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212 results for “nicotinamide”
Data set for "A Magnesium Binding Site And The Anomeric Effect Regulate The Abiotic Redox Chemistry Of Nicotinamide Nucleotides"
<p>Data associated with Sebastianelli L, Kaur H, Chen Z, Krishnamurthy R, Mansy SS (2024) A magnesium binding site and the anomeric effect regulate the abiotic redox chemistry of nicotinamide nucleotides. Chem Eur J. 30, e202400411. DOI: 10.1002/chem.202400411 [<a href="https://chemistry-europe.onlinelibrary.wiley.com/doi/abs/10.1002/chem.202400411">link</a>]</p>
Dataset related to: Low Nephron Number Induced by Maternal Protein Restriction Is Prevented by Nicotinamide Riboside Supplementation Depending on Sirtuin 3 Activation
<p>The files contain all the dataset included in the manuscript divided by figures. For each figure, individual tabs indicate data from different figure panels.</p> <p> </p> <p><strong>Abstract</strong></p> <p>A reduced nephron number at birth, due to critical gestational conditions, including maternal malnutrition, is associated with the risk of developing hypertension and chronic kidney disease in adulthood. No interventions are currently available to augment nephron number. We have recently shown that sirtuin 3 (SIRT3) has an important role in dictating proper nephron endowment. The present study explored whether SIRT3 stimulation, by means of supplementation with nicotinamide riboside (NR), a precursor of the SIRT3 co-substrate nicotinamide adenine dinucleotide (NAD<sup>+</sup>), was able to improve nephron number in a murine model of a low protein (LP) diet. Our findings show that reduced nephron number in newborn mice (day 1) born to mothers fed a LP diet was associated with impaired renal SIRT3 expression, which was restored through supplementation with NR. Glomerular podocyte density, as well as the rarefaction of renal capillaries, also improved through NR administration. In mechanistic terms, the restoration of SIRT3 expression through NR was mediated by the induction of proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α). Moreover, NR restored SIRT3 activity, as shown by the reduction of the acetylation of optic atrophy 1 (OPA1) and superoxide dismutase 2 (SOD2), which resulted in improved mitochondrial morphology and protection against oxidative damage in mice born to mothers fed the LP diet. Our results provide evidence that it is feasible to prevent nephron mass shortage at birth through SIRT3 boosting during nephrogenesis, thus providing a therapeutic option to possibly limit the long-term sequelae of reduced nephron number in adulthood.</p>
Nitrogen-15 dynamic nuclear polarization of nicotinamide derivatives in biocompatible solutions
<p>This data corresponds to the following paper:</p> <p>Title: Nitrogen-15 dynamic nuclear polarization of nicotinamide derivatives in biocompatible solutions<br> DOI: 10.1126/sciadv.add3643<br> Journal: Science Advances<br> Authors: Josh P. Peters, Arne Brahms, Vivian Janicaud, Maria Anikeeva, Eva Peschke, Frowin Ellermann, Arianna Ferrari, Dana Hellmold, Janka Held-Feindt, Na-mi Kim, Johannes Meiser, Konrad Aden, Rainer Herges, Jan-Bernd Hövener, Andrey N. Pravdivtsev</p> <p>In the upload the figures 2 - 6 are covered, so all figures from the main manuscript with acquired data.</p> <p> </p> <p>Original abstract for the manuscript:</p> <p>Dissolution dynamic nuclear polarization (dDNP) increases the sensitivity of magnetic resonance imaging by more than 10,000 times enabling <em>in vivo</em> metabolic imaging can be performed non-invasively in real-time. Here, we are developing a group of dDNP polarized tracers based on nicotinamide (NAM). We synthesized 1-<sup>15</sup>N-NAM and 1-<sup>15</sup>N nicotinic acid and hyperpolarized them with dDNP, reaching (13.0±1.9)% <sup>15</sup>N polarization. We found that the lifetime of hyperpolarized 1-<sup>15</sup>N-NAM is strongly field- and pH-dependent, with T<sub>1</sub> being as long as 41 s at a pH of 12 and 1 T while as short as a few seconds at neutral pH and fields below 1 T. The remarkably short 1-<sup>15</sup>N lifetime at low magnetic fields and neutral pH drove us to establish a unique pH neutralization procedure. Using <sup>15</sup>N dDNP and an inexpensive rodent imaging probe designed in-house, we acquired a <sup>15</sup>N MRI of 1-<sup>15</sup>N-NAM (previously hyperpolarized for more than an hour) in less than one second.</p>
Nicotinamide as an Early Alzheimer's Disease Treatment
ClinicalTrials.gov study NCT03061474. IPD Sharing: YES. Countries: 1. Publications: 4.
