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The Role of Nutrition in Gene Regulation

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

Deadline for manuscript submissions: closed (20 March 2023) | Viewed by 8307

Special Issue Editors


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Guest Editor
Department of Nutrition and Food Hygiene, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan 250012, China
Interests: molecular nutrition; spatial nutrition; diabetes and complications; nutrigenetics; functional foods
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Guest Editor
School of Public Health, Sun Yat-Sen University, Guangzhou 510080, China
Interests: phytochemicals; atherosclerosis; lipid metabolism; inflammation; immunometabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Food and nutrition determine the growth, survival, health and illness of every human being. Although food and nutrition have been studied for centuries, modern nutritional science linking gene expression to health and disease is surprisingly young. On one hand, different from the slow genetic evolution in spite of the ~200,000 year human history, our dietary patterns have changed rapidly, especially in the last few decades. This has resulted in the inadaptation of the body, characterized by dysregulated gene expression, leading to nutritional diseases such as obesity, diabetes and complications, cardiovascular diseases, cancer, etc. On the other hand, nutritional deficiencies are still threatening a large proportion of the world population, with limited mechanisms known at the molecular level. Therefore, researchers have been inspired to dissect the role of nutrition in gene regulation, which would unveil the molecular mechanism of nutritional diseases, and provide effective nutritional approaches for their intervention. In this Special Issue, we provide a platform for researchers to share novel advances in the understanding of the role of nutrition in gene regulation. The topics include, but are not limited to:

  • The role of nutrients in gene regulation associated with human health or disease.
  • The effect and molecular action of functional foods, phytochemicals and natural products on nutritional disease.
  • The effect of novel dietary patterns on gene expression associated with human health or disease.

Prof. Dr. Hao Wu
Prof. Dr. Dongliang Wang
Guest Editors

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Published Papers (3 papers)

