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477 results on '"Migaud, Marie"'

1. Subcellular NAD+ pools are interconnected and buffered by mitochondrial NAD+

Author

Høyland, Lena E., VanLinden, Magali R., Niere, Marc, Strømland, Øyvind, Sharma, Suraj, Dietze, Jörn, Tolås, Ingvill, Lucena, Eva, Bifulco, Ersilia, Sverkeli, Lars J., Cimadamore-Werthein, Camila, Ashrafi, Hanan, Haukanes, Kjellfrid F., van der Hoeven, Barbara, Dölle, Christian, Davidsen, Cédric, Pettersen, Ina K. N., Tronstad, Karl J., Mjøs, Svein A., Hayat, Faisal, Makarov, Mikhail V., Migaud, Marie E., Heiland, Ines, and Ziegler, Mathias

Published
2024
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3. Synthesis, Detection, and Metabolism of Pyridone Ribosides, Products of NAD Overoxidation.

Author

Hayat, Faisal, Deason, J, Bryan, Ru, Terkeltaub, Robert, Song, Weidan, Kraus, W, Pluth, Janice, Gassman, Natalie, and Migaud, Marie

Subjects
Humans, NAD, Nucleotides, Nucleosides, Energy Metabolism, Pyridones
Abstract

Pyridone-containing adenine dinucleotides, ox-NAD, are formed by overoxidation of nicotinamide adenine dinucleotide (NAD+) and exist in three distinct isomeric forms. Like the canonical nucleosides, the corresponding pyridone-containing nucleosides (PYR) are chemically stable, biochemically versatile, and easily converted to nucleotides, di- and triphosphates, and dinucleotides. The 4-PYR isomer is often reported with its abundance increasing with the progression of metabolic diseases, age, cancer, and oxidative stress. Yet, the pyridone-derived nucleotides are largely under-represented in the literature. Here, we report the efficient synthesis of the series of ox-NAD and pyridone nucleotides and measure the abundance of ox-NAD in biological specimens using liquid chromatography coupled with mass spectrometry (LC-MS). Overall, we demonstrate that all three forms of PYR and ox-NAD are found in biospecimens at concentrations ranging from nanomolar to midmicromolar and that their presence affects the measurements of NAD(H) concentrations when standard biochemical redox-based assays are applied. Furthermore, we used liver extracts and 1H NMR spectrometry to demonstrate that each ox-NAD isomer can be metabolized to its respective PYR isomer. Together, these results suggest a need for a better understanding of ox-NAD in the context of human physiology since these species are endogenous mimics of NAD+, the key redox cofactor in metabolism and bioenergetics maintenance.

Published
2024

5. Trigonelline is an NAD+ precursor that improves muscle function during ageing and is reduced in human sarcopenia

Author

Membrez, Mathieu, Migliavacca, Eugenia, Christen, Stefan, Yaku, Keisuke, Trieu, Jennifer, Lee, Alaina K., Morandini, Francesco, Giner, Maria Pilar, Stiner, Jade, Makarov, Mikhail V., Garratt, Emma S., Vasiloglou, Maria F., Chanvillard, Lucie, Dalbram, Emilie, Ehrlich, Amy M., Sanchez-Garcia, José Luis, Canto, Carles, Karagounis, Leonidas G., Treebak, Jonas T., Migaud, Marie E., Heshmat, Ramin, Razi, Farideh, Karnani, Neerja, Ostovar, Afshin, Farzadfar, Farshad, Tay, Stacey K. H., Sanders, Matthew J., Lillycrop, Karen A., Godfrey, Keith M., Nakagawa, Takashi, Moco, Sofia, Koopman, René, Lynch, Gordon S., Sorrentino, Vincenzo, and Feige, Jerome N.

Published
2024
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9. NAD precursors cycle between host tissues and the gut microbiome

Author

Chellappa, Karthikeyani, McReynolds, Melanie R., Lu, Wenyun, Zeng, Xianfeng, Makarov, Mikhail, Hayat, Faisal, Mukherjee, Sarmistha, Bhat, Yashaswini R., Lingala, Siddharth R., Shima, Rafaella T., Descamps, Hélène C., Cox, Timothy, Ji, Lixin, Jankowski, Connor, Chu, Qingwei, Davidson, Shawn M., Thaiss, Christoph A., Migaud, Marie E., Rabinowitz, Joshua D., and Baur, Joseph A.

