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A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 34012

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Dr. Xinhui Wang

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Guest Editor

School of Medicine, Zhejiang University, Hangzhou 310058, China
Interests: nutrition; metabolism; trace elements; diabetes; aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nutrition and metabolism are critical life-sustaining parts of human health. The nutritional and metabolic status profoundly affects the function and activity of the endocrine and immune systems. Malnutrition and the disruption of metabolic processes widely affect and exacerbate various health problems, including chronic diseases, infectious diseases, and death. On the contrary, interventions with specific nutrients or metabolites are effective in disease prevention and management. Many basic metabolic pathways are evolutionarily conserved due to their fundamental roles in vastly different species, which make it possible to use model organisms to study the interaction among nutrition, metabolism, and the pathological processes of diseases. Recent advances in nutritional evaluation, metabolic profiling, the establishment of animal models, and the development of novel analytical methods have provided insights into the basis of nutrition- and metabolism-related diseases. However, many theoretical and clinical issues remain to be explored. Therefore, for this Special Issue, we welcome high-quality original research papers and reviews in the fields of nutrition and metabolism.

We welcome submissions on research across various diseases, including obesity, diabetes, cardiovascular diseases, fatty liver disease, cancer, neurodegenerative diseases, autoimmune diseases, infectious diseases, and any other diseases related to nutrition and metabolism. The topics that will be covered include but are not limited to studies on the nutritional intervention for disease prevention and management, mechanisms of nutrient- and metabolite-regulated pathological processes, animal models for nutrition and disease, methodologies for the characterization of the metabolic status in disease, and causality between nutritional or metabolic factors and diseases.

Dr. Xinhui Wang
Guest Editor

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Keywords

nutrition
metabolism
nutrient
metabolite
disease

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Published Papers (12 papers)

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Research

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15 pages, 8208 KiB

Open AccessArticle

Causal Effects of Blood Lipid Traits on Inflammatory Bowel Diseases: A Mendelian Randomization Study

by Ziqin Yao, Feiyu Jiang, Hongbin Luo, Jiahui Zhou, Wanting Shi, Shoufang Xu, Yingying Zhang, Feng Dai, Xinran Li, Zhiwei Liu and Xinhui Wang

Metabolites 2023, 13(6), 730; https://doi.org/10.3390/metabo13060730 - 7 Jun 2023

Cited by 6 | Viewed by 2170

Abstract

Inflammatory bowel diseases (IBDs), including Crohn’s disease (CD) and ulcerative colitis (UC), have become a global health problem with a rapid growth of incidence in newly industrialized countries. Observational studies have recognized associations between blood lipid traits and IBDs, but the causality still remains unclear. To determine the causal effects of blood lipid traits, including triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) on IBDs, two-sample Mendelian randomization (MR) analyses were conducted using the summary-level genome-wide association study (GWAS) statistics of blood lipid traits and IBDs. Our univariable MR using multiplicative random-effect inverse-variance weight (IVW) method identified TC (OR: 0.674; 95% CI: 0.554, 0.820; p < 0.00625) and LDL-C (OR: 0.685; 95% CI: 0.546, 0.858; p < 0.00625) as protective factors of UC. The result of our multivariable MR analysis further provided suggestive evidence of the protective effect of TC on UC risk (OR: 0.147; 95% CI: 0.025, 0.883; p < 0.05). Finally, our MR-BMA analysis prioritized TG (MIP: 0.336;

\hat{θ}

_MACE: −0.025; PP: 0.31;

\hat{θ}

_λ: −0.072) and HDL-C (MIP: 0.254;

\hat{θ}

_MACE: −0.011; PP: 0.232;

\hat{θ}

_λ: −0.04) for CD and TC (MIP: 0.721;

\hat{θ}

_MACE: −0.257; PP: 0.648;

\hat{θ}

_λ: −0.356) and LDL-C (MIP: 0.31;

\hat{θ}

_MACE: −0.095; PP: 0.256;

\hat{θ}

_λ: −0.344) for UC as the top-ranked protective factors. In conclusion, the causal effect of TC for UC prevention was robust across all of our MR approaches, which provide the first evidence that genetically determined TC is causally associated with reduced risk of UC. The finding of this study provides important insights into the metabolic regulation of IBDs and potential metabolites targeting strategies for IBDs intervention. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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13 pages, 17396 KiB

Open AccessArticle

Multi-Omics Unravels Metabolic Alterations in the Ileal Mucosa of Neonatal Piglets Receiving Total Parenteral Nutrition

by Junkai Yan, Yuling Zhao, Lu Jiang, Ying Wang and Wei Cai

Metabolites 2023, 13(4), 555; https://doi.org/10.3390/metabo13040555 - 13 Apr 2023

