Cargando…

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

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 depen...

Descripción completa

Detalles Bibliográficos
Autores principales: Cartwright, David M, Oakey, Lucy A, Fletcher, Rachel S, Doig, Craig L, Heising, Silke, Larner, Dean P, Nasteska, Daniela, Berry, Caitlin E, Heaselgrave, Sam R, Ludwig, Christian, Hodson, David J, Lavery, Gareth G, Garten, Antje
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bioscientifica Ltd 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8494379/
https://www.ncbi.nlm.nih.gov/pubmed/34370682
http://dx.doi.org/10.1530/JOE-21-0123
_version_ 1784579301193023488
author Cartwright, David M
Oakey, Lucy A
Fletcher, Rachel S
Doig, Craig L
Heising, Silke
Larner, Dean P
Nasteska, Daniela
Berry, Caitlin E
Heaselgrave, Sam R
Ludwig, Christian
Hodson, David J
Lavery, Gareth G
Garten, Antje
author_facet Cartwright, David M
Oakey, Lucy A
Fletcher, Rachel S
Doig, Craig L
Heising, Silke
Larner, Dean P
Nasteska, Daniela
Berry, Caitlin E
Heaselgrave, Sam R
Ludwig, Christian
Hodson, David J
Lavery, Gareth G
Garten, Antje
author_sort Cartwright, David M
collection PubMed
description 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.
format Online
Article
Text
id pubmed-8494379
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Bioscientifica Ltd
record_format MEDLINE/PubMed
spelling pubmed-84943792021-10-08 Nicotinamide riboside has minimal impact on energy metabolism in mouse models of mild obesity Cartwright, David M Oakey, Lucy A Fletcher, Rachel S Doig, Craig L Heising, Silke Larner, Dean P Nasteska, Daniela Berry, Caitlin E Heaselgrave, Sam R Ludwig, Christian Hodson, David J Lavery, Gareth G Garten, Antje J Endocrinol Research 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. Bioscientifica Ltd 2021-08-09 /pmc/articles/PMC8494379/ /pubmed/34370682 http://dx.doi.org/10.1530/JOE-21-0123 Text en © The authors https://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research
Cartwright, David M
Oakey, Lucy A
Fletcher, Rachel S
Doig, Craig L
Heising, Silke
Larner, Dean P
Nasteska, Daniela
Berry, Caitlin E
Heaselgrave, Sam R
Ludwig, Christian
Hodson, David J
Lavery, Gareth G
Garten, Antje
Nicotinamide riboside has minimal impact on energy metabolism in mouse models of mild obesity
title Nicotinamide riboside has minimal impact on energy metabolism in mouse models of mild obesity
title_full Nicotinamide riboside has minimal impact on energy metabolism in mouse models of mild obesity
title_fullStr Nicotinamide riboside has minimal impact on energy metabolism in mouse models of mild obesity
title_full_unstemmed Nicotinamide riboside has minimal impact on energy metabolism in mouse models of mild obesity
title_short Nicotinamide riboside has minimal impact on energy metabolism in mouse models of mild obesity
title_sort nicotinamide riboside has minimal impact on energy metabolism in mouse models of mild obesity
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8494379/
https://www.ncbi.nlm.nih.gov/pubmed/34370682
http://dx.doi.org/10.1530/JOE-21-0123
work_keys_str_mv AT cartwrightdavidm nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT oakeylucya nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT fletcherrachels nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT doigcraigl nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT heisingsilke nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT larnerdeanp nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT nasteskadaniela nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT berrycaitline nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT heaselgravesamr nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT ludwigchristian nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT hodsondavidj nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT laverygarethg nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity
AT gartenantje nicotinamideribosidehasminimalimpactonenergymetabolisminmousemodelsofmildobesity