10
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Time-restricted feeding alters lipid and amino acid metabolite rhythmicity without perturbing clock gene expression

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Time-restricted feeding (TRF) improves metabolism independent of dietary macronutrient composition or energy restriction. To elucidate mechanisms underpinning the effects of short-term TRF, we investigated skeletal muscle and serum metabolic and transcriptomic profiles from 11 men with overweight/obesity after TRF (8 h day −1) and extended feeding (EXF, 15 h day −1) in a randomised cross-over design (trial registration: ACTRN12617000165381). Here we show that muscle core clock gene expression was similar after both interventions. TRF increases the amplitude of oscillating muscle transcripts, but not muscle or serum metabolites. In muscle, TRF induces rhythmicity of several amino acid transporter genes and metabolites. In serum, lipids are the largest class of periodic metabolites, while the majority of phase-shifted metabolites are amino acid related. In conclusion, short-term TRF in overweight men affects the rhythmicity of serum and muscle metabolites and regulates the rhythmicity of genes controlling amino acid transport, without perturbing core clock gene expression.

          Abstract

          Time restricted feeding has several health benefits. Here the authors perform a randomised cross-over study with 11 men with overweight/obesity to investigate how time restricted feeding affects skeletal muscle and serum, and report that it does not affect the core circadian machinery, but modifies periodicity in amino acid related metabolites and transporters.

          Related collections

          Most cited references30

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Organization of GC/MS and LC/MS metabolomics data into chemical libraries

          Background Metabolomics experiments involve generating and comparing small molecule (metabolite) profiles from complex mixture samples to identify those metabolites that are modulated in altered states (e.g., disease, drug treatment, toxin exposure). One non-targeted metabolomics approach attempts to identify and interrogate all small molecules in a sample using GC or LC separation followed by MS or MSn detection. Analysis of the resulting large, multifaceted data sets to rapidly and accurately identify the metabolites is a challenging task that relies on the availability of chemical libraries of metabolite spectral signatures. A method for analyzing spectrometry data to identify and Qu antify I ndividual C omponents in a S ample, (QUICS), enables generation of chemical library entries from known standards and, importantly, from unknown metabolites present in experimental samples but without a corresponding library entry. This method accounts for all ions in a sample spectrum, performs library matches, and allows review of the data to quality check library entries. The QUICS method identifies ions related to any given metabolite by correlating ion data across the complete set of experimental samples, thus revealing subtle spectral trends that may not be evident when viewing individual samples and are likely to be indicative of the presence of one or more otherwise obscured metabolites. Results LC-MS/MS or GC-MS data from 33 liver samples were analyzed simultaneously which exploited the inherent biological diversity of the samples and the largely non-covariant chemical nature of the metabolites when viewed over multiple samples. Ions were partitioned by both retention time (RT) and covariance which grouped ions from a single common underlying metabolite. This approach benefitted from using mass, time and intensity data in aggregate over the entire sample set to reject outliers and noise thereby producing higher quality chemical identities. The aggregated data was matched to reference chemical libraries to aid in identifying the ion set as a known metabolite or as a new unknown biochemical to be added to the library. Conclusion The QUICS methodology enabled rapid, in-depth evaluation of all possible metabolites (known and unknown) within a set of samples to identify the metabolites and, for those that did not have an entry in the reference library, to create a library entry to identify that metabolite in future studies.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Circadian Clocks in Human Red Blood Cells

