Special Issue "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: 5 January 2022.

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

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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 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 2400 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 (3 papers)

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Research

Article
Leptin Improves Parameters of Brown Adipose Tissue Thermogenesis in Lipodystrophic Mice
Nutrients 2021, 13(8), 2499; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13082499 - 22 Jul 2021
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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
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Communication
Leptin Receptors Are Not Required for Roux-en-Y Gastric Bypass Surgery to Normalize Energy and Glucose Homeostasis in Rats
Nutrients 2021, 13(5), 1544; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13051544 - 04 May 2021
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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
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Article
Fractalkine, sICAM-1 and Kynurenine Pathway in Restrictive Anorexia Nervosa–Exploratory Study
Nutrients 2021, 13(2), 339; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13020339 - 24 Jan 2021
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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
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