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Nutrients
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Carotenoids and Their Retinoid Conversion Products in the Regulation of...
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Carotenoids and Their Retinoid Conversion Products in the Regulation of Fat Reserves and Dysmetabolic Obesity

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Phytochemicals and Human Health".

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 11884

Special Issue Editor

Dr. Jose Atilio Canas

E-Mail Website
Guest Editor
Johns Hopkins All Children's Hospital, St Petersburg, FL, USA
Interests: bioactive compounds; phenolics; antioxidants; carotenoids; retinoids; health claims; nutrition; anti-obesity effects, reduction of chronic disease risk; thermogenesis; mitochondria; lipid storage; visceral fat
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Carotenoids belong to the tetraterpene family of compounds mainly present in fruits and vegetables. The 2015–2020 Dietary Guidelines for Americans recommends eating a variety of fruits and vegetables to lower the risk of chronic disease and “help children and adults achieve and maintain a healthy weight”. This guidance has a strong evidence base for the prevention of cardiovascular disease (CVD), but less so for the mechanisms necessary to achieve and maintain a healthy weight based on the adequate intake or systemic levels of carotenoids. Obesity when characterized as unhealthy, carries the potential to accumulate fat in the viscera and muscles, inducing chronic inflammation and insulin resistance. Adipose tissue is an important endocrine organ that mediates carotenoid and lipid storage, metabolism, adipokine secretion, insulin signaling, and subclinical inflammation. Lower concentrations of carotenoids by up to 50% have been reported in subcutaneous adipose tissue of subjects with obesity vs. non-obese subjects. Adipose tissue carotenoids and their conversion retinoid products regulate a variety of metabolic functions, such as thermogenesis, lipolysis, and fatty acid oxidation. They may also have a direct effect on adipocyte differentiation, which is likely to contribute to their effects on adiposity accrual during childhood. Studies on the effectiveness of utilizing carotenoids and their conversion products to reduce or modify the accrual of visceral adiposity are needed.

The purpose of this Special Issue is to summarize and expand the research on carotenoids and their conversion products on the (genetics, epigenetics, transcriptomics, metabolomics, and microbiomics) of adipose tissue and to propose the development of carotenoid-based nutrition therapies for the amelioration of ectopic fat accumulation. Submissions may include studies focused on the investigation of the effects of specific diets, dietary patterns, foods, mixed or single carotenoid supplementation, or bioactive compounds on changes in depot-specific body fat which could modify the biological responses and/or the risk of chronic diseases. This Special Issue welcomes the submission of manuscripts describing related original research or reviews of the scientific literature in humans (interventional, observational, cohort studies) or animal models. 

Dr. Jose Atilio Canas
Guest Editor

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

  • Bioactive compounds
  • phenolics
  • antioxidants
  • carotenoids
  • retinoids
  • health claims
  • nutrition
  • anti-obesity effects, reduction of chronic disease risk
  • thermogenesis
  • mitochondria
  • lipid storage
  • visceral fat

Published Papers (3 papers)

