دورية أكاديمية
أعرض في EDS

Nicotinamide riboside supplementation confers marginal metabolic benefits in obese mice without remodeling the muscle acetyl-proteome.

التفاصيل البيبلوغرافية
العنوان: Nicotinamide riboside supplementation confers marginal metabolic benefits in obese mice without remodeling the muscle acetyl-proteome.
المؤلفون: Williams AS; Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27701, USA., Koves TR; Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27701, USA.; Divison of Geriatrics, Duke University Medical Center, Durham, NC 27710, USA., Pettway YD; Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27701, USA., Draper JA; Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27701, USA., Slentz DH; Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27701, USA., Grimsrud PA; Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27701, USA.; Department of Medicine, Division of Endocrinology, Metabolism, and Nutrition, Duke University Medical Center, Durham, NC 27710, USA., Ilkayeva OR; Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27701, USA.; Department of Medicine, Division of Endocrinology, Metabolism, and Nutrition, Duke University Medical Center, Durham, NC 27710, USA., Muoio DM; Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27701, USA.; Department of Medicine, Division of Endocrinology, Metabolism, and Nutrition, Duke University Medical Center, Durham, NC 27710, USA.; Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.
المصدر: IScience [iScience] 2021 Dec 16; Vol. 25 (1), pp. 103635. Date of Electronic Publication: 2021 Dec 16 (Print Publication: 2022).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101724038 Publication Model: eCollection Cited Medium: Internet ISSN: 2589-0042 (Electronic) Linking ISSN: 25890042 NLM ISO Abbreviation: iScience Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Cambridge, MA] : Cell Press, [2018]-
مستخلص: Nicotinamide riboside supplements (NRS) have been touted as a nutraceutical that promotes cardiometabolic and musculoskeletal health by enhancing nicotinamide adenine dinucleotide (NAD + ) biosynthesis, mitochondrial function, and/or the activities of NAD-dependent sirtuin deacetylase enzymes. This investigation examined the impact of NRS on whole body energy homeostasis, skeletal muscle mitochondrial function, and corresponding shifts in the acetyl-lysine proteome, in the context of diet-induced obesity using C57BL/6NJ mice. The study also included a genetically modified mouse model that imposes greater demand on sirtuin flux and associated NAD + consumption, specifically within muscle tissues. In general, whole body glucose control was marginally improved by NRS when administered at the midpoint of a chronic high-fat diet, but not when given as a preventative therapy upon initiation of the diet. Contrary to anticipated outcomes, the study produced little evidence that NRS increases tissue NAD + levels, augments mitochondrial function, and/or mitigates diet-induced hyperacetylation of the skeletal muscle proteome.
Competing Interests: The authors received NR Chloride as a gift from ChromaDex Inc.
(© 2021 The Authors.)
References: Biophys J. 1999 Jan;76(1 Pt 1):469-77. (PMID: 9876159)
Mol Metab. 2018 Jan;7:1-11. (PMID: 29146412)
Mol Metab. 2021 Nov;53:101271. (PMID: 34119711)
Cell Metab. 2014 Jun 3;19(6):1042-9. (PMID: 24814483)
Cell Metab. 2020 Jan 7;31(1):131-147.e11. (PMID: 31813822)
Cell Rep. 2016 Jan 12;14(2):243-54. (PMID: 26748706)