Cited by 1 | Viewed by 1637

Abstract

Total parenteral nutrition (TPN) is life-saving therapy for the pediatric patients with intestinal failure (IF) who cannot tolerate enteral nutrition (EN). However, TPN-induced metabolic alterations are also a critical issue for the maintenance of intestinal homeostasis, and thus the global metabolomic signatures need to be addressed. In this study, ileal mucosal biopsies were collected from 12 neonatal Bama piglets receiving either EN or TPN for 14 days, and changes in the intestinal metabolism were examined by multi-omics (HM350 Metabolomics + Tandem Mass Tag (TMT)-based proteomics). As a result, a total of 240 compounds were identified by metabolomics, including 56 down-regulated and 9 up-regulated metabolites. Notably, tissue levels of fatty acyl-carnitines (decreased by 35–85%) and succinate (decreased by 89%) dramatically decreased in the TPN group, suggestive of disrupted processes of fatty acid oxidation (FAO) and the citrate cycle, respectively. Interestingly, however, no differences were found in the production of adenosine 5′-triphosphate (ATP) between groups, suggesting that these dysregulated metabolites may have mainly led to the loss of bioactive compounds rather than energy deficit. Additionally, 4813 proteins were identified by proteomics in total, including 179 down-regulated and 329 up-regulated proteins. The analysis of protein–protein interactions (PPI) indicated that most of the differentially expressed proteins were clustered into “lipid metabolism” and “innate immune responses”. In summary, this work provided new findings in TPN-induced intestinal metabolic alterations, which would be useful to the improvement of nutritional management for IF patients. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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20 pages, 3528 KiB

Open AccessArticle

Mendelian Randomization Analysis Provides Insights into the Pathogenesis of Serum Levels of Branched-Chain Amino Acids in Cardiovascular Disease

by Wenxi Jiang, Ke Lu, Zhenhuang Zhuang, Xue Wang, Xun Tang, Tao Huang, Pei Gao, Yuan Wang and Jie Du

Metabolites 2023, 13(3), 403; https://doi.org/10.3390/metabo13030403 - 9 Mar 2023

Cited by 6 | Viewed by 3619

Abstract

Several observational studies have indicated an association between high serum levels of branched-chain amino acids (BCAAs) and an increased risk of cardiovascular disease (CVD). To assess whether theses associations reflect causality, we carried out two-sample Mendelian randomization (MR). Single-nucleotide polymorphisms (SNPs) associated with BCAA were evaluated in 10 studies, including 24,925 participants. The association between SNPs and coronary artery disease (CAD) were assessed using summary estimates from the CARDIoGRAMplusC4D consortium. Further MR analysis of BCAAs and seven CVD outcomes was performed. The BCAA-raising gene functions were also analyzed. MR analyses revealed a risk-increasing causal relationship between serum BCAA concentrations and CAD (odds ratio 1.08; 95% confidence interval (CI) 1.02–1.14), which was partly mediated by blood pressure and type 2 diabetes. BCAA also demonstrated a causal relationship with ischemic CVD events induced by plaque rupture and thrombosis (false discovery rate <0.05). Two BCAA-raising genes (MRL33 and CBLN1) were preferentially associated with myocardial infarction risk in the presence of atherosclerosis (p < 0.003). Functional analysis of the BCAA-raising genes suggested the causal involvement of two pathophysiological pathways, including glucose metabolism (PPM1K and TRMT61A) related to plaque progression, and the newly discovered neuroendocrine disorders regulating blood pressure (MRPL33, CBLN1, and C2orf16) related to plaque rupture and thrombosis. This comprehensive MR analysis provided insights into the potential causal mechanisms linking BCAA with CVD risk and suggested targeting neuroendocrine disorders as a potential strategy for the prevention of CVD. These results warrant further studies to elucidate the mechanisms underlying these reported causal associations. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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9 pages, 721 KiB

Open AccessArticle

Association of Sarcopenia with Cognitive Function and Dementia Risk Score: A National Prospective Cohort Study

by Ailing Lin, Ting Wang, Chenxi Li, Fan Pu, Zeinab Abdelrahman, Mengqi Jin, Zhenqing Yang, Liming Zhang, Xingqi Cao, Kaili Sun, Tongyao Hou, Zuyun Liu, Liying Chen and Zuobing Chen

Metabolites 2023, 13(2), 245; https://doi.org/10.3390/metabo13020245 - 8 Feb 2023

