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Metabolites
Special Issues
Organismal Metabolism and Nutritional Support
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Organismal Metabolism and Nutritional Support

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

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 3341

Special Issue Editors

Prof. Dr. Lifeng Yang

E-Mail Website
Guest Editor
The Shanghai Institute of Nutrition and Health (SINH) of the Chinese Academy of Sciences (CAS), Shanghai, China
Interests: tumor metabolism; hepatocyte metabolism
Dr. Lin Wang

E-Mail Website
Guest Editor
Department of Physiology, Institute of Basic Medical Sciences, School of Basic Medicine Peking Union Medical College, Chinese Academy of Medical Sciences, 5 Dong Dan San Tiao, Beijing, China
Interests: metabolic analysis; metabolic imaging

Special Issue Information

Dear Colleagues,

The recent advancements in high throughput technologies such as metabolomics have provided us with the opportunity to explore the biomarkers of biological patient samples and helped to elucidate the functions of small molecules in driving disease progression. Currently, the application of in vivo isotope tracing and metabolic imaging technology for samples from human patients and experimental models enables us to decipher in vivo organismal metabolism under physiological conditions or its metabolic reprogramming locally within the development of chronic diseases. However, many challenges remain to be addressed, including a comprehensive metabolic landscape of organs in different stages of diseases, its cellular metabolic changes under the influence of distinct microenvironments/host dietary intake, discovery of therapeutic targets combining the study of metabolomics with that of other omics, and nutritional support to alleviate disease progression. In this Special Issue, we invite both original and review articles on both technical and biological studies focusing on organismal metabolism and nutritional support.

Prof. Dr. Lifeng Yang
Dr. Lin Wang
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

  • organismal metabolism
  • metabolomics
  • isotope tracing
  • metabolic imaging
  • nutritional support

Published Papers (2 papers)

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Research

15 pages, 3313 KiB  
Article
Untargeted Metabolomics Reveals Alterations of Rhythmic Pulmonary Metabolism in IPF
by Wei Sun, Jiuqiang Ren, Zixian Jia, Puyang Liang, Shengxi Li, Meiyue Song, Yinghao Cao, Haoran Chen, Qiang Luo, Lifeng Yang, Jing Wang, Chen Wang and Lin Wang
Metabolites 2023, 13(10), 1069; https://doi.org/10.3390/metabo13101069 - 10 Oct 2023
Cited by 1 | Viewed by 1343
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive condition characterized by the impairment of alveolar epithelial cells. Despite continued research efforts, the effective therapeutic medication is still absent due to an incomplete understanding of the underlying etiology. It has been shown that [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive condition characterized by the impairment of alveolar epithelial cells. Despite continued research efforts, the effective therapeutic medication is still absent due to an incomplete understanding of the underlying etiology. It has been shown that rhythmic alterations are of significant importance in the pathophysiology of IPF. However, a comprehensive understanding of how metabolite level changes with circadian rhythms in individuals with IPF is lacking. Here, we constructed an extensive metabolite database by utilizing an unbiased reference system culturing with 13C or 15N labeled nutrients. Using LC-MS analysis via ESI and APCI ion sources, 1300 potential water-soluble metabolites were characterized and applied to evaluate the metabolic changes with rhythm in the lung from both wild-type mice and mice with IPF. The metabolites, such as glycerophospholipids and amino acids, in WT mice exhibited notable rhythmic oscillations. The concentrations of phospholipids reached the highest during the fast state, while those of amino acids reached their peak during fed state. Similar diurnal variations in the metabolite rhythm of amino acids and phospholipids were also observed in IPF mice. Although the rhythmic oscillation of metabolites in the urea cycle remained unchanged, there was a significant up-regulation in their levels in the lungs of IPF mice. 15N-ammonia in vivo isotope tracing further showed an increase in urea cycle activity in the lungs of mice with IPF, which may compensate for the reduced efficiency of the hepatic urea cycle. In sum, our metabolomics database and method provide evidence of the periodic changes in lung metabolites, thereby offering valuable insights to advance our understanding of metabolic reprogramming in the context of IPF. Full article
(This article belongs to the Special Issue Organismal Metabolism and Nutritional Support)
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15 pages, 3281 KiB  
Article
Lactobacillus johnsonii Attenuates Liver Steatosis and Bile Acid Dysregulation in Parenteral Nutrition-Fed Rats
by Juan Xu, Yongchang Zhou, Siyang Cheng, Yuling Zhao, Junkai Yan, Ying Wang, Wei Cai and Lu Jiang
Metabolites 2023, 13(10), 1043; https://doi.org/10.3390/metabo13101043 - 29 Sep 2023
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Abstract
Parenteral nutrition (PN), a vital therapy for patients with intestinal failure, can lead to the development of parenteral nutrition-associated liver disease (PNALD). In this study, we aimed to investigate the role of Lactobacillus johnsonii (L. johnsonii) in a rat model of [...] Read more.
Parenteral nutrition (PN), a vital therapy for patients with intestinal failure, can lead to the development of parenteral nutrition-associated liver disease (PNALD). In this study, we aimed to investigate the role of Lactobacillus johnsonii (L. johnsonii) in a rat model of PNALD. Total parenteral nutrition (TPN)-fed rats were used to assess the role of L. johnsonii in liver steatosis, bile acid metabolism, gut microbiota, and hepatocyte apoptosis. We observed a depletion of L. johnsonii that was negatively correlated with the accumulation of glycochenodeoxycholic acid (GCDCA), a known apoptosis inducer, in rats subjected to TPN. L. johnsonii attenuated TPN-induced liver steatosis by inhibiting fatty acid synthesis and promoting fatty acid oxidation. TPN resulted in a decrease in bile acid synthesis and biliary bile secretion, which were partially restored by L. johnsonii treatment. The gut microbial profile revealed depletion of pathogenic bacteria in L. johnsonii-treated rats. L. johnsonii treatment reduced both hepatic GCDCA levels and hepatocyte apoptosis compared with the TPN group. In vitro, L. johnsonii treatment inhibited GCDCA-induced hepatocyte apoptosis via its bile salt hydrolase (BSH) activity. Our findings suggest that L. johnsonii protects against liver steatosis, bile acid dysregulation, and hepatocyte apoptosis in TPN-fed rats. Full article
(This article belongs to the Special Issue Organismal Metabolism and Nutritional Support)
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