic neurons to in turn increase sympathetic nerve activity and innervation of brown and white adipose tissues, thereby promoting thermogenesis and a negative whole-body energy balance.

In this Special Issue, we invite articles that expand our knowledge on these and similar periphery-brain interactions. In particular, we welcome articles that characterize or summarize novel peripheral signalling molecules, interactions or pathways that ultimately converge to regulate whole-body energy metabolism. These can include traditional adipokines such as leptin and gut hormones such as glucagon-like peptide 1, but also microbiota products and host-derived metabolites. Articles that shed light on how nutritional, pharmacological, exercise or surgical interventions promote healthier whole-body energy metabolism through periphery-brain interactions are also welcome.

Our hope is that this Special Issue stimulates a lively and insightful discussion in the burgeoning subject of periphery-brain interactions, to contribute to finding new approaches to treating obesity and its devastating comorbidities.

Dr. Mohammed Khair Hankir
Dr. Michael Bruneau Jr.
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. Nutrients 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 2900 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

  • Adipokines 
  • Gut hormones 
  • Central nervous system 
  • Peripheral nervous system 
  • Exercise 
  • Bariatric surgery 
  • Whole-body energy metabolism

Published Papers (7 papers)

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Editorial

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3 pages, 159 KiB  
Editorial
Periphery-Brain Interactions and Leptin in the Regulation of Whole-Body Energy Metabolism
by Mohammed Khair Hankir and Michael Bruneau, Jr.
Nutrients 2022, 14(8), 1594; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14081594 - 12 Apr 2022
Viewed by 1118
Abstract
In order to combat overweight and obesity as a global public health issue and prevent its impact on other debilitating cardiovascular, metabolic and renal diseases, a better understanding of the processes regulating energy metabolism are essential [...] Full article
(This article belongs to the Special Issue Periphery-Brain Interactions and Leptin in the Regulation of Whole-Body Energy Metabolism)