Published
2022
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11. Dysregulated nicotinamide adenine dinucleotide metabolome in patients hospitalized with COVID‐19.

Author

Valderrábano, Rodrigo J., Wipper, Benjamin, Pencina, Karol Mateusz, Migaud, Marie, Shang, Yili Valentine, Latham, Nancy K., Montano, Monty, Cunningham, James M., Wilson, Lauren, Peng, Liming, Memish‐Beleva, Yusnie, Bhargava, Avantika, Swain, Pamela M., Lehman, Phoebe, Lavu, Siva, Livingston, David J., and Bhasin, Shalender

Subjects
NICOTINAMIDE, OXIDATION-reduction reaction, HOSPITAL patients, CONTROL groups, METABOLITES, NAD (Coenzyme), DNA repair
Abstract

Nicotinamide adenine dinucleotide (NAD+) depletion has been postulated as a contributor to the severity of COVID‐19; however, no study has prospectively characterized NAD+ and its metabolites in relation to disease severity in patients with COVID‐19. We measured NAD+ and its metabolites in 56 hospitalized patients with COVID‐19 and in two control groups without COVID‐19: (1) 31 age‐ and sex‐matched adults with comorbidities, and (2) 30 adults without comorbidities. Blood NAD+ concentrations in COVID‐19 group were only slightly lower than in the control groups (p < 0.05); however, plasma 1‐methylnicotinamide concentrations were significantly higher in patients with COVID‐19 (439.7 ng/mL, 95% CI: 234.0, 645.4 ng/mL) than in age‐ and sex‐matched controls (44.5 ng/mL, 95% CI: 15.6, 73.4) and in healthy controls (18.1 ng/mL, 95% CI 15.4, 20.8; p < 0.001 for each comparison). Plasma nicotinamide concentrations were also higher in COVID‐19 group and in controls with comorbidities than in healthy control group. Plasma concentrations of 2‐methyl‐2‐pyridone‐5‐carboxamide (2‐PY), but not NAD+, were significantly associated with increased risk of death (HR = 3.65; 95% CI 1.09, 12.2; p = 0.036) and escalation in level of care (HR = 2.90, 95% CI 1.01, 8.38, p = 0.049). RNAseq and RTqPCR analyses of PBMC mRNA found upregulation of multiple genes involved in NAD+ synthesis as well as degradation, and dysregulation of NAD+‐dependent processes including immune response, DNA repair, metabolism, apoptosis/autophagy, redox reactions, and mitochondrial function. Blood NAD+ concentrations are modestly reduced in COVID‐19; however, NAD+ turnover is substantially increased with upregulation of genes involved in both NAD+ biosynthesis and degradation, supporting the rationale for NAD+ augmentation to attenuate disease severity. [ABSTRACT FROM AUTHOR]

Published
2024
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13. NAD+ flux is maintained in aged mice despite lower tissue concentrations

Author

McReynolds, Melanie R., Chellappa, Karthikeyani, Chiles, Eric, Jankowski, Connor, Shen, Yihui, Chen, Li, Descamps, Hélène C., Mukherjee, Sarmistha, Bhat, Yashaswini R., Lingala, Siddharth R., Chu, Qingwei, Botolin, Paul, Hayat, Faisal, Doke, Tomohito, Susztak, Katalin, Thaiss, Christoph A., Lu, Wenyun, Migaud, Marie E., Su, Xiaoyang, Rabinowitz, Joshua D., and Baur, Joseph A.

Published
2021
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15. Deprotection of nucleosides by lysine-assisted methanolysis of esters and amides.

Author

Dhuguru, Jyothi, English, Brandon, Dellinger, Ryan W., and Migaud, Marie E.

Abstract

A deacylation method was developed based on lysine-assisted methanolysis of nucleoside-derived esters and arylamides. The present methodology complements well-established deacylation methods, using a minimum molar equivalency of lysine and methanol under mild heating to generate the deacylated nucleoside and recyclable lysine and volatile methyl esters as byproducts. A variety of acylated canonical nucleosides and hydrolytically labile non-canonical nucleosides like nicotinamide riboside (NR) and its reduced form (NRH) were deprotected under such lysine-assisted conditions, demonstrating the versatility of this approach. Having determined this one-pot process's E-factor and reaction mass index, we find this method greener than the more established deacylation processes. [ABSTRACT FROM AUTHOR]

Published
2025
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18. SLC25A51 is a mammalian mitochondrial NAD+ transporter

Author

Luongo, Timothy S., Eller, Jared M., Lu, Mu-Jie, Niere, Marc, Raith, Fabio, Perry, Caroline, Bornstein, Marc R., Oliphint, Paul, Wang, Lin, McReynolds, Melanie R., Migaud, Marie E., Rabinowitz, Joshua D., Johnson, F. Brad, Johnsson, Kai, Ziegler, Mathias, Cambronne, Xiaolu A., and Baur, Joseph A.

