ArticlePloS one2015
Genetic Ablation of CD38 Protects against Western Diet-Induced Exercise Intolerance and Metabolic Inflexibility.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Genome-Wide Meta-Analysis of Blood Pressure Response to βJournal of the American Heart Association · 2019Pooled it
- Robinetin Alleviates Metabolic Failure in Liver through Suppression of p300-CD38 Axis.Biomolecules & therapeutics · 2024Article
- The Role of NADBiomedicines · 2023Review
- Triple-Isotope Tracing for Pathway Discernment of NMN-Induced NADInternational journal of molecular sciences · 2023Article
- Review
- Balancing NADCellular and molecular life sciences : CMLS · 2022Review
- Benefits in cardiac function by CD38 suppression: Improvement in NADJournal of molecular and cellular cardiology · 2022Article
- The CD38 glycohydrolase and the NAD sink: implications for pathological conditions.American journal of physiology. Cell physiology · 2022Review
- CRISPR Gene Editing of Human Primary NK and T Cells for Cancer Immunotherapy.Frontiers in oncology · 2022Review
- Critical Role of Astrocyte NADThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Optimizing the discovery and assessment of therapeutic targets in heart failure with preserved ejection fraction.ESC heart failure · 2021Review
- Importance of Adipose Tissue NAD+ Biology in Regulating Metabolic Flexibility.Endocrinology · 2021Article
- Targeting CD38-dependent NADiScience · 2021Article
- Codonopsis pilosula Polysaccharides Alleviate AβCurrent Alzheimer research · 2021Article
- Mouse Models of Heart Failure with Preserved or Reduced Ejection Fraction.The American journal of pathology · 2020Review
- Kynurenine pathway, NADExperimental gerontology · 2020Review
- Distinct physical condition and social behavior phenotypes of CD157 and CD38 knockout mice during aging.PloS one · 2020Article
- Inflamm-Aging and Brain Insulin Resistance: New Insights and Role of Life-style Strategies on Cognitive and Social Determinants in Aging and Neurodegeneration.Frontiers in neuroscience · 2020Review
- Overexpression of Sirtuin 1 protein in neurons prevents and reverses experimental diabetic neuropathy.Brain : a journal of neurology · 2019Article
- NADDiabetologia · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.