Research

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6 pages, 224 KiB  
Article
Interaction of Protein Preloads and Physical Activity on Intake of an Ultra-Processed, High Sugar/High Fat Food/Low Protein Food
by Jennifer A. Nasser, Eram Albajri, Lisa Lanza, Abigail Gilman, Mansour Altayyar, Dimitra Thomopoulos and Michael Bruneau, Jr.
Nutrients 2022, 14(4), 884; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14040884 - 19 Feb 2022
Cited by 2 | Viewed by 2158
Abstract
“Loss of control, LOC” eating is a major contributor to the development of obesity. Dietary protein is known to promote satiety, but little attention has been paid to the ability of protein, consumed in close proximity to snacking (20 min), to reduce the [...] Read more.
“Loss of control, LOC” eating is a major contributor to the development of obesity. Dietary protein is known to promote satiety, but little attention has been paid to the ability of protein, consumed in close proximity to snacking (20 min), to reduce the intake of ultra-processed, low-protein snack foods. We hypothesized that a high-protein preload (HP, 8 g of protein) consumed in close proximity to eating an ultra-processed snack food would reduce intake of the snack food as compared to a low-protein preload (LP, 1.2 g of protein). Two laboratory test meals were conducted, and the intake of ice cream (1.99 kcal/gram) after consuming dairy-based liquid preloads was measured. Habitual physical activity, a potential modulator of satiety, was assessed by a self-reporting questionnaire. Thirty (responders) out of 50 participants reduced their intake of ice cream after the HP preload, with a significant difference in intake observed between the responders and non-responders (−30 ± 25 and 18 ± 18 g, F (1, 49) = 54.36, p < 0.001 for responders and non-responders, respectively). Our data demonstrate that protein consumed in close proximity to ultra-processed snack food can reduce caloric intake by ~60 kcal, which could potentially reduce body weight by at least 5 pounds per year. Full article
(This article belongs to the Special Issue Periphery-Brain Interactions and Leptin in the Regulation of Whole-Body Energy Metabolism)
18 pages, 4105 KiB  
Article
Roux-en-Y Gastric Bypass and Caloric Restriction but Not Gut Hormone-Based Treatments Profoundly Impact the Hypothalamic Transcriptome in Obese Rats
by Ulrich Dischinger, Tobias Heckel, Thorsten Bischler, Julia Hasinger, Malina Königsrainer, Angelika Schmitt-Böhrer, Christoph Otto, Martin Fassnacht, Florian Seyfried and Mohammed Khair Hankir
Nutrients 2022, 14(1), 116; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14010116 - 28 Dec 2021
Cited by 4 | Viewed by 2166
Abstract
Background: The hypothalamus is an important brain region for the regulation of energy balance. Roux-en-Y gastric bypass (RYGB) surgery and gut hormone-based treatments are known to reduce body weight, but their effects on hypothalamic gene expression and signaling pathways are poorly studied. Methods: [...] Read more.
Background: The hypothalamus is an important brain region for the regulation of energy balance. Roux-en-Y gastric bypass (RYGB) surgery and gut hormone-based treatments are known to reduce body weight, but their effects on hypothalamic gene expression and signaling pathways are poorly studied. Methods: Diet-induced obese male Wistar rats were randomized into the following groups: RYGB, sham operation, sham + body weight-matched (BWM) to the RYGB group, osmotic minipump delivering PYY3-36 (0.1 mg/kg/day), liraglutide s.c. (0.4 mg/kg/day), PYY3-36 + liraglutide, and saline. All groups (except BWM) were kept on a free choice of high- and low-fat diets. Four weeks after interventions, hypothalami were collected for RNA sequencing. Results: While rats in the RYGB, BWM, and PYY3-36 + liraglutide groups had comparable reductions in body weight, only RYGB and BWM treatment had a major impact on hypothalamic gene expression. In these groups, hypothalamic leptin receptor expression as well as the JAK–STAT, PI3K-Akt, and AMPK signaling pathways were upregulated. No significant changes could be detected in PYY3-36 + liraglutide-, liraglutide-, and PYY-treated groups. Conclusions: Despite causing similar body weight changes compared to RYGB and BWM, PYY3-36 + liraglutide treatment does not impact hypothalamic gene expression. Whether this striking difference is favorable or unfavorable to metabolic health in the long term requires further investigation. Full article
(This article belongs to the Special Issue Periphery-Brain Interactions and Leptin in the Regulation of Whole-Body Energy Metabolism)
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10 pages, 1459 KiB  
Article
Leptin Improves Parameters of Brown Adipose Tissue Thermogenesis in Lipodystrophic Mice
by Annett Hoffmann, Thomas Ebert, Mohammed K. Hankir, Gesine Flehmig, Nora Klöting, Beate Jessnitzer, Ulrike Lössner, Michael Stumvoll, Matthias Blüher, Mathias Fasshauer, Anke Tönjes, Konstanze Miehle and Susan Kralisch
Nutrients 2021, 13(8), 2499; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13082499 - 22 Jul 2021
Cited by 4 | Viewed by 2236
Abstract
Lipodystrophy syndromes (LD) are a heterogeneous group of very rare congenital or acquired disorders characterized by a generalized or partial lack of adipose tissue. They are strongly associated with severe metabolic dysfunction due to ectopic fat accumulation in the liver and other organs [...] Read more.
