nutrients-logo

Journal Browser

Journal Browser

Diet, Adipose Tissue Dysfunction and Metabolic Disorders

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

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 10225

Special Issue Editors


E-Mail Website
Guest Editor
Centre for Sport, Exercise and Life Sciences, Institute for Health and Wellbeing, Coventry University, Priory St, Coventry CV1 5FB, UK
Interests: stress; obesity; satiety; adipose tissue inflammation

E-Mail Website
Guest Editor
Centre for Sport, Exercise and Life Sciences, Research Institute for Health and Wellbeing, Coventry University, Coventry, UK
Interests: QP Physiology; metabolism; diabetes; exercise physiology; cell metabolism; liver; NAFLD; skeletal muscle; nutrition

Special Issue Information

Dear Colleagues,

Our understanding of adipose tissue has changed enormously in the past 20 years. From being simply an energy storage vessel, adipose tissue is now known to exist in a range of types, each with a different function and origin as well as having different regulatory control and secretory products. The ability of adipose tissue to respond and adapt to a changing energy balance can determine whether an individual is predisposed to metabolic disease or will expand adipose tissue without the associated negative metabolic consequences. Additionally, the location of white adipose tissue, whether centrally as visceral fat or peripheral subcutaneous adipose tissue, can also present different risks for metabolic diseases as well as the development of other pathologies such as cardiovascular and fatty liver diseases. However, the factors which regulate healthy adipose tissue expansion and function are still to be elucidated.

As the Guest Editors of this Special Issue on “Diet, Adipose Tissue Dysfunction and Metabolic Disorders”, we hope to further contribute to this facinating area of metabolism by inviting you to submit a manuscript to Nutrients to improve our knowledge regarding the role of macronutrients in adipose tissue function and metabolism. Experimental research, systematic and meta-analyses, and narrative reviews are welcome.

Prof. Dr. Derek Renshaw
Dr. Mark Turner
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

  • adipose tissue inflammation
  • body composition
  • visceral fat
  • fibrosis
  • hypertrophy
  • hypoxia

Published Papers (4 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

14 pages, 1903 KiB  
Article
Ascophyllum nodosum and Fucus vesiculosus Extracts Improved Lipid Metabolism and Inflammation in High-Energy Diet–Induced Hyperlipidemia Rats
by Yu-Tang Tung, Chieh-Hsi Wu, Wen-Chao Chen, Chun-Hsu Pan, Yi-Wen Chen, Shu-Ping Tsao, Chia-Jung Chen and Hui-Yu Huang
Nutrients 2022, 14(21), 4665; https://doi.org/10.3390/nu14214665 - 4 Nov 2022
Cited by 2 | Viewed by 2366
Abstract
Ascophyllum nodosum and Fucus vesiculosus both contain unique polyphenols called phlorotannins. Phlorotannins reportedly possess various pharmacological activities. A previous study reported that the activity of phlorotannin is strongly correlated with the normalization of metabolic function, and phlorotannins are extremely promising nutrients for use [...] Read more.
Ascophyllum nodosum and Fucus vesiculosus both contain unique polyphenols called phlorotannins. Phlorotannins reportedly possess various pharmacological activities. A previous study reported that the activity of phlorotannin is strongly correlated with the normalization of metabolic function, and phlorotannins are extremely promising nutrients for use in the treatment of metabolic syndrome. To date, no study has explored the antihyperlipidemic effects of phlorotannins from A. nodosum and F. vesiculosus in animal models. Therefore, in the present study, we investigated the effects of phlorotannins using a rat model of high-energy diet (HED)-induced hyperlipidemia. The results showed that the rats that were fed an HED and treated with phlorotannin-rich extract from A. nodosum and F. vesiculosus had significantly lower serum fasting blood sugar (FBS), aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol (TC), triacylglyceride (TG) and free fatty acids (FFAs) levels and hepatic TG level and had higher serum insulin, high-density lipoprotein cholesterol (HDL-C) levels and lipase activity in their fat tissues than in the case with the rats that were fed the HED alone. A histopathological analysis revealed that phlorotannin-rich extract could significantly reduce the size of adipocytes around the epididymis. In addition, the rats treated with phlorotannin-rich extract had significantly lowered interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) levels and increased superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities than did those in the HED group. These results suggested that the phlorotannin-rich extract stimulated lipid metabolism and may have promoted lipase activity in rats with HED-induced hyperlipidemia. Our results indicated that A. nodosum and F. vesiculosus, marine algae typically used as health foods, have strong antihyperlipidemic effects and may, therefore, be useful for preventing atherosclerosis. These algae may be incorporated into antihyperlipidemia pharmaceuticals and functional foods. Full article
(This article belongs to the Special Issue Diet, Adipose Tissue Dysfunction and Metabolic Disorders)
Show Figures

