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Article ; Online: Ophthalmic acid is a glutathione regulating tripeptide.

Schomakers, Bauke V / Jillings, Sonia L / van Weeghel, Michel / Vaz, Frédéric M / Salomons, Gajja S / Janssens, Georges E / Houtkooper, Riekelt H

The FEBS journal

2024

Abstract: Since its discovery in 1958 in the lens of cows, ophthalmic acid (OPH) has stood in the shadow of its anti-oxidant analog: glutathione (GSH). Lacking the thiol group that gives GSH many of its important properties, ophthalmic acid's function has remained ...

Abstract	Since its discovery in 1958 in the lens of cows, ophthalmic acid (OPH) has stood in the shadow of its anti-oxidant analog: glutathione (GSH). Lacking the thiol group that gives GSH many of its important properties, ophthalmic acid's function has remained elusive, and it has been widely presumed to be an accidental product of the same enzymes. In this review, we compile evidence demonstrating that OPH is a ubiquitous metabolite found in bacteria, plants, fungi, and animals, produced through several layers of metabolic regulation. We discuss the limitations of the oft-repeated suggestions that aberrations in OPH levels should solely indicate GSH deficiency or oxidative stress. Finally, we discuss the available literature and suggest OPH's role in metabolism as a GSH-regulating tripeptide; controlling both cellular and organelle influx and efflux of GSH, as well as modulating GSH-dependent reactions and signaling. Ultimately, we hope that this review reinvigorates and directs more research into this versatile metabolite.
Language	English
Publishing date	2024-01-20
Publishing country	England
Document type	Journal Article
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.17061
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Article ; Online: Hepatic ADTRP overexpression does not influence lipid and glucose metabolism.

Defour, Merel / van Weeghel, Michel / Hermans, Jill / Kersten, Sander

American journal of physiology. Cell physiology

2021 Volume 321, Issue 4, Page(s) C585–C595

Abstract: The peroxisome proliferator-activated receptors (PPARs) are a group of transcription factors belonging to the nuclear receptor superfamily. Since most target genes of PPARs are implicated in lipid and glucose metabolism, regulation by PPARs could be used ...

Abstract	The peroxisome proliferator-activated receptors (PPARs) are a group of transcription factors belonging to the nuclear receptor superfamily. Since most target genes of PPARs are implicated in lipid and glucose metabolism, regulation by PPARs could be used as a screening tool to identify novel genes involved in lipid or glucose metabolism. Here, we identify
MeSH term(s)	3T3-L1 Cells ; Adipocytes/enzymology ; Animals ; Disease Models, Animal ; Enzyme Induction ; Esterases/biosynthesis ; Esterases/genetics ; Fasting/metabolism ; Female ; Glucose/metabolism ; Hepatocytes/enzymology ; Lipid Metabolism ; Lipidomics ; Lipids/blood ; Male ; Membrane Proteins/biosynthesis ; Membrane Proteins/genetics ; Mice ; Mice, 129 Strain ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Knockout ; Obesity/enzymology ; Obesity/genetics ; PPAR alpha/genetics ; PPAR alpha/metabolism ; PPAR gamma/metabolism
Chemical Substances	Lipids ; Membrane Proteins ; PPAR alpha ; PPAR gamma ; Ppara protein, mouse ; Pparg protein, mouse ; Adtrp protein, mouse (EC 3.1.-) ; Esterases (EC 3.1.-) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-07-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00185.2021
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Article ; Online: A metabolomic signature of decelerated physiological aging in human plasma.

Janssens, Georges E / Grevendonk, Lotte / Schomakers, Bauke V / Perez, Ruben Zapata / van Weeghel, Michel / Schrauwen, Patrick / Hoeks, Joris / Houtkooper, Riekelt H

GeroScience

2023 Volume 45, Issue 6, Page(s) 3147–3164

Abstract: The degenerative processes that occur during aging increase the risk of disease and impaired health. Meanwhile, interventions that target aging to promote healthy longevity are gaining interest, both academically and in the public. While nutritional and ... ...

