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NMN and Weight Loss, Fat Loss

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Obesity is a global epidemic that contributes to the development of a variety of metabolic disorders, including type 2 diabetes and heart disease. The disorder’s distinctive buildup of fat tissue is caused by a rise in the size and growth of mature fat cells called adipocytes. Compounds capable of regulating the size, quantity, and activity of adipocytes, as well as their mechanism of action, might make a significant contribution to obesity prevention and treatment. Recent studies have demonstrated a strong link between NMN and weight loss.

NAD+, NMN and Weight Loss

Findings of a study demonstrated that the increased synthesis of nicotinamide adenine dinucleotide (NAD+), a key component of metabolism, is required for the development of mature fat cells.


What Role Does NAD+ Play in Fat Storage?

Adipocyte maturation is a tightly regulated process. These cells develop from preadipocytes, a process controlled by a complex network of transcription factors that govern the expression of hundreds of proteins. Inflammation and metabolic inefficiency arise when preadipocyte differentiation is disturbed. Adipogenesis is known to cause metabolic alterations.

NAD+ Synthesis Upregulation Is Required for Preadipocyte Differentiation

The study discovered that NAD+ and nicotinamide mononucleotide (NMN), a precursor to NAD+, were dramatically enhanced during preadipocyte development. This was accompanied by an increase in the activity of the enzymes responsible for the synthesis of both NAD+ and NMN. Meanwhile, it also investigated if NAD+ levels had an effect on the adipogenic program. Reduced NAD+ levels effectively decreased the master regulator of adipogenesis, PPAR, and target adipogenic genes.

α-Ketoglutarate Contributes to the Activation of PPARs During Preadipocyte Differentiation

α-Ketoglutarate Contributes to the Activation of PPARs in preadipocytes to activate the gene, the PPAR DNA sequence must be demethylated, which involves the removal of molecular tags called methyl groups attached to DNA. The researchers discovered that inhibiting demethylation decreases PPAR activity and preadipocyte differentiation.

The researchers intended to discover if NAD+, α-ketoglutarate, and adipogenesis were linked. And they found that NAD+-dependent -ketoglutarate levels are required for PPAR gene demethylation and preadipocyte development.

The researchers also looked at how NAD+ and α-ketoglutarate affect obesity and found that the NAD+α-ketoglutarate axis may be a therapeutic target for obesity-related metabolic disorders.

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