Figure 1

19 pages, 1628 KiB  
Article
Suppression of Anti-Inflammatory Mediators in Metabolic Disease May Be Driven by Overwhelming Pro-Inflammatory Drivers
by Sehar Sajid, Mohammed Gulrez Zariwala, Richard Mackenzie, Mark Turner, Theo Nell, Srikanth Bellary and Derek Renshaw
Nutrients 2022, 14(11), 2360; https://doi.org/10.3390/nu14112360 - 6 Jun 2022
Cited by 2 | Viewed by 2784
Abstract
Obesity is a multifactorial disease and is associated with an increased risk of developing metabolic syndrome and co-morbidities. Dysregulated expansion of the adipose tissue during obesity induces local tissue hypoxia, altered secretory profile of adipokines, cytokines and chemokines, altered profile of local tissue [...] Read more.
Obesity is a multifactorial disease and is associated with an increased risk of developing metabolic syndrome and co-morbidities. Dysregulated expansion of the adipose tissue during obesity induces local tissue hypoxia, altered secretory profile of adipokines, cytokines and chemokines, altered profile of local tissue inflammatory cells leading to the development of low-grade chronic inflammation. Low grade chronic inflammation is considered to be the underlying mechanism that increases the risk of developing obesity associated comorbidities. The glucocorticoid induced protein annexin A1 and its N-terminal peptides are anti-inflammatory mediators involved in resolving inflammation. The aim of the current study was to investigate the role of annexin A1 in obesity and associated inflammation. To achieve this aim, the current study analysed data from two feasibility studies in clinical populations: (1) bariatric surgery patients (Pre- and 3 months post-surgery) and (2) Lipodystrophy patients. Plasma annexin A1 levels were increased at 3-months post-surgery compared to pre-surgery (1.2 ± 0.1 ng/mL, n = 19 vs. 1.6 ± 0.1 ng/mL, n = 9, p = 0.009) and positively correlated with adiponectin (p = 0.009, r = 0.468, n = 25). Plasma annexin A1 levels were decreased in patients with lipodystrophy compared to BMI matched controls (0.2 ± 0.1 ng/mL, n = 9 vs. 0.97 ± 0.1 ng/mL, n = 30, p = 0.008), whereas CRP levels were significantly elevated (3.3 ± 1.0 µg/mL, n = 9 vs. 1.4 ± 0.3 µg/mL, n = 31, p = 0.0074). The roles of annexin A1 were explored using an in vitro cell based model (SGBS cells) mimicking the inflammatory status that is observed in obesity. Acute treatment with the annexin A1 N-terminal peptide, AC2-26 differentially regulated gene expression (including PPARA (2.8 ± 0.7-fold, p = 0.0303, n = 3), ADIPOQ (2.0 ± 0.3-fold, p = 0.0073, n = 3), LEP (0.6 ± 0.2-fold, p = 0.0400, n = 3), NAMPT (0.4 ± 0.1-fold, p = 0.0039, n = 3) and RETN (0.1 ± 0.03-fold, p < 0.0001, n = 3) in mature obesogenic adipocytes indicating that annexin A1 may play a protective role in obesity and inflammation. However, this effect may be overshadowed by the continued increase in systemic inflammation associated with rapid tissue expansion in obesity. Full article
(This article belongs to the Special Issue Diet, Adipose Tissue Dysfunction and Metabolic Disorders)
Show Figures

