keyword
https://read.qxmd.com/read/38392200/nicotinamide-riboside-regulates-chemotaxis-to-decrease-inflammation-and-ameliorate-functional-recovery-following-spinal-cord-injury-in-mice
#21
JOURNAL ARTICLE
Yan Li, Chunjia Zhang, Zihan Li, Fan Bai, Yingli Jing, Han Ke, Shuangyue Zhang, Yitong Yan, Yan Yu
Changes in intracellular nicotinamide adenine dinucleotide (NAD+ ) levels have been observed in various disease states. A decrease in NAD+ levels has been noted following spinal cord injury (SCI). Nicotinamide riboside (NR) serves as the precursor of NAD+ . Previous research has demonstrated the anti-inflammatory and apoptosis-reducing effects of NR supplements. However, it remains unclear whether NR exerts a similar role in mice after SCI. The objective of this study was to investigate the impact of NR on these changes in a mouse model of SCI...
February 1, 2024: Current Issues in Molecular Biology
https://read.qxmd.com/read/38357951/the-role-of-nad-in-myocardial-ischemia-induced-heart-failure-in-sprague-dawley-rats-and-beagles
#22
JOURNAL ARTICLE
Zuowei Pei, Chenguang Yang, Ying Guo, Min Dong, Fang Wang
INTRODUCTION: Nicotinamide adenine dinucleotide (NAD+) participates in various processes that are dysregulated in cardiovascular diseases. Supplementation with NAD+ may be cardioprotective. However, whether the protective effect exerted by NAD+ in heart failure (HF) is more effective before acute myocardial infarction (MI) or after remains unclear. The left anterior descending arteries of male Sprague Dawley rats and beagles that developed HF following MI were ligated for 1 week, following which the animals were treated for 4 weeks with low, medium, and high doses of NAD+ and LCZ696...
February 13, 2024: Current Pharmaceutical Biotechnology
https://read.qxmd.com/read/38357931/a-metabolic-signature-for-nadsyn1-dependent-congenital-nad-deficiency-disorder
#23
JOURNAL ARTICLE
Justin O Szot, Hartmut Cuny, Ella Mma Martin, Delicia Z Sheng, Kavitha Iyer, Stephanie Portelli, Vivien Nguyen, Jessica M Gereis, Dimuthu Alankarage, David Chitayat, Karen Chong, Ingrid M Wentzensen, Catherine Vincent-Delormé, Alban Lermine, Emma Burkitt-Wright, Weizhen Ji, Lauren Jeffries, Lynn S Pais, Tiong Y Tan, James Pitt, Cheryl A Wise, Helen Wright, Israel D Andrews, Brianna Pruniski, Theresa A Grebe, Nicole Corsten-Janssen, Katelijne Bouman, Cathryn Poulton, Supraja Prakash, Boris Keren, Natasha J Brown, Matthew F Hunter, Oliver Heath, Saquib A Lakhani, John H McDermott, David B Ascher, Gavin Chapman, Kayleigh Bozon, Sally L Dunwoodie
Nicotinamide adenine dinucleotide (NAD) is essential for embryonic development. To date, biallelic loss-of-function variants in 3 genes encoding nonredundant enzymes of the NAD de novo synthesis pathway - KYNU, HAAO, and NADSYN1 - have been identified in humans with congenital malformations defined as congenital NAD deficiency disorder (CNDD). Here, we identified 13 further individuals with biallelic NADSYN1 variants predicted to be damaging, and phenotypes ranging from multiple severe malformations to the complete absence of malformation...
February 15, 2024: Journal of Clinical Investigation
https://read.qxmd.com/read/38352659/low-dose-naltrexone-and-nad-for-the-treatment-of-patients-with-persistent-fatigue-symptoms-after-covid-19
#24
JOURNAL ARTICLE
Anar Isman, Andy Nyquist, Bailey Strecker, Girish Harinath, Virginia Lee, Xingyu Zhang, Sajad Zalzala
A subset of patients experiences persistent fatigue symptoms after COVID-19, and patients may develop long COVID, which is characterized by lasting systemic symptoms. No treatments for this condition have been validated and are urgently warranted. In this pilot study, we assessed whether treatment with low-dose naltrexone (LDN, 4.5 mg/day) and supplementation with NAD + through iontophoresis patches could improve fatigue symptoms and quality of life in 36 patients with persistent moderate/severe fatigue after COVID-19...