Abstract	The degenerative processes that occur during aging increase the risk of disease and impaired health. Meanwhile, interventions that target aging to promote healthy longevity are gaining interest, both academically and in the public. While nutritional and physical interventions exist, efficacy is often difficult to determine. It is therefore imperative that an aging score measuring the biological aging process is available to the wider public. However, simple, interpret, and accessible biological aging scores are lacking. Here, we developed PhysiAge, a physiological aging score based on five accessible parameters that have influence on or reflect the aging process: (1) average daily step count, (2) blood glucose, (3) systolic blood pressure, (4) sex, and (5) age. Here, we found that compared to calendar age alone, PhysiAge better predicts mortality, as well as established muscle aging markers such as decrease in NAD
MeSH term(s)	Humans ; Aged ; Aging/physiology ; Longevity/physiology ; Metabolomics ; Oxidative Stress ; Plasma
Language	English
Publishing date	2023-05-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2886586-8
ISSN	2509-2723 ; 2509-2715
ISSN (online)	2509-2723
ISSN	2509-2715
DOI	10.1007/s11357-023-00827-0
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Article ; Online: Smoking cessation only partially reverses cardiac metabolic and structural remodeling in mice.

Aid, Jekaterina / Tanjeko, Ajime Tom / Serré, Jef / Eggelbusch, Moritz / Noort, Wendy / de Wit, Gerard M J / van Weeghel, Michel / Puurand, Marju / Tepp, Kersti / Gayan-Ramirez, Ghislaine / Degens, Hans / Käämbre, Tuuli / Wüst, Rob C I

Acta physiologica (Oxford, England)

2024 , Page(s) e14145

Abstract: Aims: Active cigarette smoking is a major risk factor for chronic obstructive pulmonary disease that remains elevated after cessation. Skeletal muscle dysfunction has been well documented after smoking, but little is known about cardiac adaptations to ... ...

Abstract	Aims: Active cigarette smoking is a major risk factor for chronic obstructive pulmonary disease that remains elevated after cessation. Skeletal muscle dysfunction has been well documented after smoking, but little is known about cardiac adaptations to cigarette smoking. The underlying cellular and molecular cardiac adaptations, independent of confounding lifestyle factors, and time course of reversibility by smoking cessation remain unclear. We hypothesized that smoking negatively affects cardiac metabolism and induces local inflammation in mice, which do not readily reverse upon 2-week smoking cessation. Methods: Mice were exposed to air or cigarette smoke for 14 weeks with or without 1- or 2-week smoke cessation. We measured cardiac mitochondrial respiration by high-resolution respirometry, cardiac mitochondrial density, abundance of mitochondrial supercomplexes by electrophoresis, and capillarization, fibrosis, and macrophage infiltration by immunohistology, and performed cardiac metabolome and lipidome analysis by mass spectrometry. Results: Mitochondrial protein, supercomplex content, and respiration (all p < 0.03) were lower after smoking, which were largely reversed within 2-week smoking cessation. Metabolome and lipidome analyses revealed alterations in mitochondrial metabolism, a shift from fatty acid to glucose metabolism, which did not revert to control upon smoking cessation. Capillary density was not different after smoking but increased after smoking cessation (p = 0.02). Macrophage infiltration and fibrosis (p < 0.04) were higher after smoking but did not revert to control upon smoking cessation. Conclusions: While cigarette-impaired smoking-induced cardiac mitochondrial function was reversed by smoking cessation, the remaining fibrosis and macrophage infiltration may contribute to the increased risk of cardiovascular events after smoking cessation.
Language	English
Publishing date	2024-04-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.14145
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Article ; Online: Polar metabolomics in human muscle biopsies using a liquid-liquid extraction and full-scan LC-MS.