Lipodystrophy syndromes (LD) are a heterogeneous group of very rare congenital or acquired disorders characterized by a generalized or partial lack of adipose tissue. They are strongly associated with severe metabolic dysfunction due to ectopic fat accumulation in the liver and other organs and the dysregulation of several key adipokines, including leptin. Treatment with leptin or its analogues is therefore sufficient to reverse some of the metabolic symptoms of LD in patients and in mouse models through distinct mechanisms. Brown adipose tissue (BAT) thermogenesis has emerged as an important regulator of systemic metabolism in rodents and in humans, but it is poorly understood how leptin impacts BAT in LD. Here, we show in transgenic C57Bl/6 mice overexpressing sterol regulatory element-binding protein 1c in adipose tissue (Tg (aP2-nSREBP1c)), an established model of congenital LD, that daily subcutaneous administration of 3 mg/kg leptin for 6 to 8 weeks increases body temperature without affecting food intake or body weight. This is associated with increased protein expression of the thermogenic molecule uncoupling protein 1 (UCP1) and the sympathetic nerve marker tyrosine hydroxylase (TH) in BAT. These findings suggest that leptin treatment in LD stimulates BAT thermogenesis through sympathetic nerves, which might contribute to some of its metabolic benefits by providing a healthy reservoir for excess circulating nutrients. Full article
(This article belongs to the Special Issue Periphery-Brain Interactions and Leptin in the Regulation of Whole-Body Energy Metabolism)
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16 pages, 1981 KiB  
Communication
Leptin Receptors Are Not Required for Roux-en-Y Gastric Bypass Surgery to Normalize Energy and Glucose Homeostasis in Rats
by Mohammed K. Hankir, Laura Rotzinger, Arno Nordbeck, Caroline Corteville, Ulrich Dischinger, Juna-Lisa Knop, Annett Hoffmann, Christoph Otto and Florian Seyfried
Nutrients 2021, 13(5), 1544; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13051544 - 04 May 2021
Cited by 2 | Viewed by 2571
Abstract
Sensitization to the adipokine leptin is a promising therapeutic strategy against obesity and its comorbidities and has been proposed to contribute to the lasting metabolic benefits of Roux-en-Y gastric bypass (RYGB) surgery. We formally tested this idea using Zucker fatty fa/fa rats as [...] Read more.
Sensitization to the adipokine leptin is a promising therapeutic strategy against obesity and its comorbidities and has been proposed to contribute to the lasting metabolic benefits of Roux-en-Y gastric bypass (RYGB) surgery. We formally tested this idea using Zucker fatty fa/fa rats as an established genetic model of obesity, glucose intolerance, and fatty liver due to leptin receptor deficiency. We show that the changes in body weight in these rats following RYGB largely overlaps with that of diet-induced obese Wistar rats with intact leptin receptors. Further, food intake and oral glucose tolerance were normalized in RYGB-treated Zucker fatty fa/fa rats to the levels of lean Zucker fatty fa/+ controls, in association with increased glucagon-like peptide 1 (GLP-1) and insulin release. In contrast, while fatty liver was also normalized in RYGB-treated Zucker fatty fa/fa rats, their circulating levels of the liver enzyme alanine aminotransferase (ALT) remained elevated at the level of obese Zucker fatty fa/fa controls. These findings suggest that the leptin system is not required for the normalization of energy and glucose homeostasis associated with RYGB, but that its potential contribution to the improvements in liver health postoperatively merits further investigation. Full article
(This article belongs to the Special Issue Periphery-Brain Interactions and Leptin in the Regulation of Whole-Body Energy Metabolism)
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11 pages, 303 KiB  
Article
Fractalkine, sICAM-1 and Kynurenine Pathway in Restrictive Anorexia Nervosa–Exploratory Study
by Ewa Dudzińska, Kinga Szymona, Renata Kloc, Tomasz Kocki, Paulina Gil-Kulik, Jacek Bogucki, Janusz Kocki, Roman Paduch and Ewa M. Urbańska
Nutrients 2021, 13(2), 339; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13020339 - 24 Jan 2021
Cited by 4 | Viewed by 2001
Abstract
The link between the kynurenine pathway and immunomodulatory molecules—fractalkine and soluble intercellular adhesion molecule-1 (sICAM-1)—in anorexia nervosa (AN) remains unknown. Fractalkine, sICAM-1, tryptophan (TRP), kynurenine (KYN), neuroprotective kynurenic acid (KYNA), neurotoxic 3-OH-kynurenine (3-OH-KYN), and the expression of mRNA for kynurenine aminotransferases (KAT1-3 [...] Read more.
The link between the kynurenine pathway and immunomodulatory molecules—fractalkine and soluble intercellular adhesion molecule-1 (sICAM-1)—in anorexia nervosa (AN) remains unknown. Fractalkine, sICAM-1, tryptophan (TRP), kynurenine (KYN), neuroprotective kynurenic acid (KYNA), neurotoxic 3-OH-kynurenine (3-OH-KYN), and the expression of mRNA for kynurenine aminotransferases (KAT1-3) were studied in 20 female patients with restrictive AN (mostly drug-free, all during first episode of the disease) and in 24 controls. In AN, serum fractalkine, but not sICAM-1, KYNA, KYN, TRP or 3-OH-KYN, was higher; ratios TRP/KYN, KYN/KYNA, KYN/3-OH-KYN and KYNA/3-OH-KYN were unaltered. The expression of the gene encoding KAT3, but not of genes encoding KAT1 and KAT2 (measured in blood mononuclear cells), was higher in patients with AN. In AN, fractalkine positively correlated with TRP, while sICAM-1 was negatively associated with 3-OH-KYN and positively linked with the ratio KYN/3-OH-KYN. Furthermore, TRP and fractalkine were negatively associated with the body mass index (BMI) in AN. Expression of KAT1, KAT2 and KAT3 did not correlate with fractalkine, sICAM-1 or BMI, either in AN or control. Increased fractalkine may be an independent factor associated with the restrictive type of AN. Excessive physical activity probably underlies increased expression of KAT3 observed among enrolled patients. Further, longitudinal studies on a larger cohort of patients should be aimed to clarify the contribution of fractalkine and KAT3 to the pathogenesis of AN. Full article
(This article belongs to the Special Issue Periphery-Brain Interactions and Leptin in the Regulation of Whole-Body Energy Metabolism)