March 2024: Brain, behavior, & immunity health
https://read.qxmd.com/read/38340651/the-therapeutic-perspective-of-nad-precursors-in-age-related-diseases
#25
REVIEW
Tooba Iqbal, Takashi Nakagawa
Nicotinamide adenine dinucleotide (NAD+ ) is the fundamental molecule that performs numerous biological reactions and is crucial for maintaining cellular homeostasis. Studies have found that NAD+ decreases with age in certain tissues, and age-related NAD+ depletion affects physiological functions and contributes to various aging-related diseases. Supplementation of NAD+ precursor significantly elevates NAD+ levels in murine tissues, effectively mitigates metabolic syndrome, enhances cardiovascular health, protects against neurodegeneration, and boosts muscular strength...
February 2, 2024: Biochemical and Biophysical Research Communications
https://read.qxmd.com/read/38336100/supplementation-of-nicotinamide-mononucleotide-diminishes-cox-2-associated-inflammatory-responses-in-macrophages-by-activating-kynurenine-ahr-signaling
#26
JOURNAL ARTICLE
Jing Liu, Wenxuan Hou, Zhaoyun Zong, Yuling Chen, Xiaohui Liu, Ran Zhang, Haiteng Deng
Cyclooxygenase-2 (COX-2) is an inducible enzyme responsible for prostaglandin synthesis during inflammation and immune responses. Our previous results show that NAD+ level decreased in activated macrophages while nicotinamide mononucleotide (NMN) supplementation suppressed the inflammatory responses via restoring NAD+ level and downregulating COX-2. However, whether NMN downregulates COX-2 in mouse model of inflammation, and its underlying mechanism needs to be further explored. In the present study, we established LPS- and alum-induced inflammation model and demonstrated that NMN suppressed the inflammatory responses in vivo...
February 7, 2024: Free Radical Biology & Medicine
https://read.qxmd.com/read/38331947/loss-of-sarm1-reduces-retinal-ganglion-cell-loss-in-chronic-glaucoma
#27
JOURNAL ARTICLE
Huilan Zeng, Jordan E Mayberry, David Wadkins, Nathan Chen, Daniel W Summers, Markus H Kuehn
Glaucoma is one of the leading causes of irreversible blindness worldwide and vision loss in the disease results from the deterioration of retinal ganglion cells (RGC) and their axons. Metabolic dysfunction of RGC plays a significant role in the onset and progression of the disease in both human patients and rodent models, highlighting the need to better define the mechanisms regulating cellular energy metabolism in glaucoma. This study sought to determine if Sarm1, a gene involved in axonal degeneration and NAD+ metabolism, contributes to glaucomatous RGC loss in a mouse model with chronic elevated intraocular pressure (IOP)...
February 8, 2024: Acta Neuropathologica Communications
https://read.qxmd.com/read/38323474/integrated-stress-response-potentiates-ponatinib-induced-cardiotoxicity
#28
JOURNAL ARTICLE
Gege Yan, Zhenbo Han, Youjeong Kwon, Jordan Jousma, Sarath Babu Nukala, Benjamin L Prosser, Xiaoping Du, Sandra Pinho, Sang-Bing Ong, Won Hee Lee, Sang-Ging Ong
BACKGROUND: Mitochondrial dysfunction is a primary driver of cardiac contractile failure; yet, the cross talk between mitochondrial energetics and signaling regulation remains obscure. Ponatinib, a tyrosine kinase inhibitor used to treat chronic myeloid leukemia, is among the most cardiotoxic tyrosine kinase inhibitors and causes mitochondrial dysfunction. Whether ponatinib-induced mitochondrial dysfunction triggers the integrated stress response (ISR) to induce ponatinib-induced cardiotoxicity remains to be determined...
