Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice
NAD+ availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD+ intermediate, has been shown to enhance NAD+ biosynthesis and ameliorate various pathologies in mouse disease models. In this study, we conducted a 12-month-long NMN administration t...
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| Published in | Cell metabolism Vol. 24; no. 6; pp. 795 - 806 |
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| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
13.12.2016
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| Subjects | |
| Online Access | Get full text |
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| Abstract | NAD+ availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD+ intermediate, has been shown to enhance NAD+ biosynthesis and ameliorate various pathologies in mouse disease models. In this study, we conducted a 12-month-long NMN administration to regular chow-fed wild-type C57BL/6N mice during their normal aging. Orally administered NMN was quickly utilized to synthesize NAD+ in tissues. Remarkably, NMN effectively mitigates age-associated physiological decline in mice. Without any obvious toxicity or deleterious effects, NMN suppressed age-associated body weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and plasma lipid profile, and ameliorated eye function and other pathophysiologies. Consistent with these phenotypes, NMN prevented age-associated gene expression changes in key metabolic organs and enhanced mitochondrial oxidative metabolism and mitonuclear protein imbalance in skeletal muscle. These effects of NMN highlight the preventive and therapeutic potential of NAD+ intermediates as effective anti-aging interventions in humans.
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•NMN suppresses age-associated body weight gain and enhances energy metabolism•NMN improves insulin sensitivity, eye function, and other features with no toxicity•NMN prevents age-associated gene expression changes in a tissue-specific manner•NMN is an effective anti-aging intervention that could be translated to humans
Mills et al. conducted a 12-month-long administration of nicotinamide mononucleotide (NMN), a key natural NAD+ intermediate, to normal wild-type mice, demonstrating that NMN effectively mitigates age-associated physiological decline in mice without any obvious toxicity. These results highlight the significant potential of NMN as an effective anti-aging intervention in humans. |
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| AbstractList | NAD+ availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD+ intermediate, has been shown to enhance NAD+ biosynthesis and ameliorate various pathologies in mouse disease models. In this study, we conducted a 12-month-long NMN administration to regular chow-fed wild-type C57BL/6N mice during their normal aging. Orally administered NMN was quickly utilized to synthesize NAD+ in tissues. Remarkably, NMN effectively mitigates age-associated physiological decline in mice. Without any obvious toxicity or deleterious effects, NMN suppressed age-associated body weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and plasma lipid profile, and ameliorated eye function and other pathophysiologies. Consistent with these phenotypes, NMN prevented age-associated gene expression changes in key metabolic organs and enhanced mitochondrial oxidative metabolism and mitonuclear protein imbalance in skeletal muscle. These effects of NMN highlight the preventive and therapeutic potential of NAD+ intermediates as effective anti-aging interventions in humans.