Schomakers, Bauke V / Hermans, Jill / Jaspers, Yorrick R J / Salomons, Gajja / Vaz, Frédéric M / van Weeghel, Michel / Houtkooper, Riekelt H

STAR protocols

2022 Volume 3, Issue 2, Page(s) 101302

Abstract: We describe here a user-friendly analysis protocol for semi-targeted polar metabolomics in human muscle biopsies using Zwitterionic Hydrophilic Interaction Liquid Chromatography and high-resolution full-scan mass spectrometry. Previously, this protocol ... ...

Abstract	We describe here a user-friendly analysis protocol for semi-targeted polar metabolomics in human muscle biopsies using Zwitterionic Hydrophilic Interaction Liquid Chromatography and high-resolution full-scan mass spectrometry. Previously, this protocol has been used for
MeSH term(s)	Biopsy ; Chromatography, Liquid/methods ; Humans ; Liquid-Liquid Extraction ; Metabolomics/methods ; Muscles ; Tandem Mass Spectrometry/methods
Language	English
Publishing date	2022-04-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2022.101302
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Article ; Online: Discovery of novel diagnostic biomarkers for Sjögren-Larsson syndrome by untargeted lipidomics.

Vaz, Frédéric M / Staps, Pippa / van Klinken, Jan Bert / van Lenthe, Henk / Vervaart, Martin / Wanders, Ronald J A / Pras-Raves, Mia L / van Weeghel, Michel / Salomons, Gajja S / Ferdinandusse, Sacha / Wevers, Ron A / Willemsen, Michèl A A P

Biochimica et biophysica acta. Molecular and cell biology of lipids

2024 Volume 1869, Issue 2, Page(s) 159447

Abstract: Aim: Sjögren-Larsson syndrome (SLS) is a rare neurometabolic disorder that mainly affects brain, eye and skin and is caused by deficiency of fatty aldehyde dehydrogenase. Our recent finding of a profoundly disturbed brain tissue lipidome in SLS prompted ...

Abstract	Aim: Sjögren-Larsson syndrome (SLS) is a rare neurometabolic disorder that mainly affects brain, eye and skin and is caused by deficiency of fatty aldehyde dehydrogenase. Our recent finding of a profoundly disturbed brain tissue lipidome in SLS prompted us to search for similar biomarkers in plasma as no functional test in blood is available for SLS. Methods and results: We performed plasma lipidomics and used a newly developed bioinformatics tool to mine the untargeted part of the SLS plasma and brain lipidome to search for SLS biomarkers. Plasma lipidomics showed disturbed ether lipid metabolism in known lipid classes. Untargeted lipidomics of both plasma and brain (white and grey matter) uncovered two new endogenous lipid classes highly elevated in SLS. The first biomarker group were alkylphosphocholines/ethanolamines containing different lengths of alkyl-chains where some alkylphosphocholines were > 600-fold elevated in SLS plasma. The second group of biomarkers were a set of 5 features of unknown structure. Fragmentation studies suggested that they contain ubiquinol and phosphocholine and one feature was also found as a glucuronide conjugate in plasma. The plasma features were highly distinctive for SLS with levels >100-1000-fold the level in controls, if present at all. We speculate on the origin of the alkylphosphocholines/ethanolamines and the nature of the ubiquinol-containing metabolites. Conclusions: The metabolites identified in this study represent novel endogenous lipid classes thus far unknown in humans. They represent the first plasma metabolite SLS-biomarkers and may also yield more insight into SLS pathophysiology.
MeSH term(s)	Humans ; Sjogren-Larsson Syndrome/diagnosis ; Sjogren-Larsson Syndrome/metabolism ; Lipidomics ; Skin/metabolism ; Ethanolamines ; Lipids
Chemical Substances	Ethanolamines ; Lipids
Language	English
Publishing date	2024-01-03
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	60-7
ISSN	1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbalip.2023.159447
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Article ; Online: Muscle abnormalities worsen after post-exertional malaise in long COVID.