Cited by 7 | Viewed by 2156

Abstract

The relationship between skeletal muscle and cognitive disorders has drawn increasing attention. This study aims to examine the associations of sarcopenia with cognitive function and dementia risk score. Data on 1978 participants (aged 65 years and older) from the 2011 wave of the China Health and Retirement Longitudinal Study, with four follow-up waves to 2018, were used. Cognitive function was assessed by four dimensions, with a lower score indicating lower cognitive function. Dementia risk was assessed by a risk score using the Rotterdam Study Basic Dementia Risk Model (BDRM), with a higher score indicating a greater risk. Sarcopenia was defined when low muscle mass plus low muscle strength or low physical performance were met. We used generalized estimating equations to examine the associations of sarcopenia. In the fully adjusted models, sarcopenia was significantly associated with lower cognitive function (standardized, β = −0.15; 95% CIs: −0.26, −0.04) and a higher BDRM score (standardized, β = 0.42; 95% CIs: 0.29, 0.55). Our findings may provide a new avenue for alleviating the burden of cognitive disorders by preventing sarcopenia. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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10 pages, 1555 KiB

Open AccessArticle

Appraising the Effects of Metabolic Traits on the Risk of Glaucoma: A Mendelian Randomization Study

by Kai Wang, Fangkun Yang, Xin Liu, Xueqi Lin, Houfa Yin, Qiaomei Tang, Li Jiang and Ke Yao

Metabolites 2023, 13(1), 109; https://doi.org/10.3390/metabo13010109 - 9 Jan 2023

Cited by 6 | Viewed by 2882

Abstract

Metabolic traits are associated with the risk of developing glaucoma in observational studies. To assess whether theses associations reflect causality, we conducted a Mendelian randomization (MR) study. Our study included up to 20,906 glaucoma cases and 438,188 controls. Genetic instruments associated with the concerned 11 exposures at the genome-wide significance level were selected from corresponding genome-wide association studies. Summary-level data for glaucoma were obtained from the UK Biobank, the GERA study, and the FinnGen consortium. Univariable and multivariable MR analyses were conducted separately in two populations. Our results showed that higher genetic liability to type 2 diabetes (T2D) was causally and independently associated with an increased risk of glaucoma (odds ratio [OR], 1.11; 95% confidence interval [CI], 1.06–1.16; p = 4.4 × 10⁻⁶). The association for T2D persisted after multivariable adjustment. In addition, higher genetically predicted systolic blood pressure (SBP), fasting glucose (FG), and HbA1c, were also suggestively associated with glaucoma risk. The OR was 1.08 (95% CI, 1.01–1.16; p = 0.035) for SBP, 1.24 (95% CI, 1.05–1.47; p = 0.011) for FG, and 1.28 (95% CI, 1.01–1.61; p = 0.039) for HbA1c. No evidence was observed to support the causal effects of body mass index and blood lipids for glaucoma. This study suggests a causal role for diabetes, as well as possible roles for higher SBP, FG, and HbA1c in the development of glaucoma. Further validation is needed to assess the potential of these risk factors as pharmacological targets for glaucoma prevention. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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10 pages, 392 KiB

Open AccessArticle

Causal Effects of Circulating Lipid Traits on Epithelial Ovarian Cancer: A Two-Sample Mendelian Randomization Study

by Hongen Meng, Rong Wang, Zijun Song and Fudi Wang

Metabolites 2022, 12(12), 1175; https://doi.org/10.3390/metabo12121175 - 25 Nov 2022

Cited by 2 | Viewed by 1999

Abstract

Ovarian cancer (OC), and particularly epithelial OC (EOC), is an increasing challenge for women. Circulating lipids play different roles in the occurrence and development of OC, but no causal relationship has been confirmed. We used two-sample Mendelian randomization (MR) to evaluate the genetic effects of circulating Apolipoprotein A1 (APOA1), Apolipoprotein B (APOB), high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and triglyc-erides (TG) on EOC risks based on summary data obtained from the UK Biobank and the Ovarian Cancer Association Consortium. We used the inverse-variance weight as the main statistical method and the MR-Egger, weighted median, and MR-PRESSO for sensitivity analysis. A 1-SD increment in HDL gave odds ratios (OR) and 95% confidence intervals (CI) of OR = 0.80 (95% CI: 0.69–0.93), OR = 0.77 (95% CI: 0.66–0.90), and OR = 0.76 (95% CI: 0.63–0.90) for low malignant potential OC (LMPOC), low-grade low malignant OC (LGLMSOC), and low malignant serous OC (LMSOC), respectively. Genetic liability due to TG was associated with an increased risk of LGLMSOC and LGSOC and a suggestive association with an increased risk of LMSOC (p = 0.001, p = 0.007, and p = 0.027, respectively). Circulating HDL was negatively associated with the risk of LMPOC, LGLMSOC, and LMSOC, while elevated circulating TG levels genetically predicted an increased risk of LGLMSOC and LGSOC. Further research is needed to investigate the causal effects of lipids on EOC and potential intervention and therapeutic targets. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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14 pages, 2596 KiB