Published
2020
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26. Quantitative Analysis of NAD Synthesis-Breakdown Fluxes

Author

Liu, Ling, Su, Xiaoyang, Quinn, William J., III, Hui, Sheng, Krukenberg, Kristin, Frederick, David W., Redpath, Philip, Zhan, Le, Chellappa, Karthikeyani, White, Eileen, Migaud, Marie, Mitchison, Timothy J., Baur, Joseph A., and Rabinowitz, Joshua D.

Published
2018
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32. Loss of NAD Homeostasis Leads to Progressive and Reversible Degeneration of Skeletal Muscle

Author

Frederick, David W., Loro, Emanuele, Liu, Ling, Davila, Antonio, Jr., Chellappa, Karthikeyani, Silverman, Ian M., Quinn, William J., III, Gosai, Sager J., Tichy, Elisia D., Davis, James G., Mourkioti, Foteini, Gregory, Brian D., Dellinger, Ryan W., Redpath, Philip, Migaud, Marie E., Nakamaru-Ogiso, Eiko, Rabinowitz, Joshua D., Khurana, Tejvir S., and Baur, Joseph A.

Published
2016
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35. An abundant biliary metabolite derived from dietary omega-3 polyunsaturated fatty acids regulates triglycerides

Author

Grevengoed, Trisha J., Trammell, Samuel A.J., Svenningsen, Jens S., Makarov, Mikhail V., Nielsen, Thomas Svava, Jacobsen, Jens Christian Brings, Treebak, Jonas T., Calder, Philip C., Migaud, Marie E., and Gillum, Benjamin F. Cravatand Matthew P.

Subjects
Identification and classification, Care and treatment, Physiological aspects, Composition, Models, Research, Health aspects, Hyperlipidemia -- Models -- Care and treatment, Metabolites -- Identification and classification -- Health aspects, Omega 3 fatty acids -- Health aspects -- Physiological aspects, Pharmacological research, Bile acids -- Composition -- Health aspects, Lipid metabolism -- Health aspects, Triglycerides -- Health aspects -- Physiological aspects, Dietary supplements -- Research, Pharmacology, Experimental, Omega-3 fatty acids -- Health aspects -- Physiological aspects
Abstract

Introduction Omega-3 fatty acids are essential to many cellular functions, but are not made by mammals and instead are found in highest abundance in fatty fish and fish oil supplements [...], Omega-3 fatty acids from fish oil reduce triglyceride levels in mammals, yet the mechanisms underlying this effect have not been fully clarified, despite the clinical use of omega-3 ethyl esters to treat severe hypertriglyceridemia and reduce cardiovascular disease risk in humans. Here, we identified in bile a class of hypotriglyceridemic omega-3 fatty acid-derived N-acyl taurines (NATs) that, after dietary omega-3 fatty acid supplementation, increased to concentrations similar to those of steroidal bile acids. The biliary docosahexaenoic acid-containing (DHA-containing) NAT C22:6 NAT was increased in human and mouse plasma after dietary omega-3 fatty acid supplementation and potently inhibited intestinal triacylglycerol hydrolysis and lipid absorption. Supporting this observation, genetic elevation of endogenous NAT levels in mice impaired lipid absorption, whereas selective augmentation of C22:6 NAT levels protected against hypertriglyceridemia and fatty liver. When administered pharmacologically, C22:6 NAT accumulated in bile and reduced high-fat diet-induced, but not sucrose-induced, hepatic lipid accumulation in mice, suggesting that C22:6 NAT is a negative feedback mediator that limits excess intestinal lipid absorption. Thus, biliary omega-3 NATs may contribute to the hypotriglyceridemic mechanism of action of fish oil and could influence the design of more potent omega-3 fatty acid-based therapeutics.