[Display omitted]
•NMN suppresses age-associated body weight gain and enhances energy metabolism•NMN improves insulin sensitivity, eye function, and other features with no toxicity•NMN prevents age-associated gene expression changes in a tissue-specific manner•NMN is an effective anti-aging intervention that could be translated to humans
Mills et al. conducted a 12-month-long administration of nicotinamide mononucleotide (NMN), a key natural NAD+ intermediate, to normal wild-type mice, demonstrating that NMN effectively mitigates age-associated physiological decline in mice without any obvious toxicity. These results highlight the significant potential of NMN as an effective anti-aging intervention in humans. NAD+ availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD+ intermediate, has been shown to enhance NAD+ biosynthesis and ameliorate various pathologies in mouse disease models. In this study, we conducted a 12-month-long NMN administration to regular chow-fed wild-type C57BL/6N mice during their normal aging. Orally administered NMN was quickly utilized to synthesize NAD+ in tissues. Remarkably, NMN effectively mitigates age-associated physiological decline in mice. Without any obvious toxicity or deleterious effects, NMN suppressed age-associated body weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and plasma lipid profile, and ameliorated eye function and other pathophysiologies. Consistent with these phenotypes, NMN prevented age-associated gene expression changes in key metabolic organs and enhanced mitochondrial oxidative metabolism and mitonuclear protein imbalance in skeletal muscle. These effects of NMN highlight the preventive and therapeutic potential of NAD+ intermediates as effective anti-aging interventions in humans.NAD+ availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD+ intermediate, has been shown to enhance NAD+ biosynthesis and ameliorate various pathologies in mouse disease models. In this study, we conducted a 12-month-long NMN administration to regular chow-fed wild-type C57BL/6N mice during their normal aging. Orally administered NMN was quickly utilized to synthesize NAD+ in tissues. Remarkably, NMN effectively mitigates age-associated physiological decline in mice. Without any obvious toxicity or deleterious effects, NMN suppressed age-associated body weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and plasma lipid profile, and ameliorated eye function and other pathophysiologies. Consistent with these phenotypes, NMN prevented age-associated gene expression changes in key metabolic organs and enhanced mitochondrial oxidative metabolism and mitonuclear protein imbalance in skeletal muscle. These effects of NMN highlight the preventive and therapeutic potential of NAD+ intermediates as effective anti-aging interventions in humans. NAD + availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD + intermediate, has been shown to enhance NAD + biosynthesis and ameliorate various pathologies in mouse disease models. In this study, we conducted a 12 month-long NMN administration to regular chow-fed wild-type C57BL/6N mice during their normal aging. Orally administered NMN was quickly utilized to synthesize NAD + in tissues. Remarkably, NMN effectively mitigates age-associated physiological decline in mice. Without any obvious toxicity or deleterious effects, NMN suppressed age-associated body weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and plasma lipid profile, and ameliorated eye function and other pathophysiologies. Consistent with these phenotypes, NMN prevented age-associated gene expression changes in key metabolic organs and enhanced mitochondrial oxidative metabolism and mitonuclear protein imbalance in skeletal muscle. These effects of NMN highlight the preventive and therapeutic potential of NAD + intermediates as effective anti-aging interventions in humans. NAD availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD intermediate, has been shown to enhance NAD biosynthesis and ameliorate various pathologies in mouse disease models. In this study, we conducted a 12-month-long NMN administration to regular chow-fed wild-type C57BL/6N mice during their normal aging. Orally administered NMN was quickly utilized to synthesize NAD in tissues. Remarkably, NMN effectively mitigates age-associated physiological decline in mice. Without any obvious toxicity or deleterious effects, NMN suppressed age-associated body weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and plasma lipid profile, and ameliorated eye function and other pathophysiologies. Consistent with these phenotypes, NMN prevented age-associated gene expression changes in key metabolic organs and enhanced mitochondrial oxidative metabolism and mitonuclear protein imbalance in skeletal muscle. These effects of NMN highlight the preventive and therapeutic potential of NAD intermediates as effective anti-aging interventions in humans. |
| Author | Sasaki, Yo Kubota, Shunsuke Migaud, Marie E. Uchida, Koji Imai, Shin-ichiro Yoshino, Jun Apte, Rajendra S. Grozio, Alessia Mills, Kathryn F. Stein, Liana R. Redpath, Philip Yoshida, Shohei |
