| Autor: |
Shian-Huey Chiang, W Wallace Harrington, Guizhen Luo, Naphtali O Milliken, John C Ulrich, Jing Chen, Deepak K Rajpal, Ying Qian, Tiffany Carpenter, Rusty Murray, Robert S Geske, Stephen A Stimpson, Henning F Kramer, Curt D Haffner, J David Becherer, Frank Preugschat, Andrew N Billin |
| Jazyk: |
angličtina |
| Rok vydání: |
2015 |
| Předmět: |
|
| Zdroj: |
PLoS ONE, Vol 10, Iss 8, p e0134927 (2015) |
| Druh dokumentu: |
article |
| ISSN: |
1932-6203 |
| DOI: |
10.1371/journal.pone.0134927 |
| Popis: |
Nicotinamide adenine dinucleotide (NAD+) is a key cofactor required for essential metabolic oxidation-reduction reactions. It also regulates various cellular activities, including gene expression, signaling, DNA repair and calcium homeostasis. Intracellular NAD+ levels are tightly regulated and often respond rapidly to nutritional and environmental changes. Numerous studies indicate that elevating NAD+ may be therapeutically beneficial in the context of numerous diseases. However, the role of NAD+ on skeletal muscle exercise performance is poorly understood. CD38, a multi-functional membrane receptor and enzyme, consumes NAD+ to generate products such as cyclic-ADP-ribose. CD38 knockout mice show elevated tissue and blood NAD+ level. Chronic feeding of high-fat, high-sucrose diet to wild type mice leads to exercise intolerance and reduced metabolic flexibility. Loss of CD38 by genetic mutation protects mice from diet-induced metabolic deficit. These animal model results suggest that elevation of tissue NAD+ through genetic ablation of CD38 can profoundly alter energy homeostasis in animals that are maintained on a calorically-excessive Western diet. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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