Published
2021
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36. Nicotinamide Adenine Dinucleotide in Aging Biology: Potential Applications and Many Unknowns.

Author

Bhasin, Shalender, Seals, Douglas, Migaud, Marie, Musi, Nicolas, and Baur, Joseph A

Subjects
NICOTINAMIDE adenine dinucleotide phosphate, HEART metabolism disorders, WEIGHT gain
Abstract

Recent research has unveiled an expansive role of NAD+ in cellular energy generation, redox reactions, and as a substrate or cosubstrate in signaling pathways that regulate health span and aging. This review provides a critical appraisal of the clinical pharmacology and the preclinical and clinical evidence for therapeutic effects of NAD+ precursors for age-related conditions, with a particular focus on cardiometabolic disorders, and discusses gaps in current knowledge. NAD+ levels decrease throughout life; age-related decline in NAD+ bioavailability has been postulated to be a contributor to many age-related diseases. Raising NAD+ levels in model organisms by administration of NAD+ precursors improves glucose and lipid metabolism; attenuates diet-induced weight gain, diabetes, diabetic kidney disease, and hepatic steatosis; reduces endothelial dysfunction; protects heart from ischemic injury; improves left ventricular function in models of heart failure; attenuates cerebrovascular and neurodegenerative disorders; and increases health span. Early human studies show that NAD+ levels can be raised safely in blood and some tissues by oral NAD+ precursors and suggest benefit in preventing nonmelanotic skin cancer, modestly reducing blood pressure and improving lipid profile in older adults with obesity or overweight; preventing kidney injury in at-risk patients; and suppressing inflammation in Parkinson disease and SARS-CoV-2 infection. Clinical pharmacology, metabolism, and therapeutic mechanisms of NAD+ precursors remain incompletely understood. We suggest that these early findings provide the rationale for adequately powered randomized trials to evaluate the efficacy of NAD+ augmentation as a therapeutic strategy to prevent and treat metabolic disorders and age-related conditions. [ABSTRACT FROM AUTHOR]

Published
2023
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44. Defining NAD(P)(H) Catabolism.

Author

Dhuguru, Jyothi, Dellinger, Ryan W., and Migaud, Marie E.

Abstract

Dietary vitamin B3 components, such as nicotinamide and nicotinic acid, are precursors to the ubiquitous redox cofactor nicotinamide adenine dinucleotide (NAD+). NAD+ levels are thought to decline with age and disease. While the drivers of this decline remain under intense investigation, strategies have emerged seeking to functionally maintain NAD+ levels through supplementation with NAD+ biosynthetic intermediates. These include marketed products, such as nicotinamide riboside (NR) and its phosphorylated form (NMN). More recent developments have shown that NRH (the reduced form of NR) and its phosphorylated form NMNH also increases NAD+ levels upon administration, although they initially generate NADH (the reduced form of NAD+). Other means to increase the combined levels of NAD+ and NADH, NAD(H), include the inhibition of NAD+-consuming enzymes or activation of biosynthetic pathways. Multiple studies have shown that supplementation with an NAD(H) precursor changes the profile of NAD(H) catabolism. Yet, the pharmacological significance of NAD(H) catabolites is rarely considered although the distribution and abundance of these catabolites differ depending on the NAD(H) precursor used, the species in which the study is conducted, and the tissues used for the quantification. Significantly, some of these metabolites have emerged as biomarkers in physiological disorders and might not be innocuous. Herein, we review the known and emerging catabolites of the NAD(H) metabolome and highlight their biochemical and physiological function as well as key chemical and biochemical reactions leading to their formation. Furthermore, we emphasize the need for analytical methods that inform on the full NAD(H) metabolome since the relative abundance of NAD(H) catabolites informs how NAD(H) precursors are used, recycled, and eliminated. [ABSTRACT FROM AUTHOR]

Published
2023
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48. Nicotinamide Riboside and Dihydronicotinic Acid Riboside Synergistically Increase Intracellular NAD+ by Generating Dihydronicotinamide Riboside

Author

Ciarlo, Eleonora, primary, Joffraud, Magali, additional, Hayat, Faisal, additional, Giner, Maria Pilar, additional, Giroud-Gerbetant, Judith, additional, Sanchez-Garcia, Jose Luis, additional, Rumpler, Marie, additional, Moco, Sofia, additional, Migaud, Marie E., additional, and Cantó, Carles, additional

Published
2022
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