52
views
0
recommends
+1 Recommend
2 collections
    1
    shares

          The flagship journal of the Society for Endocrinology. Learn more

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

      Nicotinamide riboside has minimal impact on energy metabolism in mouse models of mild obesity

      research-article

      Read this article at

      ScienceOpenPublisherPMC
          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

          Supplementation with precursors of NAD has been shown to prevent and reverse insulin resistance, mitochondrial dysfunction, and liver damage in mouse models of diet-induced obesity. We asked whether the beneficial effects of supplementation with the NAD precursor nicotinamide riboside (NR) are dependent on mouse strain. We compared the effects of NR supplementation on whole-body energy metabolism and mitochondrial function in mildly obese C57BL/6N and C57BL/6J mice, two commonly used strains to investigate metabolism. Male C57BL/6N and C57BL/6J mice were fed a high-fat diet (HFD) or standard chow with or without NR supplementation for 8 weeks. Body and organ weights, glucose tolerance, and metabolic parameters as well as mitochondrial O 2 flux in liver and muscle fibers were assessed. We found that NR supplementation had no influence on body or organ weight, glucose metabolism or hepatic lipid accumulation, energy expenditure, or metabolic flexibility but increased mitochondrial respiration in soleus muscle in both mouse strains. Strain-dependent differences were detected for body and fat depot weight, fasting blood glucose, hepatic lipid accumulation, and energy expenditure. We conclude that, in mild obesity, NR supplementation does not alter metabolic phenotype in two commonly used laboratory mouse strains.

          Related collections

          Most cited references66

          • Record: found
          • Abstract: found
          • Article: not found

          Organelle isolation: functional mitochondria from mouse liver, muscle and cultured fibroblasts.

          Mitochondria participate in key metabolic reactions of the cell and regulate crucial signaling pathways including apoptosis. Although several approaches are available to study mitochondrial function in situ are available, investigating functional mitochondria that have been isolated from different tissues and from cultured cells offers still more unmatched advantages. This protocol illustrates a step-by-step procedure to obtain functional mitochondria with high yield from cells grown in culture, liver and muscle. The isolation procedures described here require 1-2 hours, depending on the source of the organelles. The polarographic analysis can be completed in 1 hour.
            • Record: found
            • Abstract: found
            • Article: not found

            NAD⁺ repletion improves mitochondrial and stem cell function and enhances life span in mice.

            Adult stem cells (SCs) are essential for tissue maintenance and regeneration yet are susceptible to senescence during aging. We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD(+)) and its effect on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence. Treatment with the NAD(+) precursor nicotinamide riboside (NR) induced the mitochondrial unfolded protein response and synthesis of prohibitin proteins, and this rejuvenated MuSCs in aged mice. NR also prevented MuSC senescence in the mdx (C57BL/10ScSn-Dmd(mdx)/J) mouse model of muscular dystrophy. We furthermore demonstrate that NR delays senescence of neural SCs and melanocyte SCs and increases mouse life span. Strategies that conserve cellular NAD(+) may reprogram dysfunctional SCs and improve life span in mammals.
              • Record: found
              • Abstract: found
              • Article: not found

              Nicotinamide mononucleotide, a key NAD(+) intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice.

              Type 2 diabetes (T2D) has become epidemic in our modern lifestyle, likely due to calorie-rich diets overwhelming our adaptive metabolic pathways. One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis, and the NAD(+)-dependent protein deacetylase SIRT1. Here, we show that NAMPT-mediated NAD(+) biosynthesis is severely compromised in metabolic organs by high-fat diet (HFD). Strikingly, nicotinamide mononucleotide (NMN), a product of the NAMPT reaction and a key NAD(+) intermediate, ameliorates glucose intolerance by restoring NAD(+) levels in HFD-induced T2D mice. NMN also enhances hepatic insulin sensitivity and restores gene expression related to oxidative stress, inflammatory response, and circadian rhythm, partly through SIRT1 activation. Furthermore, NAD(+) and NAMPT levels show significant decreases in multiple organs during aging, and NMN improves glucose intolerance and lipid profiles in age-induced T2D mice. These findings provide critical insights into a potential nutriceutical intervention against diet- and age-induced T2D. Copyright © 2011 Elsevier Inc. All rights reserved.

                Author and article information

                Journal
                J Endocrinol
                J Endocrinol
                JOE
                The Journal of Endocrinology
                Bioscientifica Ltd (Bristol )
                0022-0795
                1479-6805
                09 August 2021
                01 October 2021
                : 251
                : 1
                : 111-123
                Affiliations
                [1 ]Institute of Metabolism and Systems Research , College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
                [2 ]School of Science and Technology , Nottingham Trent University, Nottingham, UK
                [3 ]Pediatric Research Center , Hospital for Child and Adolescent Medicine, Leipzig University, Leipzig, Germany
                Author notes
                Correspondence should be addressed to A Garten: a.garten@ 123456bham.ac.uk

                *(G G Lavery and A Garten contributed equally as joint last authors)

                Author information
                http://orcid.org/0000-0002-5354-287X
                Article
                JOE-21-0123
                10.1530/JOE-21-0123
                8494379
                34370682
                95f6b520-4fd3-4768-9041-4c130748b1c1
                © The authors

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 14 July 2021
                : 09 August 2021
                Categories
                Research

                Endocrinology & Diabetes
                vitamin b3,nad,c57bl/6j,high-fat diet,impaired glucose tolerance,mitochondrial function,mouse strain,energy expenditure

                Comments

                Comment on this article

                Related Documents Log