Figure 1

17 pages, 2150 KiB  
Article
Proanthocyanidins Restore the Metabolic Diurnal Rhythm of Subcutaneous White Adipose Tissue According to Time-Of-Day Consumption
by Marina Colom-Pellicer, Romina M. Rodríguez, Jorge R. Soliz-Rueda, Leonardo Vinícius Monteiro de Assis, Èlia Navarro-Masip, Sergio Quesada-Vázquez, Xavier Escoté, Henrik Oster, Miquel Mulero and Gerard Aragonès
Nutrients 2022, 14(11), 2246; https://doi.org/10.3390/nu14112246 - 27 May 2022
Cited by 2 | Viewed by 2421
Abstract
Consumption of grape seed proanthocyanidin extract (GSPE) has beneficial effects on the functionality of white adipose tissue (WAT). However, although WAT metabolism shows a clear diurnal rhythm, whether GSPE consumption could affect WAT rhythmicity in a time-dependent manner has not been studied. Ninety-six [...] Read more.
Consumption of grape seed proanthocyanidin extract (GSPE) has beneficial effects on the functionality of white adipose tissue (WAT). However, although WAT metabolism shows a clear diurnal rhythm, whether GSPE consumption could affect WAT rhythmicity in a time-dependent manner has not been studied. Ninety-six male Fischer rats were fed standard (STD, two groups) or cafeteria (CAF, four groups) diet for 9 weeks (n = 16 each group). From week 6 on, CAF diet animals were supplemented with vehicle or 25 mg GSPE/kg of body weight either at the beginning of the light/rest phase (ZT0) or at the beginning of the dark/active phase (ZT12). The two STD groups were also supplemented with vehicle at ZT0 or ZT12. In week 9, animals were sacrificed at 6 h intervals (n = 4) to analyze the diurnal rhythms of subcutaneous WAT metabolites by nuclear magnetic resonance spectrometry. A total of 45 metabolites were detected, 19 of which presented diurnal rhythms in the STD groups. Although most metabolites became arrhythmic under CAF diet, GSPE consumption at ZT12, but not at ZT0, restored the rhythmicity of 12 metabolites including compounds involved in alanine, aspartate, and glutamate metabolism. These results demonstrate that timed GSPE supplementation may restore, at least partially, the functional dynamics of WAT when it is consumed at the beginning of the active phase. This study opens an innovative strategy for time-dependent polyphenol treatment in obesity and metabolic diseases. Full article
(This article belongs to the Special Issue Diet, Adipose Tissue Dysfunction and Metabolic Disorders)
Show Figures

Graphical abstract

Review

Jump to: Research

16 pages, 1089 KiB  
Review
Adipose Tissue Dysfunction in Obesity: Role of Mineralocorticoid Receptor
by Mirko Parasiliti-Caprino, Martina Bollati, Fabio Dario Merlo, Ezio Ghigo, Mauro Maccario and Simona Bo
Nutrients 2022, 14(22), 4735; https://doi.org/10.3390/nu14224735 - 9 Nov 2022
Cited by 5 | Viewed by 2089
Abstract
The mineralocorticoid receptor (MR) acts as an essential regulator of blood pressure, volume status, and electrolyte balance. However, in recent decades, a growing body of evidence has suggested that MR may also have a role in mediating pro-inflammatory, pro-oxidative, and pro-fibrotic changes in [...] Read more.
The mineralocorticoid receptor (MR) acts as an essential regulator of blood pressure, volume status, and electrolyte balance. However, in recent decades, a growing body of evidence has suggested that MR may also have a role in mediating pro-inflammatory, pro-oxidative, and pro-fibrotic changes in several target organs, including the adipose tissue. The finding that MR is overexpressed in the adipose tissue of patients with obesity has led to the hypothesis that this receptor can contribute to adipokine dysregulation and low-grade chronic inflammation, alterations that are linked to the development of obesity-related metabolic and cardiovascular complications. Moreover, several studies in animal models have investigated the role of MR antagonists (MRAs) in preventing the metabolic alterations observed in obesity. In the present review we will focus on the potential mechanisms by which MR activation can contribute to adipose tissue dysfunction in obesity and on the possible beneficial effects of MRAs in this setting. Full article
(This article belongs to the Special Issue Diet, Adipose Tissue Dysfunction and Metabolic Disorders)
Show Figures

Figure 1

Back to TopTop