February 7, 2024: Circulation Research
https://read.qxmd.com/read/38316756/function-of-nad-metabolism-in-white-adipose-tissue-lessons-from-mouse-models
#29
REVIEW
So Young Kwon, Yoon Jung Park
Nicotinamide adenine dinucleotide (NAD) is an endogenous substance in redox reactions and regulates various functions in metabolism. NAD and its precursors are known for their anti-ageing and anti-obesity properties and are mainly active in the liver and muscle. Boosting NAD+ through supplementation with the precursors, such as nicotinamide mononucleotide (NMN) or nicotinamide riboside (NR), enhances insulin sensitivity and circadian rhythm in the liver, and improves mitochondrial function in the muscle. Recent evidence has revealed that the adipose tissue could be another direct target of NAD supplementation by attenuating inflammation and fat accumulation...
February 5, 2024: Adipocyte
https://read.qxmd.com/read/38308646/c-peptide-in-diabetes-a-player-in-a-dual-hormone-disorder
#30
REVIEW
Ali Dakroub, Ali Dbouk, Aref Asfour, Suzanne A Nasser, Ahmed F El-Yazbi, Amirhossein Sahebkar, Assaad A Eid, Rabah Iratni, Ali H Eid
C-peptide, a byproduct of insulin synthesis believed to be biologically inert, is emerging as a multifunctional molecule. C-peptide serves an anti-inflammatory and anti-atherogenic role in type 1 diabetes mellitus (T1DM) and early T2DM. C-peptide protects endothelial cells by activating AMP-activated protein kinase α, thus suppressing the activity of NAD(P)H oxidase activity and reducing reactive oxygen species (ROS) generation. It also prevents apoptosis by regulating hyperglycemia-induced p53 upregulation and mitochondrial adaptor p66shc overactivation, as well as reducing caspase-3 activity and promoting expression of B-cell lymphoma-2...
February 3, 2024: Journal of Cellular Physiology
https://read.qxmd.com/read/38302501/the-use-of-a-systems-approach-to-increase-nad-in-human-participants
#31
JOURNAL ARTICLE
John D Henderson, Sophia N Z Quigley, Shruti S Chachra, Nichola Conlon, Dianne Ford
Reversal or mitigation against an age-related decline in NAD+ has likely benefits, and this premise has driven academic and commercial endeavour to develop dietary supplements that achieve this outcome. We used a systems-based approach to improve on current supplements by targeting multiple points in the NAD+ salvage pathway. In a double-blind, randomised, crossover trial, the supplement - Nuchido TIME+® (NT) - increased NAD+ concentration in whole blood. This was associated with an increase in SIRT1 and an increase in nicotinamide phosphoribosyltransferase (NAMPT) in peripheral blood mononucleocytes, lower concentrations of pro-inflammatory cytokines in plasma, including a reduction in interleukin 2 (IL2), a reduction in glycated serum protein and a shift in the glycosylation profile of immunoglobulin G (IgG) toward a younger biological age, all of which are likely to promote a healthier ageing trajectory...
February 1, 2024: NPJ Aging
https://read.qxmd.com/read/38282024/nmnat2-supports-vesicular-glycolysis-via-nad-homeostasis-to-fuel-fast-axonal-transport
#32
JOURNAL ARTICLE
Sen Yang, Zhen-Xian Niou, Andrea Enriquez, Jacob LaMar, Jui-Yen Huang, Karen Ling, Paymaan Jafar-Nejad, Jonathan Gilley, Michael P Coleman, Jason M Tennessen, Vidhya Rangaraju, Hui-Chen Lu
BACKGROUND: Bioenergetic maladaptations and axonopathy are often found in the early stages of neurodegeneration. Nicotinamide adenine dinucleotide (NAD), an essential cofactor for energy metabolism, is mainly synthesized by Nicotinamide mononucleotide adenylyl transferase 2 (NMNAT2) in CNS neurons. NMNAT2 mRNA levels are reduced in the brains of Alzheimer's, Parkinson's, and Huntington's disease. Here we addressed whether NMNAT2 is required for axonal health of cortical glutamatergic neurons, whose long-projecting axons are often vulnerable in neurodegenerative conditions...