Appelman, Brent / Charlton, Braeden T / Goulding, Richie P / Kerkhoff, Tom J / Breedveld, Ellen A / Noort, Wendy / Offringa, Carla / Bloemers, Frank W / van Weeghel, Michel / Schomakers, Bauke V / Coelho, Pedro / Posthuma, Jelle J / Aronica, Eleonora / Joost Wiersinga, W / van Vugt, Michèle / Wüst, Rob C I

Nature communications

2024 Volume 15, Issue 1, Page(s) 17

Abstract: A subgroup of patients infected with SARS-CoV-2 remain symptomatic over three months after infection. A distinctive symptom of patients with long COVID is post-exertional malaise, which is associated with a worsening of fatigue- and pain-related symptoms ...

Abstract	A subgroup of patients infected with SARS-CoV-2 remain symptomatic over three months after infection. A distinctive symptom of patients with long COVID is post-exertional malaise, which is associated with a worsening of fatigue- and pain-related symptoms after acute mental or physical exercise, but its underlying pathophysiology is unclear. With this longitudinal case-control study (NCT05225688), we provide new insights into the pathophysiology of post-exertional malaise in patients with long COVID. We show that skeletal muscle structure is associated with a lower exercise capacity in patients, and local and systemic metabolic disturbances, severe exercise-induced myopathy and tissue infiltration of amyloid-containing deposits in skeletal muscles of patients with long COVID worsen after induction of post-exertional malaise. This study highlights novel pathways that help to understand the pathophysiology of post-exertional malaise in patients suffering from long COVID and other post-infectious diseases.
MeSH term(s)	Humans ; Post-Acute COVID-19 Syndrome ; SARS-CoV-2 ; Case-Control Studies ; COVID-19/complications ; Fatigue/etiology ; Musculoskeletal Abnormalities ; Muscle, Skeletal ; Pain ; Plaque, Amyloid
Language	English
Publishing date	2024-01-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-44432-3
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Article ; Online: Hepatic ADTRP overexpression does not influence lipid and glucose metabolism

Defour, Merel / van Weeghel, Michel / Hermans, Jill / Kersten, Sander

American Journal of Physiology - Cell Physiology

2021 Volume 321, Issue 4

Abstract	The peroxisome proliferator-activated receptors (PPARs) are a group of transcription factors belonging to the nuclear receptor superfamily. Since most target genes of PPARs are implicated in lipid and glucose metabolism, regulation by PPARs could be used as a screening tool to identify novel genes involved in lipid or glucose metabolism. Here, we identify Adtrp, a serine hydrolase enzyme that was reported to catalyze the hydrolysis of fatty acid esters of hydroxy fatty acids (FAHFAs), as a novel PPAR-regulated gene. Adtrp was significantly upregulated by PPARa activation in mouse primary hepatocytes, liver slices, and whole liver. In addition, Adtrp was upregulated by PPARc activation in 3L3-L1 adipocytes and in white adipose tissue. ChIP-SEQ identified a strong PPAR-binding site in the immediate upstream promoter of the Adtrp gene. Adenoviral-mediated hepatic overexpression of Adtrp in diet-induced obese mice caused a modest increase in plasma nonesterified fatty acids but did not influence diet-induced obesity, liver triglyceride levels, liver lipidomic profiles, liver transcriptomic profiles, plasma cholesterol, triglyceride, glycerol, and glucose levels. Moreover, hepatic Adtrp overexpression did not lead to significant changes in FAHFA levels in plasma or liver and did not influence glucose and insulin tolerance. Finally, hepatic overexpression of Adtrp did not influence liver triglycerides and levels of plasma metabolites after a 24-h fast. Taken together, our data suggest that despite being a PPAR-regulated gene, hepatic Adtrp does not seem to play a major role in lipid and glucose metabolism and does not regulate FAHFA levels.
Keywords	ADTRP ; FAHFAs ; Liver ; Metabolism ; PPAR
Language	English
Publishing country	nl
Document type	Article ; Online
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Probing metabolic memory in the hepatic response to fasting.

