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Nicotinamide mononucleotide improves the quality of porcine oocytes deteriorated by heat stress

ABSTRACT: Nicotinamide mononucleotide improves the quality of porcine oocytes deteriorated by heat stress

PROVIDER: PRJNA768784 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16204458_1.fastq.gz	Fastqsanger.gz
	SRR16204458_2.fastq.gz	Fastqsanger.gz
	SRR16204459_1.fastq.gz	Fastqsanger.gz
	SRR16204459_2.fastq.gz	Fastqsanger.gz
	SRR16204460_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Nicotinamide mononucleotide improves the quality of porcine oocytes deteriorated by heat stress

Project description:Elevated ambient temperature results in heat stress which is a major concern for productivity and product quality due to its negative impact on animal health, productivity and product quality. As global warming becomes more and more serious, the impact of heat stress (HS) on animal husbandry cannot be ignored. However, the effect of NMN on the quality of porcine oocytes after heat stress and the prevention strategies are not yet fully understood. Here, we report that nicotinamide mononucleotide (NMN) treatment ameliorates the quality of porcine oocytes exposed to heat stress. Specifically, we found that HS caused oocyte meiosis failure by disrupting the dynamics and arrangement of meiotic organelles, showing obvious damage to cytoskeleton assembly. Furthermore, heat stress can cause damage to oocyte mitochondria, which is an indicator of oocyte cytoplasmic maturation. On the contrary, supplementation of NMN can improve this phenomenon, maintain the normal chromosome/spindle structure, and the dynamics of CGs and its core content ovastacin.

2022-06-22 | GSE185338 | GEO

Nicotinamide mononucleotide supplementation reverses the declining quality of maternally aged oocytes

Project description:Advanced maternal age, defined as 35 years or older, is associated with a decline in both ovarian reserve and oocyte quality, which leads to the female infertility, pregnancy loss, fetal anomalies, stillbirth, and obstetric complications. At present, the effective approaches to counteract the maternal age-related decay of oocyte quality are still not fully determined. Here, we report that in vivo supplementation of nicotinamide mononucleotide (NMN) efficaciously ameliorates the quality of oocytes from naturally aged mice by recovering nicotinamide adenine dinucleotide (NAD + ) levels in oocytes. NMN supplementation increases the number of antral follicles, ovulated oocytes and matured oocytes from aged mice. Specifically, NMN supplementation maintains the normal spindle/chromosome structure and dynamics of cortical granule component ovastacin to ensure the meiotic competency and fertilization ability of aged oocytes. Moreover, single cell transcriptome analysis shows that the beneficial effect of NMN on the aged oocytes is mediated by the restoration of the mitochondrial function, thereby reducing the accumulated ROS to suppress the occurrence of apoptosis. To sum up, our data reveal that supplementation of NMN is a feasible approach to prevent oocyte quality from advanced maternal age-related deterioration, contributing to improve the reproductive outcome of aged women and the assisted reproductive technology.

2023-07-01 | GSE153920 | GEO

Nicotinamide mononucleotide supplementation reverses the declining quality of maternally aged oocytes

Project description:Nicotinamide mononucleotide supplementation reverses the declining quality of maternally aged oocytes

| PRJNA644537 | ENA

Supplementation of nicotinamide mononucleotide improves the quality of postovulatory aged porcine oocytes.

Project description: Not available

| S-EPMC9345308 | biostudies-literature

RNA-Sequencing of Aged Mouse Oocytes with in vivo Nicotinamide Mononucleotide (NMN) Treatment

Project description:RNA-Sequencing of Aged Mouse Oocytes with in vivo Nicotinamide Mononucleotide (NMN) Treatment

| PRJNA759861 | ENA

Reduced Nicotinamide Mononucleotide (NMNH) Potently Enhances NAD+, Suppresses Glycolysis and Cell Growth

Project description:In the present study, we developed a chemical method to produce dihydro nicotinamide mononucleotide (NMNH), which is the reduced-form of nicotinamide mononucleotide (NMN). We demonstrated that NMNH was a better nicotinamide adenine dinucleotide (NAD+) enhancer compared to NMN both in vitro and in vivo mediated by mononucleotide adenylyltransferase (NMNAT). Additionally, NMNH increased the reduced NAD (NADH) levels in cells and in mouse liver. Metabolomic analysis revealed that NMNH inhibited glycolysis and TCA cycle. In vitro experiments demonstrated that NMNH induced cell cycle arrest and suppressed cell growth. Nevertheless, NMNH treatment did not cause observable difference in mice. Taken together, our work demonstrates that NMNH is a potent NAD+ enhancer, and suppresses glycometabolism and cell growth.

2022-02-25 | PXD022547 | Pride

Effect of nicotinamide mononucleotide on doxorubicin-induced cardiac injury in mice

Project description:Doxorubicin (DOX) is the cornerstone of chemotherapy regimens for many malignancies, but its clinical usage is limited by severe cardiotoxicity. Accumulating evidence suggest that nicotinamide adenine dinucleotide (NAD+) depletion contributes to DOX-induced cardiotoxicity, making NAD+ boosting an appealing strategy. Nicotinamide mononucleotide (NMN) is an NAD+ precursor that shows promising therapeutic effects in various diseases. To understand the impact of NMN on gene expression in myocardial tissue of DOX-exposed mice, a RNA-seq assay was carried out.

2023-06-03 | GSE233644 | GEO

Slc12a8 is a nicotinamide mononucleotide transporter that counteracts aging

Project description:Slc12a8 is a nicotinamide mononucleotide transporter that counteracts aging

| PRJNA485337 | ENA

Subacute toxicity study of nicotinamide mononucleotide via oral administration

Project description:Subacute toxicity study of nicotinamide mononucleotide via oral administration

| PRJNA662085 | ENA

Nicotinamide mononucleotide, a key NAD+ precursor, treats the pathophysiology of diet- and age-induced diabetes

Project description:Type 2 diabetes (T2D) has become an epidemic in our modern lifestyle, likely due to calorie-rich diets overwhelming our adaptive metabolic pathways. One such pathway is mediated by nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD+ biosynthesis, and the NAD+-dependent protein deacetylase SIRT1. Here we show that NAMPT-mediated NAD+ biosynthesis is severely compromised in metabolic organs by high-fat diet (HFD). Strikingly, nicotinamide mononucleotide (NMN), a product of the NAMPT reaction and a key NAD+ intermediate, ameliorates glucose intolerance by restoring NAD+ levels in HFD-induced T2D mice. NMN also enhances hepatic insulin sensitivity and restores gene expression related to oxidative stress, inflammatory response, and circadian rhythm, partly through SIRT1 activation. Furthermore, NAD+ and NAMPT levels show significant decreases in multiple organs during aging, and NMN improves glucose intolerance and lipid profiles in age-induced T2D mice. These findings provide critical insights into a novel intervention against diet- and age-induced T2D. 4 regular chow fed mice (RC1-4) vs 4 high-fat diet fed (HFD) (HFD1a-4a) mice were analyzed on one chip (Chip-A). 4 HFD mice (HFD1b-4b) vs 4 HFD-NMN treated mice (NMN1-4) were examined on the other chip (Chip-B).

2011-12-05 | E-GEOD-31647 | biostudies-arrayexpress

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