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Research

17 pages, 2341 KiB  
Article
Supplementation with Natto and Red Yeast Rice Alters Gene Expressions in Cholesterol Metabolism Pathways in ApoE-/- Mice with Concurrent Changes in Gut Microbiota
by Haiyan Zhou, Wenjing Liu, Yiqian Lv, Ke Liu, Yin Wang, Shuangli Meng, Tong Kang, Yuechao Bao and Huicui Meng
Nutrients 2023, 15(4), 973; https://doi.org/10.3390/nu15040973 - 15 Feb 2023
Cited by 2 | Viewed by 2399
Abstract
We aimed to examine the effect of natto and red yeast rice (NR) supplementation on lipid and lipoprotein profiles, gene expressions of cholesterol metabolism, and the composition of gut microbiota in ApoE-/- mice. Forty-one male ApoE-/- mice aged 7–8 wks old [...] Read more.
We aimed to examine the effect of natto and red yeast rice (NR) supplementation on lipid and lipoprotein profiles, gene expressions of cholesterol metabolism, and the composition of gut microbiota in ApoE-/- mice. Forty-one male ApoE-/- mice aged 7–8 wks old were randomly fed a control diet (CD), CD + NR (oral gavage at 0.3 g/kg BW/day), high-fat and high-cholesterol diet (HFD), or HFD + NR for 12 wks. Fasting blood samples, liver and intestine tissues and fecal samples were collected at week 12. Biochemical parameters, gene expressions in cholesterol metabolism and gut microbiota composition and diversity were measured using standard methods. NR supplementation had no significant effect on lipid and lipoprotein profiles. Compared with the HFD group, HFD + NR resulted in higher mRNA expressions of HMGCR and CYP7A1 (both P-NR < 0.05) and ABCA1 (P-diet*NR = 0.0134, P-NR = 0.0407), lower mRNA expression of PCSK9 (P-diet*NR = 0.0002), lower fasting glucose concentrations (P-diet*NR = 0.0011), and lower relative abundance of genera Bacteroides and Lactococcus (both P-NR < 0.01) and Coriobacteriaceae_UCG-002 (P-diet*NR = 0.0007). The relative abundance of Lactococcus was inversely correlated with HMGCR and CYP7A1, and the relative abundance of Coriobacteriaceae_UCG-002 was positively correlated with PCSK9 and inversely correlated with ABCA1 (all P < 0.05). These findings suggest that NR supplementation may regulate gene expressions in cholesterol metabolism via changes in the gut microbiota in HFD-fed ApoE-/- mice. Full article
(This article belongs to the Special Issue The Role of Nutrition in Gene Regulation)
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15 pages, 6567 KiB  
Article
Local Application of Krill Oil Accelerates the Healing of Artificially Created Wounds in Diabetic Mice
by Wenhao Hao, Huali Meng, Hui Li, Yan Zheng, Chunhong Song, Ziping Jiang, Xue Bai, Zhiyue Zhang, Lei Du, Pei Liu and Hao Wu
Nutrients 2022, 14(19), 4139; https://doi.org/10.3390/nu14194139 - 05 Oct 2022
Cited by 1 | Viewed by 2016
Abstract
Diabetes mellitus (DM) impairs the wound healing process, seriously threatening the health of the diabetic population. To date, few effective approaches have been developed for the treatment of diabetic wounds. Krill oil (KO) contains bioactive components that have potent anti-inflammatory and anti-oxidative activities. [...] Read more.
Diabetes mellitus (DM) impairs the wound healing process, seriously threatening the health of the diabetic population. To date, few effective approaches have been developed for the treatment of diabetic wounds. Krill oil (KO) contains bioactive components that have potent anti-inflammatory and anti-oxidative activities. As prolonged inflammation is a crucial contributor to DM-impaired wound healing, we speculated that the local application of KO would accelerate diabetic wound healing. Therefore, KO was applied to artificially created wounds of type 2 diabetic mice induced by streptozotocin and high-fat diet. The diabetic mice had a delayed wound healing process compared with the non-diabetic control mice, with excessive inflammation, impaired collagen deposition, and depressed neovascularization in the wound area. These effects were dramatically reversed by KO. In vitro, KO blocked the TNF-α-induced macrophage inflammation, fibroblast dysfunction, and endothelial angiogenic impairment. The present study in mice suggests that KO local application could be a viable approach in the management of diabetic wounds. Full article
(This article belongs to the Special Issue The Role of Nutrition in Gene Regulation)
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14 pages, 3123 KiB  
Article
Supplementation of Lycium barbarum Polysaccharide Combined with Aerobic Exercise Ameliorates High-Fat-Induced Nonalcoholic Steatohepatitis via AMPK/PPARα/PGC-1α Pathway
by Dou-Dou Li, Jia-Min Ma, Ming-Jing Li, Lu-Lu Gao, Yan-Na Fan, Yan-Nan Zhang, Xiu-Juan Tao and Jian-Jun Yang
Nutrients 2022, 14(15), 3247; https://doi.org/10.3390/nu14153247 - 08 Aug 2022
Cited by 8 | Viewed by 2803
Abstract
Nonalcoholic steatohepatitis (NASH) is a subtype of nonalcoholic fatty liver disease (NAFLD). Either Lycium barbarum polysaccharide (LBP) or aerobic exercise (AE) has been reported to be beneficial to hepatic lipid metabolism. However, whether the combination of LBP with AE improves lipid accumulation of [...] Read more.
Nonalcoholic steatohepatitis (NASH) is a subtype of nonalcoholic fatty liver disease (NAFLD). Either Lycium barbarum polysaccharide (LBP) or aerobic exercise (AE) has been reported to be beneficial to hepatic lipid metabolism. However, whether the combination of LBP with AE improves lipid accumulation of NASH remains unknown. Our study investigated the influence of 10 weeks of treatment of LBP, AE, and the combination (LBP plus AE) on high-fat-induced NASH in Sprague–Dawley rats. The results showed that LBP or AE reduced the severity of the NASH. LBP plus AE treatment more effectively ameliorated liver damage and lowered levels of serum lipid and inflammation. In addition, the combination can also regulate genes involved in hepatic fatty acid synthesis and oxidation. LBP plus AE activated AMPK, thereby increasing the expression of PPARα which controls hepatic fatty acid oxidation and its coactivator PGC-1α. Our study demonstrated the improvement of LBP plus AE on NASH via enhancing fatty acid oxidation (FAO) which was dependent on AMPK/PPARα/PGC-1α pathway. Full article
(This article belongs to the Special Issue The Role of Nutrition in Gene Regulation)
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