SFEBES2018 Poster Presentations Obesity & metabolism (24 abstracts)
A Direct Comparison of Metabolic Responses to NAD repletion in C57BL/6J and C57BL/6N diet-induced obesity mouse models
Antje Garten 1, , David Cartwright 2 , Lucy Oakey 2 , Rachel Fletcher 2 , Daniela Nasteska 2 , David Hodson 2 , Dean Larner 2 , Craig Doig 2 , Christian Ludwig 2 , Katarina Kluckova 2 & Gareth Lavery 2
1Leipzig University, Leipzig, Germany; 2University of Birmingham, Birmingham, UK.
Background and Aim: Supplementation with precursors of nicotinamide adenine dinucleotide (NAD), was shown to be beneficial in preventing metabolic dysfunction in mice, which is induced by feeding a high fat diet. We compared the effect of nicotinamide riboside (NR) supplementationon whole-body energy metabolism and mitochondrial function in two widely used diet-induced obesity mouse models.
Methods: Mice were fed a high fat diet (HFD, 60% fat) or standard chow with or without supplementation of 3 g/l NR in the drinking water for 8 weeks. Body and organ weights, liver lipids as well as glucose tolerance were measured. Metabolic phenotype was determined by indirect calorimetry, mitochondrial O2 flux in liver, muscles and heart was measured by high resolution respirometry.
Results: NR supplementation had a slight positive effect on fasting blood glucose and on energy expenditure of B6/N mice on HFD. In B6/J mice, NR influenced substrate usage as determined by respiratory exchange ratio both in chow and HFD-fed mice. Mitochondrial O2 flux and citrate synthase activity were significantly increased by NR supplementation specifically in heart muscle fibers of B6/N, but not B6/J mice on HFD. No effect on mitochondrial function was found in the other examined tissues. The mitochondrial enzyme nicotinamide nucleotide transhydrogenase (Nnt) was found to be 2-fold upregulatedin hearts of B6/N mice on HFD+NR, which was reflected by lower levels of the oxidative stress marker 4-hydroxynonenal.
Conclusion: The effect of NR supplementation in diet-induced obesity is influenced by mouse genotype and possibly related to cellular redox status.
Volume 59
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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