| AuthorAffiliation | 1 Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA 6 Center for Human Nutrition, Division of Geriatrics and Nutritional Science, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA 4 Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA 2 Oriental Yeast Co., Tokyo, Japan 3 Department of Ophthalmology, Washington University School of Medicine, St. Louis, MO 63110, USA 5 School of Pharmacy, Queen’s University Belfast, UK |
| AuthorAffiliation_xml | – name: 6 Center for Human Nutrition, Division of Geriatrics and Nutritional Science, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA – name: 2 Oriental Yeast Co., Tokyo, Japan – name: 5 School of Pharmacy, Queen’s University Belfast, UK – name: 3 Department of Ophthalmology, Washington University School of Medicine, St. Louis, MO 63110, USA – name: 4 Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA – name: 1 Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA |
| Author_xml | – sequence: 1 givenname: Kathryn F. surname: Mills fullname: Mills, Kathryn F. organization: Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA – sequence: 2 givenname: Shohei surname: Yoshida fullname: Yoshida, Shohei organization: Oriental Yeast Company, Tokyo 174-0051, Japan – sequence: 3 givenname: Liana R. surname: Stein fullname: Stein, Liana R. organization: Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA – sequence: 4 givenname: Alessia surname: Grozio fullname: Grozio, Alessia organization: Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA – sequence: 5 givenname: Shunsuke surname: Kubota fullname: Kubota, Shunsuke organization: Department of Ophthalmology, Washington University School of Medicine, St. Louis, MO 63110, USA – sequence: 6 givenname: Yo surname: Sasaki fullname: Sasaki, Yo organization: Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA – sequence: 7 givenname: Philip surname: Redpath fullname: Redpath, Philip organization: School of Pharmacy, Queen’s University Belfast, Belfast, Northern Ireland BT7 1NN, UK – sequence: 8 givenname: Marie E. surname: Migaud fullname: Migaud, Marie E. organization: School of Pharmacy, Queen’s University Belfast, Belfast, Northern Ireland BT7 1NN, UK – sequence: 9 givenname: Rajendra S. surname: Apte fullname: Apte, Rajendra S. organization: Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA – sequence: 10 givenname: Koji surname: Uchida fullname: Uchida, Koji organization: Oriental Yeast Company, Tokyo 174-0051, Japan – sequence: 11 givenname: Jun surname: Yoshino fullname: Yoshino, Jun email: jyoshino@wustl.edu organization: Division of Geriatrics and Nutritional Science, Department of Medicine, Center for Human Nutrition, Washington University School of Medicine, St. Louis, MO 63110, USA – sequence: 12 givenname: Shin-ichiro surname: Imai fullname: Imai, Shin-ichiro email: imaishin@wustl.edu organization: Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28068222$$D View this record in MEDLINE/PubMed |
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| PublicationDateYYYYMMDD | 2016-12-13 |
| PublicationDate_xml | – month: 12 year: 2016 text: 2016-12-13 day: 13 |
| PublicationDecade | 2010 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | Cell metabolism |
| PublicationTitleAlternate | Cell Metab |
| PublicationYear | 2016 |
| Publisher | Elsevier Inc |
| Publisher_xml | – name: Elsevier Inc |
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| Snippet | NAD+ availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD+ intermediate, has been shown to enhance... NAD availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD intermediate, has been shown to enhance NAD... NAD + availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD + intermediate, has been shown to enhance... |
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| SubjectTerms | Administration, Oral aging Aging - drug effects Aging - genetics Aging - physiology Animals anti-aging Bone Density - drug effects Cell Respiration - drug effects Darkness Drinking - drug effects Eating - drug effects energy metabolism Energy Metabolism - drug effects eye function Food Gene Expression Regulation - drug effects glucose metabolism Insulin - pharmacology insulin sensitivity Lipids - blood Lymphocytes - drug effects Lymphocytes - metabolism Male Mice, Inbred C57BL mitochondria Mitochondria - drug effects Mitochondria - metabolism Muscle, Skeletal - drug effects Muscle, Skeletal - metabolism Myeloid Cells - drug effects Myeloid Cells - metabolism NAD NAD - metabolism NAD+ precursor nicotinamide mononucleotide Nicotinamide Mononucleotide - administration & dosage Nicotinamide Mononucleotide - blood Nicotinamide Mononucleotide - pharmacology NMN Physical Conditioning, Animal Time Factors Weight Gain - drug effects |
| Title | Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice |
| URI | https://dx.doi.org/10.1016/j.cmet.2016.09.013 https://www.ncbi.nlm.nih.gov/pubmed/28068222 https://www.proquest.com/docview/1857380685 https://pubmed.ncbi.nlm.nih.gov/PMC5668137 |
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