January 29, 2024: Molecular Neurodegeneration
https://read.qxmd.com/read/38281710/nad-in-pathological-cardiac-remodeling-metabolic-regulation-and-beyond
#33
REVIEW
Ignacio Norambuena-Soto, Yingfeng Deng, Charles Brenner, Sergio Lavandero, Zhao V Wang
Nicotinamide adenine dinucleotide (NAD) coenzymes are carriers of high energy electrons in metabolism and also play critical roles in numerous signaling pathways. NAD metabolism is decreased in various cardiovascular diseases. Importantly, stimulation of NAD biosynthesis protects against heart disease under different pathological conditions. In this review, we describe pathways for both generation and catabolism of NAD coenzymes and the respective changes of these pathways in the heart under cardiac diseases, including pressure overload, myocardial infarction, cardiometabolic disease, cancer treatment cardiotoxicity, and heart failure...
January 26, 2024: Biochimica et Biophysica Acta. Molecular Basis of Disease
https://read.qxmd.com/read/38276975/gut-microbiome-mediates-ferroptosis-resistance-for-colorectal-cancer-development
#34
JOURNAL ARTICLE
Ruoxi Zhang, Rui Kang, Daolin Tang
Colorectal cancer (CRC) is a prevalent cancer type in the United States, affecting both genders and influenced by genetics and environmental factors. The role of the gut microbiome in CRC development and therapy response is a burgeoning field of study. A recent study uncovered that trans-3-indoleacrylic acid (IDA), a microbial metabolite from P. anaerobius, promotes CRC by inhibiting ferroptosis, a type of non-apoptotic cell death driven by unrestricted lipid peroxidation and subsequent membrane damage. IDA activates aryl hydrocarbon receptor (AHR), a nuclear transcription factor, leading to the expression of aldehyde dehydrogenase 1 family member A3 (ALDH1A3)...
January 26, 2024: Cancer Research
https://read.qxmd.com/read/38266764/dietary-nmn-supplementation-enhances-motor-and-nmj-function-in-als
#35
JOURNAL ARTICLE
Samuel Lundt, Nannan Zhang, Luis Polo-Parada, Xinglong Wang, Shinghua Ding
Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease that causes the degeneration of motor neurons in the motor cortex and spinal cord. Patients with ALS experience muscle weakness and atrophy in the limbs which eventually leads to paralysis and death. NAD+ is critical for energy metabolism, such as glycolysis and oxidative phosphorylation, but is also involved in non-metabolic cellular reactions. In the current study, we determined whether the supplementation of nicotinamide mononucleotide (NMN), an NAD+ precursor, in the diet had beneficial impacts on disease progression using a SOD1G93A mouse model of ALS...
January 22, 2024: Experimental Neurology
https://read.qxmd.com/read/38264909/indole-3-propionic-acid-protects-against-heart-failure-with-preserved-ejection-fraction
#36
JOURNAL ARTICLE
Yu-Chen Wang, Yen Chin Koay, Calvin Pan, Zhiqiang Zhou, W H Wilson Tang, Jennifer Wilcox, Xinmin S Li, Alexia Zagouras, Francine Marques, Hooman Allayee, Federico E Rey, David M Kaye, John F O'Sullivan, Stanley L Hazen, Yang Cao, Aldons J Lusis
BACKGROUND: Heart failure with preserved ejection fraction (HFpEF) is a common but poorly understood form of heart failure, characterized by impaired diastolic function. It is highly heterogeneous with multiple comorbidities, including obesity and diabetes, making human studies difficult. METHODS: Metabolomic analyses in a mouse model of HFpEF showed that levels of indole-3-propionic acid (IPA), a metabolite produced by gut bacteria from tryptophan, were reduced in the plasma and heart tissue of HFpEF mice as compared with controls...