            Summary Circadian (~24 hour) clocks are fundamentally important for coordinated physiology in organisms as diverse as cyanobacteria and humans. All current models of the clockwork in eukaryotic cells are based on transcription-translation feedback loops. Non-transcriptional mechanisms in the clockwork have been difficult to study in mammalian systems. We circumvented these problems by developing novel assays using human red blood cells (RBCs), which have no nucleus (or DNA), and therefore cannot perform transcription. Our results show that transcription is, in fact, not required for circadian oscillations in humans, and that non-transcriptional events appear sufficient to sustain cellular circadian rhythms. Using RBCs, we found that peroxiredoxins, highly conserved antioxidant proteins, undergo ~24 hour redox cycles, which persist for many days under constant conditions (i.e. in the absence of external cues). Moreover, these rhythms are entrainable (i.e. tunable by environmental stimuli), and temperature-compensated, both key features of circadian rhythms. We anticipate our findings will facilitate more sophisticated cellular clock models, highlighting the interdependency of transcriptional and non-transcriptional oscillations in potentially all eukaryotic cells.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Time-Restricted Feeding Prevents Obesity and Metabolic Syndrome in Mice Lacking a Circadian Clock

              Increased susceptibility of circadian clock mutant mice to metabolic diseases has led to the idea that a molecular clock is necessary for metabolic homeostasis. However, these mice often lack a normal feeding-fasting cycle. We tested whether time-restricted feeding (TRF) could prevent obesity and metabolic syndrome in whole-body Cry1;Cry2 and in liver-specific Bmal1 and Rev-erbα/β knockout mice. When provided access to food ad libitum, these mice rapidly gained weight and showed genotype-specific metabolic defects. However, when fed the same diet under TRF (food access restricted to 10 hr during the dark phase) they were protected from excessive weight gain and metabolic diseases. Transcriptome and metabolome analyses showed that TRF reduced the accumulation of hepatic lipids and enhanced cellular defenses against metabolic stress. These results suggest that the circadian clock maintains metabolic homeostasis by sustaining daily rhythms in feeding and fasting and by maintaining balance between nutrient and cellular stress responses.
                Bookmark

                Author and article information

                Contributors
                Juleen.Zierath@ki.se
                john.hawley@acu.edu.au
                Journal
                Nat Commun
                Nat Commun
                Nature Communications
                Nature Publishing Group UK (London )
                2041-1723
                16 September 2020
                16 September 2020
                2020
                : 11
                : 4643
                Affiliations
                [1 ]GRID grid.5254.6, ISNI 0000 0001 0674 042X, Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, , University of Copenhagen, ; Copenhagen, Denmark
                [2 ]GRID grid.411958.0, ISNI 0000 0001 2194 1270, Exercise and Nutrition Research Program, Mary MacKillop Institute for Health Research, , Australian Catholic University, ; Fitzroy, VIC 3000 Australia
                [3 ]GRID grid.266093.8, ISNI 0000 0001 0668 7243, Center for Epigenetics and Metabolism, INSERM U1233, Department of Biological Chemistry, School of Medicine, , University of California, Irvine, ; Irvine, CA USA
                [4 ]GRID grid.4714.6, ISNI 0000 0004 1937 0626, Department of Molecular Medicine and Surgery, , Karolinska Institutet, ; Stockholm, Sweden
                Author information
                http://orcid.org/0000-0002-4164-7690
                http://orcid.org/0000-0002-8932-0160
                http://orcid.org/0000-0001-7091-3954
                http://orcid.org/0000-0002-0158-519X
                http://orcid.org/0000-0001-6891-7497
                http://orcid.org/0000-0002-0886-9881
                Article
                18412
                10.1038/s41467-020-18412-w
                7495469
                32938935
                a51b6327-bd55-486f-ba1f-4999750a0e54
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 2 May 2019
                : 16 August 2020
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100009708, Novo Nordisk Fonden (Novo Nordisk Foundation);
                Award ID: NNF14OC0011493
                Award ID: NNF18CC003490
                Award Recipient :
                Funded by: FundRef https://doi.org/10.13039/501100004359, Vetenskapsrådet (Swedish Research Council);
                Award ID: 2015-00165
                Award Recipient :
                Categories
                Article
                Custom metadata
                © The Author(s) 2020

                Uncategorized
                metabolic disorders,endocrinology
                Uncategorized
                metabolic disorders, endocrinology

                Comments

                Comment on this article