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Research

17 pages, 2741 KiB  
Article
Protective Effects of Individual and Combined Low Dose Beta-Carotene and Metformin Treatments against High-Fat Diet-Induced Responses in Mice
by Bojan Stojnić, Alba Serrano, Lana Sušak, Andreu Palou, M. Luisa Bonet and Joan Ribot
Nutrients 2021, 13(10), 3607; https://doi.org/10.3390/nu13103607 - 14 Oct 2021
Cited by 5 | Viewed by 2239
Abstract
Anti-obesity activity has been reported for beta-carotene (BC) supplementation at high doses and metformin (MET). We studied whether BC treatment at a closer to dietary dose and MET treatment at a lower than therapeutic dose are effective in ameliorating unwanted effects of an [...] Read more.
Anti-obesity activity has been reported for beta-carotene (BC) supplementation at high doses and metformin (MET). We studied whether BC treatment at a closer to dietary dose and MET treatment at a lower than therapeutic dose are effective in ameliorating unwanted effects of an obesogenic diet and whether their combination is advantageous. Obesity-prone mice were challenged with a high-fat diet (HFD, 45% energy as fat) for 4 weeks while receiving a placebo or being treated orally with BC (3 mg/kg/day), MET (100 mg/kg/day), or their combination (BC+MET); a fifth group received a placebo and was kept on a normal-fat diet (10% energy as fat). HFD-induced increases in body weight gain and inguinal white adipose tissue (WAT) adipocyte size were attenuated maximally or selectively in the BC+MET group, in which a redistribution towards smaller adipocytes was noted. Cumulative energy intake was unaffected, yet results suggested increased systemic energy expenditure and brown adipose tissue activation in the treated groups. Unwanted effects of HFD on glucose control and insulin sensitivity were attenuated in the treated groups, especially BC and BC+MET, in which hepatic lipid content was also decreased. Transcriptional analyses suggested effects on skeletal muscle and WAT metabolism could contribute to better responses to the HFD, especially in the MET and BC+MET groups. The results support the benefits of the BC+MET cotreatment. Full article
(This article belongs to the Special Issue Carotenoids and Their Retinoid Conversion Products in the Regulation of Fat Reserves and Dysmetabolic Obesity)
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21 pages, 2556 KiB  
Article
Vitamin A5/X, a New Food to Lipid Hormone Concept for a Nutritional Ligand to Control RXR-Mediated Signaling
by Wojciech Krężel, Aurea Rivas, Monika Szklenar, Marion Ciancia, Rosana Alvarez, Angel R. de Lera and Ralph Rühl
Nutrients 2021, 13(3), 925; https://doi.org/10.3390/nu13030925 - 12 Mar 2021
Cited by 9 | Viewed by 3874
Abstract
Vitamin A is a family of derivatives synthesized from carotenoids acquired from the diet and can be converted in animals to bioactive forms essential for life. Vitamin A1 (all-trans-retinol/ATROL) and provitamin A1 (all-trans-β,β-carotene/ATBC) are precursors of all-trans-retinoic [...] Read more.
Vitamin A is a family of derivatives synthesized from carotenoids acquired from the diet and can be converted in animals to bioactive forms essential for life. Vitamin A1 (all-trans-retinol/ATROL) and provitamin A1 (all-trans-β,β-carotene/ATBC) are precursors of all-trans-retinoic acid acting as a ligand for the retinoic acid receptors. The contribution of ATROL and ATBC to formation of 9-cis-13,14-dihydroretinoic acid (9CDHRA), the only endogenous retinoid acting as retinoid X receptor (RXR) ligand, remains unknown. To address this point novel and already known retinoids and carotenoids were stereoselectively synthesized and administered in vitro to oligodendrocyte cell culture and supplemented in vivo (orally) to mice with a following high-performance liquid chromatography-mass spectrometry (HPLC-MS)/UV-Vis based metabolic profiling. In this study, we show that ATROL and ATBC are at best only weak and non-selective precursors of 9CDHRA. Instead, we identify 9-cis-13,14-dihydroretinol (9CDHROL) and 9-cis-13,14-dihydro-β,β-carotene (9CDHBC) as novel direct nutritional precursors of 9CDHRA, which are present endogenously in humans and the human food chain matrix. Furthermore, 9CDHROL displayed RXR-dependent promnemonic activity in working memory test similar to that reported for 9CDHRA. We also propose that the endogenous carotenoid 9-cis-β,β-carotene (9CBC) can act as weak, indirect precursor of 9CDHRA via hydrogenation to 9CDHBC and further metabolism to 9CDHROL and/or 9CDHRA. In summary, since classical vitamin A1 is not an efficient 9CDHRA precursor, we conclude that this group of molecules constitutes a new class of vitamin or a new independent member of the vitamin A family, named “Vitamin A5/X”. Full article
(This article belongs to the Special Issue Carotenoids and Their Retinoid Conversion Products in the Regulation of Fat Reserves and Dysmetabolic Obesity)
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30 pages, 627 KiB  
Article
Association of Antioxidant Vitamins A, C, E and Carotenoids with Cognitive Performance over Time: A Cohort Study of Middle-Aged Adults
by May A. Beydoun, Jose A. Canas, Marie T. Fanelli-Kuczmarski, Ana I. Maldonado, Danielle Shaked, Mika Kivimaki, Michele K. Evans and Alan B. Zonderman
Nutrients 2020, 12(11), 3558; https://doi.org/10.3390/nu12113558 - 20 Nov 2020
Cited by 21 | Viewed by 5255
Abstract
Carotenoids may strengthen the association of antioxidant vitamins A, C, and E with favorable cognitive outcomes over time, though a few prospective studies have examined this hypothesis. We evaluated the longitudinal data from 1251 participants in the Healthy Aging in Neighborhoods of Diversity [...] Read more.
Carotenoids may strengthen the association of antioxidant vitamins A, C, and E with favorable cognitive outcomes over time, though a few prospective studies have examined this hypothesis. We evaluated the longitudinal data from 1251 participants in the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) study (Age at visit 1 in 2004–2009 (v1): 30–65 years). Vitamins A, C, and E dietary intakes and total and individual dietary carotenoids were computed using two 24-h recalls at v1. Cognitive tests, covering global mental status and domains of memory/learning, attention, psychomotor speed, visuo-spatial, language/verbal, and executive function were conducted at v1 and/or v2 (2009–2013); mean ± SD follow-up: 4.66 ± 0.93 years. Mixed-effects linear regression models detected an interaction between vitamin E and total (and individual) carotenoids for three of 11 cognitive tests at v1, with only one meeting the statistical significance upon multiple testing correction whereby vitamin E was linked with greater verbal memory performance in the uppermost total carotenoid tertile (γ0a = +0.26 ± 0.08, p = 0.002), a synergism largely driven by carotenoid lycopene. Vitamins A and C showed no consistent interactions with carotenoids. In conclusion, we provide partial evidence for synergism between vitamin E and carotenoids in relation to better baseline cognitive performance, pending further studies with time-dependent exposures and randomized trials directly examining this synergism. Full article
(This article belongs to the Special Issue Carotenoids and Their Retinoid Conversion Products in the Regulation of Fat Reserves and Dysmetabolic Obesity)
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