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Metabolites
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Diet, Physical Activity, Obesity, and Metabolic Profiles in Relation to...
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Diet, Physical Activity, Obesity, and Metabolic Profiles in Relation to Cancer

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

Deadline for manuscript submissions: closed (15 June 2023) | Viewed by 5931

Special Issue Editors

Dr. Ying Wang

E-Mail Website
Guest Editor
Department of Population Science, American Cancer Society, Atlanta, GA 30303, USA
Interests: nutrition; physical activity; obesity; metabolomics; prostate cancer; lung cancer
Dr. Donghai Liang

E-Mail Website
Co-Guest Editor
Rollins School of Public Health, Atlanta, GA, USA
Interests: air pollution; biomarkers; data science; exposome; exposure assessment; maternal and child health

Special Issue Information

Dear Colleagues,

Modifiable risk factors such as diet, physical activity, and body weight play an important role in cancer incidence and mortality rates. The mechanisms through which these risk factors may affect cancer risk is still largely unknown. High-throughput technologies such as metabolomics, proteomics, and lipidomics can measure hundreds and thousands of small molecules in the human metabolome. The metabolic profile of the human metabolome captures both endogenous and exogenous metabolites, and thus could be a promising source for identifying novel biomarkers of environmental risk factors and furthering our understanding of the mechanisms through which risk factors may affect cancer risk and mortality rates. Furthermore, metabolome-wide association studies, which are non-hypothesis driven, are useful in identifying new risk factors of cancer and generating new hypotheses. Newly identified biomarkers or hypotheses need to be validated in other studies with larger sample sizes or with different populations. In this Special Issue, we welcome the submission of studies that aim to identify cancer risk biomarkers or prognostic biomarkers using multi-omics technologies in human studies or to understand the mediation effects of lifestyle factors on cancer through metabolic profiling.

Dr. Ying Wang
Dr. Donghai Liang
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. Metabolites 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 2700 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

  • metabolomics
  • diet
  • physical activity
  • obesity
  • cancer

Published Papers (3 papers)