Nicotinamide Adenine Dinucleotide Molecular Dynamics
<p>Nicotinamide Adenine Dinucleotide. Molecular dynamics of NAD molecule is solvated with water (transparent) in UCSF Chimera software for 22 nanoseconds.<br>By Victor Padilla Sanchez, PhD - Washington Metropolitan University, President.<br>Email: drvictorpadilla@aol.com<br>Website: https://www.drvictorpadillasanchez.com</p>
Data from: Hepatic steatosis induced by nicotine plus Coca-Cola™ is prevented by nicotinamide riboside (NR)
<p><strong>Introduction.</strong> Cigarettes containing nicotine (Nic) are a risk factor for the development of cardiovascular and metabolic diseases. We reported that Nic delivered via injections or e-cigarette vapor led to hepatic steatosis in mice fed with a high-fat diet. High-fructose corn syrup (HFCS) is the main sweetener in sugar-sweetened beverages (SSBs) in the US. Increased consumption of SSBs with HFCS is associated with increased risks of non-alcoholic fatty liver disease (NAFLD). Nicotinamide riboside (NR) increases mitochondrial nicotinamide adenine dinucleotide (NAD<sup>+</sup>) and protects mice against hepatic steatosis. This study evaluated if Nic plus Coca-Cola™ (Coke) with HFCS can cause hepatic steatosis and that can be protected by NR.</p> <p><strong>Methods.</strong> C57BL6 mice received twice daily intraperitoneal (IP) injections of Nic or saline and were given Coke (HFCS), or Coke with sugar, and NR supplementation for 10 weeks.</p> <p><strong>Results.</strong> Our results show that Nic+Coke caused increased caloric intake and induced hepatic steatosis, and the addition of NR prevented these changes. Western blot analysis showed lipogenesis markers were activated (increased cleavage of the sterol regulatory element-binding protein 1 [SREBP1c] and reduction of phospho-Acetyl-CoA Carboxylase [p-ACC]) in the Nic+Coke compared to the Sal+Water group. The hepatic detrimental effects of Nic+Coke were mediated by decreased NAD<sup>+</sup> signaling, increased oxidative stress, and mitochondrial damage. NR reduced oxidative stress and prevented mitochondrial damage by restoring protein levels of Sirtuin1 (Sirt1) and peroxisome proliferator-activated receptor coactivator 1-alpha (PGC1a) signaling.</p> <p><strong>Discussion.</strong> We conclude that Nic+Coke has an additive effect on producing hepatic steatosis, and NR is protective. This study suggests concern for the development of NAFLD in subjects who consume nicotine and drink SSBs with HFCS.</p>
Effects of Nicotinamide Riboside on Bioenergetics and Oxidative Stress in Mild Cognitive Impairment/Alzheimer's Dementia
ClinicalTrials.gov study NCT04430517. IPD Sharing: YES. Countries: 1. Publications: 0.
Nicotinamide Riboside in Ulcerative Colitis
ClinicalTrials.gov study NCT05561738. IPD Sharing: YES. Countries: 1. Publications: 9.
Trial of Nicotinamide Riboside and Co-enzyme Q10 in Chronic Kidney Disease
ClinicalTrials.gov study NCT03579693. IPD Sharing: NO. Countries: 1. Publications: 2.
Benefits of Nicotinamide Riboside Upon Cognition and Sleep
ClinicalTrials.gov study NCT05500170. IPD Sharing: YES. Countries: 1. Publications: 0.
Pilot Study to Evaluate the Effect of Nicotinamide Riboside on Immune Activation in Psoriasis
ClinicalTrials.gov study NCT04271735. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Study to Evaluate the Effect of Nicotinamide Riboside on Immunity
ClinicalTrials.gov study NCT02812238. IPD Sharing: Not stated. Countries: 1. Publications: 5.
Nicotinamide Riboside in LVAD Recipients
ClinicalTrials.gov study NCT03727646. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Kinetics and Metabolism of Nicotinamide Provided as a Dietary Supplementation
ClinicalTrials.gov study NCT07156929. IPD Sharing: YES. Countries: 1. Publications: 1.
Nicotinamide Riboside in Systolic Heart Failure
ClinicalTrials.gov study NCT03423342. IPD Sharing: YES. Countries: 1. Publications: 1.
Nicotinamide Riboside With and Without Resveratrol to Improve Functioning in Peripheral Artery Disease
ClinicalTrials.gov study NCT03743636. IPD Sharing: NO. Countries: 1. Publications: 1.
The COMBINE Study: The CKD Optimal Management With BInders and NicotinamidE
ClinicalTrials.gov study NCT02258074. IPD Sharing: YES. Countries: 1. Publications: 5.
RNA seq data from: A randomized, placebo-controlled trial shows that nicotinamide riboside reduces airway inflammation in COPD
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Data from: Hepatic steatosis induced by nicotine plus Coca-Cola™ is prevented by nicotinamide riboside (NR)
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Nicotinamide riboside and pterostilbene cooperatively delay motor neuron failure in ALS SOD1G93A mice
<p>Oxidative stress-induced damage is a major mechanism in the pathophysiology of amyotrophic lateral sclerosis (ALS). A recent human clinical trial showed that the combination of nicotinamide riboside (NR) and pterostilbene (PT), molecules with potential to interfere in that mechanism, was efficacious in ALS patients. We examined the effect of these molecules in SOD1G93A transgenic mice, a well-stablished model of ALS. Assessment of neuromotor activity and coordination was correlated with histopathology, and measurement of proinflammatory cytokines in the cerebrospinal fluid. Cell death, Nrf2- and redox-dependent enzymes and metabolites, and sirtuin activities were studied in isolated motor neurons. NR and PT increased survival and ameliorated ALSassociated loss of neuromotor functions in SOD1G93A transgenic mice. NR and PT also decreased the microgliosis and astrogliosis associated with ALS progression. Increased levels of proinflammatory cytokines were observed in the cerebrospinal fluid of mice and humans with ALS. NR and PT ameliorated TNFα-induced oxidative stress and motor neuron death in vitro. Our results support the involvement of oxidative stress, specific Nrf2-dependent antioxidant defenses, and sirtuins in the pathophysiology of ALS. NR and PT interfere with the mechanisms leading to the release of proapoptotic molecular signals by mitochondria, and also promote mitophagy</p>
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