Am J Physiol Cell Physiol. 2004 Mar;286(3):C565-72. (PMID: 14602577)
J Physiol. 2020 Feb;598(4):731-754. (PMID: 31710095)
Cell Metab. 2014 Dec 2;20(6):1059-68. (PMID: 25470550)
Nutrients. 2019 Oct 13;11(10):. (PMID: 31614949)
Am J Clin Nutr. 2020 Aug 1;112(2):413-426. (PMID: 32320006)
Am J Physiol Endocrinol Metab. 2009 Oct;297(4):E849-55. (PMID: 19638507)
Cell Metab. 2016 Aug 9;24(2):269-82. (PMID: 27508874)
Am J Clin Nutr. 2018 Aug 1;108(2):343-353. (PMID: 29992272)
Science. 2015 Mar 20;347(6228):1374-7. (PMID: 25792330)
Sci Rep. 2016 May 27;6:26933. (PMID: 27230286)
Nucleic Acids Res. 2017 Jan 4;45(D1):D1100-D1106. (PMID: 27924013)
J Clin Endocrinol Metab. 2021 Apr 23;106(5):1437-1447. (PMID: 33524145)
Science. 2016 Jun 17;352(6292):1436-43. (PMID: 27127236)
Cell Metab. 2015 Jul 7;22(1):65-76. (PMID: 26154055)
Annu Rev Biochem. 2004;73:417-35. (PMID: 15189148)
J Exp Biol. 1996 Feb;199(Pt 2):509-12. (PMID: 8930003)
J Biol Chem. 2015 Jan 16;290(3):1546-58. (PMID: 25411251)
Proteomics. 2011 Mar;11(6):1064-74. (PMID: 21298793)
Cell Metab. 2018 Oct 2;28(4):656-666.e1. (PMID: 30017358)
Cell Metab. 2020 Mar 3;31(3):564-579.e7. (PMID: 32130883)
Int J Obes (Lond). 2020 Oct;44(10):2080-2091. (PMID: 32796919)
Nat Methods. 2007 Nov;4(11):923-5. (PMID: 17952086)
Am J Physiol Cell Physiol. 2008 Jan;294(1):C79-87. (PMID: 17942641)
Cell Metab. 2018 Mar 6;27(3):513-528. (PMID: 29249689)
Cell Metab. 2018 Mar 6;27(3):667-676.e4. (PMID: 29514072)
Trends Endocrinol Metab. 2012 Sep;23(9):420-8. (PMID: 22819213)
Eur J Nutr. 2020 Sep;59(6):2427-2437. (PMID: 31494696)
Cell Rep. 2018 Sep 25;24(13):3593-3606.e10. (PMID: 30257218)
J Exp Biol. 1995 Aug;198(Pt 8):1775-82. (PMID: 7636446)
Methods Enzymol. 2014;542:163-81. (PMID: 24862266)
Hepatology. 2016 Apr;63(4):1190-204. (PMID: 26404765)
EMBO Mol Med. 2014 Apr 06;6(6):721-31. (PMID: 24711540)
Nat Commun. 2016 Oct 10;7:12948. (PMID: 27721479)
J Chromatogr B Analyt Technol Biomed Life Sci. 2005 Dec 27;829(1-2):123-35. (PMID: 16275131)
Nat Methods. 2011 Sep 11;8(10):821-7. (PMID: 21983960)
Trends Biochem Sci. 2007 Jan;32(1):12-9. (PMID: 17161604)
J Proteome Res. 2011 Dec 2;10(12):5354-62. (PMID: 22073976)
Cell Metab. 2012 Jun 6;15(6):838-47. (PMID: 22682224)
Nucleic Acids Res. 2016 Jan 4;44(D1):D1251-7. (PMID: 26450961)
Nat Protoc. 2007;2(2):287-95. (PMID: 17406588)
Cell Rep. 2015 Oct 20;13(3):533-545. (PMID: 26456827)
Mol Cell. 2011 Oct 21;44(2):177-90. (PMID: 21856199)
Cell Metab. 2018 May 01;27(5):1067-1080.e5. (PMID: 29685734)
Cell Rep. 2019 Aug 13;28(7):1717-1728.e6. (PMID: 31412242)
Life Sci. 2018 Oct 15;211:1-7. (PMID: 30195617)
Cell. 2004 May 14;117(4):495-502. (PMID: 15137942)
Cell Metab. 2012 May 2;15(5):764-77. (PMID: 22560225)
Biochemistry. 2013 Apr 23;52(16):2793-809. (PMID: 23547908)
Cell Rep. 2019 Feb 5;26(6):1557-1572.e8. (PMID: 30726738)
Proc Natl Acad Sci U S A. 2019 Nov 19;116(47):23822-23828. (PMID: 31694884)
J Cell Biol. 1981 Dec;91(3 Pt 2):227s-255s. (PMID: 7033239)
Sci Transl Med. 2016 Oct 19;8(361):361ra139. (PMID: 27798264)
معلومات مُعتمدة: F32 DK105922 United States DK NIDDK NIH HHS; P30 DK124723 United States DK NIDDK NIH HHS; R01 DK089312 United States DK NIDDK NIH HHS
فهرسة مساهمة: Keywords: Nutrition; Physiology; Proteomics
تواريخ الأحداث: Date Created: 20220114 Latest Revision: 20240510
رمز التحديث: 20240510
مُعرف محوري في PubMed: PMC8741497
DOI: 10.1016/j.isci.2021.103635
PMID: 35028529
قاعدة البيانات: MEDLINE
الوصف
تدمد:2589-0042
DOI:10.1016/j.isci.2021.103635