Nicotinamide mononucleotide (NMN) is a nucleotide best known for its role as an intermediate in the biosynthesis of nicotinamide adenine dinucleotide (NAD+). In the absence of a suitable transporter, NMN enters mammalian cells as nicotinamide riboside, which is subsequently converted to NMN and NAD+. Primarily mediated through involvement in NAD+ biosynthesis, NMN pharmacological activities include its role in cellular biochemical functions, cardioprotection, diabetes, Alzheimer's disease, and obesity-related complications.
Publishing in Scientific Reports, Wakino and colleagues at Tokushima University in Japan found that injections of 500 mg/kg/day of NMN reduced kidney damage in a mouse model of a disease called focal segmental glomerulus Sclerosis, whose pathology is similar to age-related glomerulosclerosis. NMN restores a large number of cells critical to kidney waste filtration, called podocytes. What's more, by promoting the essential molecule of cellular health, nicotinamide adenine dinucleotide (NAD+), NMN increased the activation of the longevity-promoting enzyme Sirtuin-1, thereby reducing the enzyme associated with kidney tissue damage. These findings provide the first evidence that NMN can restore waste-filtering cells in kidney disease.
NMN reverses kidney dysfunction
Because higher levels of urinary protein are associated with kidney damage and impaired filtration, the team modeled glomerulosclerosis by injecting mice with a chemotherapy drug (doxorubicin) that causes kidney damage. Urinary protein levels were significantly increased in mice that simulated kidney disease. However, treating these mice with NMN reduced urinary protein levels, suggesting reduced kidney damage and corrected protein filtration.
Since NMN reduced urinary protein levels, it can be speculated that NMN preserves the abundance of podocytes, the waste-filtering cells of the kidney. The mice with kidney disease were found to have reduced numbers of podocytes and, as expected, NMN increased these numbers. These findings suggest that NMN improves renal function by restoring waste-filtering podocytes and maintaining urinary protein levels.
NMN restores kidney function
Doxorubicin-induced glomerulosclerosis mice (ADR) had significantly increased albumin-to-creatinine ratio (ACR), an indicator of urinary protein abundance, but improved NMN (NMN500) compared to normal mice (Cont) had this effect. Furthermore, the number of podocytes decreased in ADR mice, but NMN restored their numbers.
Sirtuin-1 is an enzyme that, when activated, has been linked to increased lifespan. In addition, low Sirtuin-1 levels have been linked to age-related diseases such as glomerulosclerosis. Since Sirtuin-1 uses NAD+ for fuel and NMN increases NAD+ levels, they studied how NMN affects Sirtuin-1 levels in mice with kidney disease. It was found that NMN restored lower Sirtuin-1 levels in the mouse kidneys.
Higher Sirtuin-1 levels from NMNs were also associated with renal tissue preservation in the face of doxorubicin treatment. Although doxorubicin-induced kidney disease triggers more tissue damage (damage), NMN restores kidney tissue damage. Better organizational structural integrity leads to better functional capabilities.
NMN reduces kidney tissue damage. Various shades of pink mark kidney tissue and adipocytes. The white separation that separates the tissue is the lesion. Doxorubicin (ADR)-treated mice had significantly more lesions (lesions), but adding NMN treatment prevented lesion accumulation.
NMN protects kidney waste filtration
By increasing NAD+ levels and activating Sirtuin-1, NMN reduces kidney damage and restores kidney function. Mouse studies of the beneficial effects of NMN on the kidneys have examined models of renal scarring (fibrosis). NMN also restores kidney waste-filtering cells, thereby improving kidney function. Since kidney dialysis and transplantation are the only means of treatment for age-related glomerulosclerosis, the use of NMN or related NAD+ metabolites may offer new, less invasive ways to alleviate kidney disease.
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