| 包装 | 价格(元) |
| 100mg | 电议 |
| 500mg | 电议 |
Cell lines | Hepa1-6 cells |
Preparation Method | β-Nicotinamide mononucleotide was added to the cell medium |
Reaction Conditions | 0.5-1 mMβ-Nicotinamide mononucleotide |
Applications | Intracellular NAD + levels were significantly reduced by knocking down or knocking down Nampt or treated with the Nampt inhibitor FK866, whereas NAD + levels were significantly increased by supplementation with NAD + precursors NAM or β-Nicotinamide mononucleotide. |
Animal models | Nampt+/- female mice |
Preparation Method | For GTTs, mice were injected with PBS or β-Nicotinamide mononucleotide (500 mg/kg body weight) and fasted for 14 hrs; dextrose (3 g/kg body weight) was then injected intraperitoneally. |
Dosage form | 500 mg/kg β-Nicotinamide mononucleotide for 0、15、30、60,120min |
Applications | After β-Nicotinamide mononucleotide administration, there was no difference in blood glucose levels in GTTs between Nampt+/- and control female mice. In addition, β-Nicotinamide mononucleotide-treated Nampt+/- and control mice also had similar plasma insulin levels at each time point. β-Nicotinamide mononucleotide administration corrects the defect in GSIS observed in Nampt+/- mice. |
| 产品描述 | β-nicotinamide mononucleotide is a product of the nicotinamide phosphoribosyltransferase (NAMPT) reaction and a key NAD+ intermediate. The pharmacological activities of β-nicotinamide mononucleotide include its role in cellular biochemical functions, cardioprotection, diabetes, Alzheimer's disease, and complications associated with obesity[1]. Intracellular NAD + levels were significantly reduced by knocking down or knocking down Nampt or treated with the Nampt inhibitor FK866, whereas NAD + levels were significantly increased by supplementation with NAD + precursors NAM or β-Nicotinamide mononucleotide[3].Treatment of β-nicotinamide mononucleotide, a precursor of NAD+, to HEK293 cells activated and improved the rate of mtDNA replication by increasing nucleotides in mitochondria and decreasing their degradation products: nucleosides. β-Nicotinamide mononucleotide metabolism plays a role in supporting mtDNA replication by maintaining the nucleotide pool balance in the mitochondria[7]. After β-Nicotinamide mononucleotide administration, there was no difference in blood glucose levels in GTTs between Nampt+/- and control female mice. In addition, β-Nicotinamide mononucleotide-treated Nampt+/- and control mice also had similar plasma insulin levels at each time point. β-Nicotinamide mononucleotide administration corrects the defect in GSIS observed in Nampt+/- mice[2]. β-nicotinamide mononucleotide ameliorates glucose intolerance by restoring NAD+ levels in HFD-induced T2D mice. β-nicotinamide mononucleotide also enhances hepatic insulin sensitivity and restores gene expression related to oxidative stress, inflammatory response, and circadian rhythm, partly through SIRT1 activation[4].In a mouse model induced by doxorubicin administered in divided low doses as in the clinics, supplementing mice with a precursor of NAD+ prevented the mtDNA depletion and cardiac dysfunction[5].When investigated whether β-Nicotinamide mononucleotide is superior to nicotinamide (Nam) as a precursor of NAD+ in whole animal experiments. β-Nicotinamide mononucleotide is retained in the body for longer than Nam[6]. References: |
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