Open AccessFeature PaperArticle

Vitamin B6 Inhibits High Glucose-Induced Islet β Cell Apoptosis by Upregulating Autophagy

by Yu Zhang, Xi-an Zhou, Chuxin Liu, Qingwu Shen and Yanyang Wu

Metabolites 2022, 12(11), 1048; https://doi.org/10.3390/metabo12111048 - 31 Oct 2022

Cited by 14 | Viewed by 2024

Abstract

Vitamin B6 may alleviate diabetes by regulating insulin secretion and increasing insulin sensitivity, but its mechanism remains to be explored. In this study, vitamin B6-mediated autophagy and high glucose-induced apoptosis were tested to investigate the mechanism by which vitamin B6 regulates insulin release. The results showed that 20 mM glucose increased the apoptosis rate from 10.39% to 22.44%. Vitamin B6 reduced the apoptosis rate of RIN-m5F cells from 22.44% to 11.31%. Our data also showed that the vitamin B6 content in processed eggs was decreased and that the hydrothermal process did not affect the bioactivity of vitamin B6. Vitamin B6 increased the number of autophagosomes and the ratio of autophagosome marker protein microtubule associated protein 1 light chain 3 beta to microtubule associated protein 1 light chain 3 alpha (LC3-II/LC3-I). It also decreased the amount of sequetosome 1 (SQSTM1/p62) and inhibited the phosphorylation of p70 ribosomal protein S6 kinase (p70S6K) under normal and high glucose stress. Another study showed that vitamin B6 inhibited the apoptosis rate, whereas the autophagy inhibitor 3-methyladenine (3-MA) blocked the protective effect of vitamin B6 against apoptosis induced by high glucose. The hydrothermal process decreased the vitamin B6 content in eggs but had no effect on the cytoprotective function of vitamin B6 in RIN-m5f cells. In conclusion, we demonstrated that vitamin B6-mediated autophagy protected RIN-m5f cells from high glucose-induced apoptosis might via the mTOR-dependent pathway. Our data also suggest that low temperatures and short-term hydrothermal processes are beneficial for dietary eggs. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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Review

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20 pages, 3455 KiB

Open AccessReview

The Metabolism and Immune Environment in Diffuse Large B-Cell Lymphoma

by Jianbo Wu, Fuqing Meng, Danyang Ran, Yalong Song, Yunkun Dang, Fan Lai, Longyan Yang, Mi Deng, Yuqin Song and Jun Zhu

Metabolites 2023, 13(6), 734; https://doi.org/10.3390/metabo13060734 - 8 Jun 2023

Cited by 2 | Viewed by 2197

Abstract

Cells utilize different metabolic processes to maintain their growth and differentiation. Tumor cells have made some metabolic changes to protect themselves from malnutrition. These metabolic alterations affect the tumor microenvironment and macroenvironment. Developing drugs targeting these metabolic alterations could be a good direction. In this review, we briefly introduce metabolic changes/regulations of the tumor macroenvironment and microenvironment and summarize potential drugs targeting the metabolism in diffuse large B-cell lymphoma. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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22 pages, 1419 KiB

Open AccessReview

Integrated Control of Fatty Acid Metabolism in Heart Failure

by Xiaoting Li and Xukun Bi

Metabolites 2023, 13(5), 615; https://doi.org/10.3390/metabo13050615 - 29 Apr 2023

Cited by 8 | Viewed by 3867

Abstract

Disrupted fatty acid metabolism is one of the most important metabolic features in heart failure. The heart obtains energy from fatty acids via oxidation. However, heart failure results in markedly decreased fatty acid oxidation and is accompanied by the accumulation of excess lipid moieties that lead to cardiac lipotoxicity. Herein, we summarized and discussed the current understanding of the integrated regulation of fatty acid metabolism (including fatty acid uptake, lipogenesis, lipolysis, and fatty acid oxidation) in the pathogenesis of heart failure. The functions of many enzymes and regulatory factors in fatty acid homeostasis were characterized. We reviewed their contributions to the development of heart failure and highlighted potential targets that may serve as promising new therapeutic strategies. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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15 pages, 1936 KiB

