NMN Human Trial Show Improved Muscle Glucose Metabolism

NMN trial data just released suggests benefits for pre-diabetics and diabetics.

In recent years, there has been considerable interest and increasing studies in the naturally occurring molecule nicotinamide mononucleotide (NMN) and its potential influence on aging. A diverse myriad of benefits have been shown with NMN supplementation. (https://www.frontiersin. org/articles/10.3389/fcell.2020.00246/full).

In previous studies NMN mainly invoicing mice, it has been shown to improve metabolism and in particular boost mitochondrial function (https://pubmed.ncbi.nlm.nih.gov/30801823/), increase cognitive function (https://www. sciencedirect.com/science/article/pii/S221323171930240X) and improve DNA repair (https://www.nature.com/articles/s41598-020-57506-9).

DNA damage can occur from environmental, dietary, or internal sources. As we get older, the body’s mechanisms to repair this DNA damage deteriorate.

Scientists have now found that supplemental NMN boost NAD+ levels, which allows for the DNA repair protein PARP1 to be fully functioning and effective.

This is important because accumulated damage to DNA and proteins will accelerate the aging process and increase the risk of developing several types of chronic diseases as we age.


Nicotinamide mononucleotide (NMN) is a direct precursor of the coenzyme NAD+, which serves critical functions in our cells and declines with age.

NMN human trial results

Researchers at Washington University School of Medicine in St. Louis have published the results of a human trial that suggest clinically relevant results in people given NMN. This is the first randomized clinical trial to examine the effects of NMN administration on human metabolism.

This clinical trial saw women with prediabetes given 250 mg of NMN orally each day for a period of 10 weeks; the remaining were given a placebo.

Administration of NMN improved the ability of insulin to increase glucose uptake in skeletal muscle. This uptake is typically dysfunctional in people experiencing prediabetes, type 2 diabetes, or obesity. Insulin boosts glucose uptake and storage in muscle, and people with insulin resistance have an increased risk of developing Type 2 diabetes.

The researchers also observed that there was an increased expression of genes associated with muscle structure and remodelling in participants given NMN.

The researchers reported that administration of NMN did not appear to reduce blood glucose levels or blood pressure. It also did not appear to have an impact on blood lipid profile, raise insulin sensitivity in the liver, or reduce the presence of fat in the liver.

In rodents, obesity and aging impair nicotinamide adenine dinucleotide (NAD+) biosynthesis, which contributes to metabolic dysfunction. Nicotinamide mononucleotide (NMN) availability is a rate-limiting factor in mammalian NAD+ biosynthesis. A 10-week, randomized, placebo-controlled, double -blind trial was also conducted to evaluate the effect of NMN supplementation on metabolic function in postmenopausal women with prediabetes who were overweight or obese. Insulin-stimulated glucose disposal, assessed by using the hyperinsulinemic-euglycemic clamp, and skeletal muscle insulin signalling (phosphorylation of AKT and mTOR) increased after NMN supplementation, but did not change after placebo treatment. NMN supplementation up-regulated the expression of platelet-derived growth factor receptor β and other genes related to muscle remodelling. These results demonstrate NMN increases muscle insulin sensitivity, insulin signalling and remodelling in women with prediabetes who are overweight or obese.


The results of this study are interesting as it points to benefits of NMN supplementation for the prevention or management of prediabetes or diabetes in people. Regular exercise, an active lifestyle and a healthy diet are also important contributing factors to prevention or even remission (reversal) of pre-diabetic or diabetic conditions in individuals (https://www.webmd.com/diabetes/can-you-reverse-type-2-diabetes).

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