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Research

14 pages, 450 KiB  
Article
Dietary Inflammatory and Insulinemic Potentials, Plasma Metabolome and Risk of Colorectal Cancer
by Dong Hoon Lee, Qi Jin, Ni Shi, Fenglei Wang, Alaina M. Bever, Jun Li, Liming Liang, Frank B. Hu, Mingyang Song, Oana A. Zeleznik, Xuehong Zhang, Amit Joshi, Kana Wu, Justin Y. Jeon, Jeffrey A. Meyerhardt, Andrew T. Chan, A. Heather Eliassen, Clary B. Clish, Steven K. Clinton, Edward L. Giovannucci and Fred K. Tabungadd Show full author list remove Hide full author list
Metabolites 2023, 13(6), 744; https://doi.org/10.3390/metabo13060744 - 12 Jun 2023
Cited by 1 | Viewed by 1634
Abstract
The inflammatory and insulinemic potentials of diets have been associated with colorectal cancer risk. However, it is unknown whether the plasma metabolite profiles related to inflammatory diets, or to insulinemic diets, underlie this association. The aim of this study was to evaluate the [...] Read more.
The inflammatory and insulinemic potentials of diets have been associated with colorectal cancer risk. However, it is unknown whether the plasma metabolite profiles related to inflammatory diets, or to insulinemic diets, underlie this association. The aim of this study was to evaluate the association between metabolomic profile scores related to the food-based empirical dietary inflammatory patterns (EDIP), the empirical dietary index for hyperinsulinemia (EDIH), and plasma inflammation (CRP, IL-6, TNFα-R2, adiponectin) and insulin (C-peptide) biomarkers, and colorectal cancer risk. Elastic net regression was used to derive three metabolomic profile scores for each dietary pattern among 6840 participants from the Nurses’ Health Study and Health Professionals Follow-up Study, and associations with CRC risk were examined using multivariable-adjusted logistic regression, in a case-control study of 524 matched pairs nested in both cohorts. Among 186 known metabolites, 27 were significantly associated with both the EDIP and inflammatory biomarkers, and 21 were significantly associated with both the EDIH and C-peptide. In men, odds ratios (ORs) of colorectal cancer, per 1 standard deviation (SD) increment in metabolomic score, were 1.91 (1.31–2.78) for the common EDIP and inflammatory-biomarker metabolome, 1.12 (0.78–1.60) for EDIP-only metabolome, and 1.65 (1.16–2.36) for the inflammatory-biomarkers-only metabolome. However, no association was found for EDIH-only, C-peptide-only, and the common metabolomic signatures in men. Moreover, the metabolomic signatures were not associated with colorectal cancer risk among women. Metabolomic profiles reflecting pro-inflammatory diets and inflammation biomarkers were associated with colorectal cancer risk in men, while no association was found in women. Larger studies are needed to confirm our findings. Full article
(This article belongs to the Special Issue Diet, Physical Activity, Obesity, and Metabolic Profiles in Relation to Cancer)
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13 pages, 1293 KiB  
Article
A Metabolomic Signature of Obesity and Risk of Colorectal Cancer: Two Nested Case–Control Studies
by Mingjia Yang, Chen Zhu, Lingbin Du, Jianv Huang, Jiayi Lu, Jing Yang, Ye Tong, Meng Zhu, Ci Song, Chong Shen, Juncheng Dai, Xiangfeng Lu, Zekuan Xu, Ni Li, Hongxia Ma, Zhibin Hu, Dongfeng Gu, Guangfu Jin, Dong Hang and Hongbing Shen
Metabolites 2023, 13(2), 234; https://doi.org/10.3390/metabo13020234 - 05 Feb 2023
Cited by 2 | Viewed by 2254
Abstract
Obesity is a leading contributor to colorectal cancer (CRC) risk, but the metabolic mechanisms linking obesity to CRC are not fully understood. We leveraged untargeted metabolomics data from two 1:1 matched, nested case–control studies for CRC, including 223 pairs from the US Prostate, [...] Read more.
Obesity is a leading contributor to colorectal cancer (CRC) risk, but the metabolic mechanisms linking obesity to CRC are not fully understood. We leveraged untargeted metabolomics data from two 1:1 matched, nested case–control studies for CRC, including 223 pairs from the US Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial and 190 pairs from a prospective Chinese cohort. We explored serum metabolites related to body mass index (BMI), constructed a metabolomic signature of obesity, and examined the association between the signature and CRC risk. In total, 72 of 278 named metabolites were correlated with BMI after multiple testing corrections (p FDR < 0.05). The metabolomic signature was calculated by including 39 metabolites that were independently associated with BMI. There was a linear positive association between the signature and CRC risk in both cohorts (p for linear < 0.05). Per 1-SD increment of the signature was associated with 38% (95% CI: 9–75%) and 28% (95% CI: 2–62%) higher risks of CRC in the US and Chinese cohorts, respectively. In conclusion, we identified a metabolomic signature for obesity and demonstrated the association between the signature and CRC risk. The findings offer new insights into the underlying mechanisms of CRC, which is critical for improved CRC prevention. Full article
(This article belongs to the Special Issue Diet, Physical Activity, Obesity, and Metabolic Profiles in Relation to Cancer)
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13 pages, 13032 KiB  
Article
Palmitic Acid Promotes Lung Metastasis of Melanomas via the TLR4/TRIF-Peli1-pNF-κB Pathway
by Xuedan Zhang, Xiaoyu Li, Guohang Xiong, Fang Yun, Yu Feng, Qinxuan Ni, Na Wu, Lijuan Yang, Zihan Yi, Qiao Zhang, Zhe Yang, Yingmin Kuang, Buqing Sai and Yuechun Zhu
Metabolites 2022, 12(11), 1132; https://doi.org/10.3390/metabo12111132 - 17 Nov 2022
Cited by 7 | Viewed by 1534
Abstract
A high-fat diet plays an important role in aggravating cancers. Palmitic acid (PA) is one of the components of saturated fatty acids; it has been reported to promote tumor proliferation in melanomas, but the signal transduction pathway mediated by palmitic acid remains unclear. [...] Read more.
A high-fat diet plays an important role in aggravating cancers. Palmitic acid (PA) is one of the components of saturated fatty acids; it has been reported to promote tumor proliferation in melanomas, but the signal transduction pathway mediated by palmitic acid remains unclear. This study showed that palmitic acid can promote the lung metastasis of melanomas. Moreover, the interaction between palmitic acid and toll-like receptor 4 (TLR4) was predicted by molecular docking. The experimental results proved that palmitic acid could promote the TLR4 and Toll/IL-1 receptor domain-containing adaptor-inducing IFN-β (TRIF) expression. The expression of Pellino1 (Peli1) and the phosphorylation of NF-kappa B (pNF-κB) were downregulated after the suppression of TLR4 and the silencing of Peli1 also inhibited the phosphorylation of NF-κB. Therefore, we concluded that palmitic acid promoted the lung metastasis of melanomas through the TLR4/TRIF-Peli1-pNF-κB pathway. Full article
(This article belongs to the Special Issue Diet, Physical Activity, Obesity, and Metabolic Profiles in Relation to Cancer)
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