Review

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20 pages, 399 KiB  
Review
The Implication of Physiological Ketosis on The Cognitive Brain: A Narrative Review
by Mansour Altayyar, Jennifer A. Nasser, Dimitra Thomopoulos and Michael Bruneau, Jr.
Nutrients 2022, 14(3), 513; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14030513 - 25 Jan 2022
Cited by 12 | Viewed by 6643
Abstract
Optimal cognitive functions are necessary for activities of daily living and self-independence. Cognitive abilities are acquired during early childhood as part of progressive neurodevelopmental milestones; unfortunately, regressive changes can occur as part of physiological aging, or more ominously, pathological diseases, such as Alzheimer’s [...] Read more.
Optimal cognitive functions are necessary for activities of daily living and self-independence. Cognitive abilities are acquired during early childhood as part of progressive neurodevelopmental milestones; unfortunately, regressive changes can occur as part of physiological aging, or more ominously, pathological diseases, such as Alzheimer’s disease (AD). Cases of AD and its milder subset, mild cognitive impairment (MCI), are rising and would impose a burdensome impact beyond the individual level. Various dietary and nutritional approaches have potential for promising results in managing cognitive deterioration. Glucose is the core source of bioenergy in the body; however, glucose brain metabolism could be affected in aging cells or due to disease development. Ketone bodies are an efficient alternate fuel source that could compensate for the deficient glycolytic metabolism upon their supra-physiologic availability in the blood (ketosis), which, in turn, could promote cognitive benefits and tackle disease progression. In this review, we describe the potential of ketogenic approaches to produce cognitive benefits in healthy individuals, as well as those with MCI and AD. Neurophysiological changes of the cognitive brain in response to ketosis through neuroimaging modalities are also described in this review to provide insight into the ketogenic effect on the brain outside the framework of purely molecular explanations. Full article
(This article belongs to the Special Issue Periphery-Brain Interactions and Leptin in the Regulation of Whole-Body Energy Metabolism)
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