Open AccessFeature PaperReview

Non-Negligible Role of Trace Elements in Influenza Virus Infection

by Shan Xu, Duanyang Wang, Wenqi Zhao, Qinglin Wei and Yigang Tong

Metabolites 2023, 13(2), 184; https://doi.org/10.3390/metabo13020184 - 26 Jan 2023

Cited by 2 | Viewed by 1932

Abstract

Influenza virus has continuously spread around the globe for more than 100 years since the first influenza epidemic in 1918. The rapid and unpredictable gene variation of the influenza virus could possibly bring about another pandemic in future, which might threaten to overwhelm us without adequate preparation. Consequently, it is extremely urgent to identify effective broad-spectrum antiviral treatments for a variety of influenza virus variants. As essential body components, trace elements are great potential candidates with an as yet poorly understood ability to protect the host from influenza infection. Herein, we have summarized the present state of knowledge concerning the function of trace elements in influenza virus replication along with an analysis of their potential molecular mechanisms. Modulation of host immune responses to the influenza virus is one of the most common modes to achieve the anti-influenza activity of trace elements, such as selenium and zinc. Simultaneously, some antioxidant and antiviral signal pathways can be altered with the participation of trace elements. More interestingly, some micro-elements including selenium, zinc, copper and manganese, directly target viral proteins and regulate their stability and activity to influence the life cycle of the influenza virus. Further verification of the antiviral effect and the mechanism will promote the application of trace elements as adjuvants in the clinic. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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15 pages, 1481 KiB

Open AccessReview

Regeneration of Pancreatic β-Cells for Diabetes Therapeutics by Natural DYRK1A Inhibitors

by Yichuan Guo, Lingqiao Li, Yuanfa Yao and Hanbing Li

Metabolites 2023, 13(1), 51; https://doi.org/10.3390/metabo13010051 - 29 Dec 2022

Cited by 5 | Viewed by 4164

Abstract

The pathogenesis of diabetes mellitus is characterized by insulin resistance and islet β-cell dysfunction. Up to now, the focus of diabetes treatment has been to control blood glucose to prevent diabetic complications. There is an urgent need to develop a therapeutic approach to restore the mass and function of β-cells. Although exogenous islet cell transplantation has been used to help patients control blood glucose, it is costly and has very narrow application scenario. So far, small molecules have been reported to stimulate β-cell proliferation and expand β-cell mass, increasing insulin secretion. Dual-specificity tyrosine-regulated kinase 1A (DYRK1A) inhibitors can induce human β-cell proliferation in vitro and in vivo, and show great potential in the field of diabetes therapeutics. From this perspective, we elaborated on the mechanism by which DYRK1A inhibitors regulate the proliferation of pancreatic β-cells, and summarized several effective natural DYRK1A inhibitors, hoping to provide clues for subsequent structural optimization and drug development in the future. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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Other

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20 pages, 1239 KiB

Open AccessSystematic Review

Blueberry Consumption and Changes in Obesity and Diabetes Mellitus Outcomes: A Systematic Review

by Mayara Souza de Oliveira, Felipe Mateus Pellenz, Bianca Marmontel de Souza and Daisy Crispim

Metabolites 2023, 13(1), 19; https://doi.org/10.3390/metabo13010019 - 22 Dec 2022

Cited by 8 | Viewed by 3822

Abstract

Low-grade inflammation and oxidative stress are key mechanisms involved in obesity and related disorders. Polyphenols from blueberry (BB) and bilberries (BiB) might protect against oxidative damage and inflammation. To summarize the effects of BiB or BB consumption in parameters related to obesity and its comorbidities, a search of the literature was performed in PubMed, Embase, and Cochrane Library repositories to identify all studies that evaluated associations of whole BB or BiB with obesity and associated disorders. Thirty-one studies were eligible for inclusion in this review: eight clinical trials and 23 animal studies. In humans, BB consumption only consistently decreased oxidative stress and improved endothelial function. In rodents, BB or BiB consumption caused positive effects on glucose tolerance, nuclear factor-kappa B (Nf-κb) activity, oxidative stress, and triglyceride (TG) content in the liver and hepatic steatosis. The high content of anthocyanins present in BB and BiB seems to attenuate oxidative stress. The decrease in oxidative stress may have a positive impact on glucose tolerance and endothelial function. Moreover, in rodents, these berries seem to protect against hepatic steatosis, through the decreased accumulation of hepatic TGs. BB and BiB might also attenuate inflammation by decreasing Nf-κb activity and immune cell recruitment into the adipose tissue. Full article

(This article belongs to the Special Issue Nutrition and Metabolism in Human Diseases)

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