Defour, Merel / Hooiveld, Guido J E J / van Weeghel, Michel / Kersten, Sander

Physiological genomics

2020 Volume 52, Issue 12, Page(s) 602–617

Abstract: Tissues may respond differently to a particular stimulus if they have been previously exposed to that same stimulus. Here, we tested the hypothesis that a strong metabolic stimulus such as fasting may influence the hepatic response to a subsequent fast ... ...

Abstract	Tissues may respond differently to a particular stimulus if they have been previously exposed to that same stimulus. Here, we tested the hypothesis that a strong metabolic stimulus such as fasting may influence the hepatic response to a subsequent fast and thus elicit a memory effect. Overnight fasting in mice significantly increased plasma free fatty acids, glycerol, β-hydroxybutyrate, and liver triglycerides, and decreased plasma glucose, plasma triglycerides, and liver glycogen levels. In addition, fasting dramatically changed the liver transcriptome, upregulating genes involved in gluconeogenesis and in uptake, oxidation, storage, and mobilization of fatty acids, and downregulating genes involved in fatty acid synthesis, fatty acid elongation/desaturation, and cholesterol synthesis. Fasting also markedly impacted the liver metabolome, causing a decrease in the levels of numerous amino acids, glycolytic-intermediates, TCA cycle intermediates, and nucleotides. However, these fasting-induced changes were unaffected by two previous overnight fasts. Also, no significant effect was observed of prior fasting on glucose tolerance. Finally, analysis of the effect of fasting on the transcriptome in hepatocyte humanized mouse livers indicated modest similarity in gene regulation in mouse and human liver cells. In general, genes involved in metabolic pathways were upregulated or downregulated to a lesser extent in human liver cells than in mouse liver cells. In conclusion, we found that previous exposure to fasting in mice did not influence the hepatic response to a subsequent fast, arguing against the concept of metabolic memory in the liver. Our data provide a useful resource for the study of liver metabolism during fasting.
MeSH term(s)	3-Hydroxybutyric Acid/blood ; Animals ; Blood Glucose/analysis ; Cells, Cultured ; Fasting/blood ; Fatty Acids, Nonesterified/blood ; Gluconeogenesis/genetics ; Glucose Tolerance Test ; Glycerol/blood ; Glycogen/metabolism ; Hepatocytes/metabolism ; Humans ; Liver/metabolism ; Male ; Metabolic Networks and Pathways/genetics ; Metabolome ; Mice ; Mice, Inbred C57BL ; Transcriptome ; Triglycerides/blood
Chemical Substances	Blood Glucose ; Fatty Acids, Nonesterified ; Triglycerides ; Glycogen (9005-79-2) ; Glycerol (PDC6A3C0OX) ; 3-Hydroxybutyric Acid (TZP1275679)
Language	English
Publishing date	2020-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2038823-8
ISSN	1531-2267 ; 1094-8341
ISSN (online)	1531-2267
ISSN	1094-8341
DOI	10.1152/physiolgenomics.00117.2020
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Article ; Online: Biotechnological production of reduced and oxidized NAD

Zapata-Pérez, Rubén / García-Saura, Antonio Ginés / Scantlebery, Angelique M L / Schomakers, Bauke V / Rabadán-Ros, Rubén / van Weeghel, Michel / Houtkooper, Riekelt H / Sánchez-Ferrer, Álvaro

Food research international (Ottawa, Ont.)

2023 Volume 165, Page(s) 112560

Abstract: Dysregulation of nicotinamide adenine dinucleotide ( ... ...

Abstract	Dysregulation of nicotinamide adenine dinucleotide (NAD
MeSH term(s)	NAD ; Biotechnology ; Cell Culture Techniques ; Homeostasis ; Nucleotides
Chemical Substances	NAD (0U46U6E8UK) ; Nucleotides
Language	English
Publishing date	2023-02-02
Publishing country	Canada
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1111695-x
ISSN	1873-7145 ; 0963-9969
ISSN (online)	1873-7145
ISSN	0963-9969
DOI	10.1016/j.foodres.2023.112560
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