January 24, 2024: Circulation Research
https://read.qxmd.com/read/38256175/nad-precursors-reverse-experimental-diabetic-neuropathy-in-mice
#37
JOURNAL ARTICLE
Krish Chandrasekaran, Neda Najimi, Avinash R Sagi, Sushuma Yarlagadda, Mohammad Salimian, Muhammed Ikbal Arvas, Ahmad F Hedayat, Yanni Kevas, Anand Kadakia, Tibor Kristian, James W Russell
Abnormal NAD+ signaling has been implicated in axonal degeneration in diabetic peripheral neuropathy (DPN). We hypothesized that supplementing NAD+ precursors could alleviate DPN symptoms through increasing the NAD+ levels and activating the sirtuin-1 (SIRT1) protein. To test this, we exposed cultured Dorsal Root Ganglion neurons (DRGs) to Nicotinamide Riboside (NR) or Nicotinamide Mononucleotide (NMN), which increased the levels of NAD+ , the SIRT1 protein, and the deacetylation activity that is associated with increased neurite growth...
January 16, 2024: International Journal of Molecular Sciences
https://read.qxmd.com/read/38254035/%C3%AE-ketoglutarate-improves-cardiac-insufficiency-through-nad-sirt1-signaling-mediated-mitophagy-and-ferroptosis-in-pressure-overload-induced-mice
#38
JOURNAL ARTICLE
Hao Yu, Daojing Gan, Zhen Luo, Qilin Yang, Dongqi An, Hao Zhang, Yingchun Hu, Zhuang Ma, Qingchun Zeng, Dingli Xu, Hao Ren
BACKGROUND: In heart failure (HF), mitochondrial dysfunction and metabolic remodeling lead to a reduction in energy productivity and aggravate cardiomyocyte injury. Supplementation with α-ketoglutarate (AKG) alleviated myocardial hypertrophy and fibrosis in mice with HF and improved cardiac insufficiency. However, the myocardial protective mechanism of AKG remains unclear. We verified the hypothesis that AKG improves mitochondrial function by upregulating NAD+ levels and activating silent information regulator 2 homolog 1 (SIRT1) in cardiomyocytes...
January 22, 2024: Molecular Medicine
https://read.qxmd.com/read/38236698/evidence-for-cytochrome-p450-3a4-mediated-metabolic-activation-of-sco-267
#39
JOURNAL ARTICLE
Cui Li, Xiaokun Li, Ali Fan, Ning He, Dongmei Wu, Hongyan Yu, Kun Wang, Weijie Jiao, Xu Zhao
SCO-267 is a potent G-protein-coupled receptor 40 agonist that is undergoing clinical development for the treatment of type 2 diabetes mellitus. The current work was undertaken to investigate the bioactivation potential of SCO-267 in vitro and in vivo. Three SCO-267-derived glutathione (GSH) conjugates (M1-M3) were found both in rat and human liver microsomal incubations supplemented with GSH and nicotinamide adenine dinucleotide phosphate. Two GSH conjugates (M1-M2) together with two N-acetyl-cysteine conjugates (M4-M5) were detected in the bile of rats receiving SCO-267 at 10 mg/kg...
January 18, 2024: Biopharmaceutics & Drug Disposition
https://read.qxmd.com/read/38228611/nad-dependent-upr-mt-activation-underlies-intestinal-aging-caused-by-mitochondrial-dna-mutations
#40
JOURNAL ARTICLE
Liang Yang, Zifeng Ruan, Xiaobing Lin, Hao Wang, Yanmin Xin, Haite Tang, Zhijuan Hu, Yunhao Zhou, Yi Wu, Junwei Wang, Dajiang Qin, Gang Lu, Kerry M Loomes, Wai-Yee Chan, Xingguo Liu
Aging in mammals is accompanied by an imbalance of intestinal homeostasis and accumulation of mitochondrial DNA (mtDNA) mutations. However, little is known about how accumulated mtDNA mutations modulate intestinal homeostasis. We observe the accumulation of mtDNA mutations in the small intestine of aged male mice, suggesting an association with physiological intestinal aging. Using polymerase gamma (POLG) mutator mice and wild-type mice, we generate male mice with progressive mtDNA mutation burdens. Investigation utilizing organoid technology and in vivo intestinal stem cell labeling reveals decreased colony formation efficiency of intestinal crypts and LGR5-expressing intestinal stem cells in response to a threshold mtDNA mutation burden...
January 16, 2024: Nature Communications
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