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Chemical Structure| 1094-61-7 Chemical Structure| 1094-61-7
Chemical Structure| 1094-61-7

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CAS No.: 1094-61-7

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Nicotinamide mononucleotide (NMN), one of the key precursors of NAD+ and products of the NAMPT reaction , is converted to NAD+ by nicotinamide mononucleotide adenylyltransferase.

Synonyms: β-NM; NMN; Nicotinamide Mononucleotide

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Kei Takahash ; Emiko Sato ; Seiko Yamakoshi ; Mizuki Ogane ; Akiyo Sekimoto ; Takamasa Ishikawa , et al.

Abstract: Podocytes are key components of the glomerular filtration barrier, and their injury leads to proteinuria, chronic kidney disease (CKD), and nephrotic syndrome. Effective treatments for these conditions are not well established, and prevention of podocyte injury is a crucial challenge. Nicotinamide (NAM), a form of vitamin B3, has been reported to exert beneficial effects in various renal disease models due to its antioxidant and anti-inflammatory properties and its ability to replenish nicotinamide adenine dinucleotide (NAD+ ). However, its impact on adriamycin (ADR)-induced nephropathy, a model of nephrotic syndrome caused by podocyte injury, remains unclear. We investigated the effects of NAM administration in a mouse model of ADR nephropathy. BALB/c mice were intravenously administered ADR to induce nephropathy. In the NAM-treated group, mice received 0.6% NAM in drinking water ad libitum starting 7 days before ADR administration. After 14 days, NAM treatment decreased albuminuria, glomerular sclerosis, and podocyte injury, and reduced inflammation and oxidative stress markers in the kidneys. NAM and NAD+ levels were decreased in ADR-treated kidneys, and the expression of the NAD+ -consuming enzymes SIRT1 and poly(ADP-ribose) polymerase 1 (PARP-1) was decreased and increased, respectively. Nicotinamide N-methyltransferase expression was increased. NAM canceled these abnormalities. In cultured rat podocytes, NAD+ alleviated ADR-induced cytotoxicity, apoptosis, and inflammation. These findings suggest that NAM prevents ADR nephropathy and podocyte injury, likely through NAD+ replenishment.

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Jooman Park ; Ruoci Hu ; Yanyu Qian ; Shaolei Xiong ; Asma Sana El-Sabbagh ; Meram Ibrahim , et al.

Abstract: Thermogenic beige adipocytes are recognized as potential therapeutic targets for combating metabolic diseases. However, the metabolic advantages that they offer are compromised with aging. Here we show that treating mice with (E2), a hormone that decreases with age, can counteract the age-related decline in beige adipogenesis when exposed to cold temperature while concurrently enhancing energy expenditure and improving tolerance in mice. Mechanistically, we found that phosphoribosyl (NAMPT) plays a pivotal role in facilitating the formation of E2-induced beige adipocytes, which subsequently suppresses the onset of age-related endoplasmic reticulum (ER) stress. Furthermore, we found that targeting signaling, either genetically or pharmacologically, can restore the formation of beige adipocytes by increasing the number of perivascular adipocyte progenitor cells. Conversely, the absence of signaling prevents this process. Together, our findings shed light on the mechanisms regulating the age-dependent impairment of beige adipocyte formation and underscore the E2-NAMPT-controlled ER stress pathway as a key regulator of this process.

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Park, Jooman ; Hu, Ruoci ; Xiong, Shaolei ; Qian, Yanyu ; El-Sabbagh, Asma Sana ; Ibrahim, Meram , et al.

Abstract: Thermogenic beige adipocytes are recognized as potential therapeutic targets for combating metabolic diseases. However, the metabolic advantages they offer are compromised with aging. Here, we show that treating mice with estrogen (E2), a hormone that decreases with age, to mice can counteract the aging- related decline in beige adipocyte formation when subjected to cold, while concurrently enhancing energy expenditure and improving glucose tolerance. Mechanistically, we find that nicotinamide phosphoribosyltranferase (NAMPT) plays a pivotal role in facilitating the formation of E2-induced beige adipocytes, which subsequently suppresses the onset of age-related ER stress. Furthermore, we found that targeting NAMPT signaling, either genetically or pharmacologically, can restore the formation of beige adipocytes by increasing the number of perivascular adipocyte progenitor cells. Conversely, the absence of NAMPT signaling prevents this process. In conclusion, our findings shed light on the mechanisms governing the age-dependent impairment of beige adipocyte formation and underscore the E2-NAMPT controlled ER stress as a key regulator of this process. Highlights: Estrogen restores beige adipocyte failure along with improved energy metabolism in old mice.Estrogen enhances the thermogenic gene program by mitigating age-induced ER stress.Estrogen enhances the beige adipogenesis derived from SMA+ APCs.Inhibiting the NAMPT signaling pathway abolishes estrogen-promoted beige adipogenesis.

Keywords: Aging ; Beige adipocyte formation ; Estrogen ; ER stress ; NAMPT

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Product Details of β-Nicotinamide mononucleotide

CAS No. :1094-61-7
Formula : C11H15N2O8P
M.W : 334.22
SMILES Code : O=P(OC[C@H]1O[C@@H]([N+]2=CC=CC(C(N)=O)=C2)[C@H](O)[C@@H]1O)([O-])O
Synonyms :
β-NM; NMN; Nicotinamide Mononucleotide
MDL No. :MFCD00038748
InChI Key :DAYLJWODMCOQEW-TURQNECASA-N
Pubchem ID :14180

Safety of β-Nicotinamide mononucleotide

GHS Pictogram:
Signal Word:Warning
Hazard Statements:H315-H319-H335
Precautionary Statements:P261-P305+P351+P338
 

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