New Breakthrough for NMN in Type 2 Diabetes
In the long journey against type 2 diabetes, scientists continue to explore new therapeutic strategies. Recently, a study published in the International Journal of Molecular Sciences revealed potential new mechanisms of Nicotinamide Mononucleotide (NMN) in type 2 diabetes through in-depth proteomic analysis: acting through unexpected effects in adipose tissue rather than mitochondrial biogenesis.
(Image 1: Study paper header titled "Nicotinamide Mononucleotide (NMN) Works in Type 2 Diabetes through Unexpected Effects in Adipose Tissue, Not by Mitochondrial Biogenesis")
(Image 2: Diagram showing organ-specific effects of NMN in high-fat diet (HFD) mice)
Figure 1. NMN acts on type 2 diabetes through unexpected effects in adipose tissue, rather than mitochondrial biogenesis.
(Image 3: Summary diagram of health benefits of restoring $\text{NAD}^+$ levels via NMN supplementation in mouse models and published human clinical trials)
Figure 2. Health benefits of restoring $\text{NAD}^+$ levels through NMN supplementation.
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease characterized by insulin resistance and elevated blood glucose levels. Because impaired glucose uptake is a hallmark of T2DM, previous studies have shown that NMN can improve age-related diseases—including type 2 diabetes—by boosting $\text{NAD}^+$ levels. However, how NMN influences diabetes treatment at the molecular level has not been fully clarified.
In this new study, researchers used a comprehensive proteomic approach to investigate the effects of NMN across different tissues in a mouse model of type 2 diabetes. They found that NMN treatment significantly improved glucose uptake capacity in mice, but this effect was not achieved through the conventional mitochondrial biogenesis pathway.
(Image 4: Diagrams and graphs showing mouse muscle and liver insulin resistance pathways, along with IPGTT glucose levels before and after NMN treatment)
Figure 3. NMN significantly improves blood glucose uptake in HFD mice, but not through insulin resistance pathways in muscle or liver.
(Image 5: Enrichment charts, gene network diagrams, and histological tissue stainings for PRAT and EAT in HFD vs. HFD+NMN mice)
Figure 4. NMN stimulates adipocyte proliferation by upregulating the mTOR pathway.
(Image 6: Heatmaps, gene networks, and enrichment charts for differential protein expression in mouse brain)
Figure 5. Significant changes induced by NMN treatment in the brain proteome of HFD mice.
Overall, this study not only deepens our understanding of NMN's mechanisms of action, but also provides new perspectives for future diabetes research. As research continues to advance, we look forward to NMN playing a greater role in clinical settings and bringing new hope to patients with diabetes.
BONTAC owns its manufacturing facility and holds multiple international certifications, including SELF GRAS, FSSC 22000, FDA, DMF, HALAL, and KOSHER, serving as a stable supplier to more than 100 enterprise clients globally. BONTAC has accumulated 173 domestic and international patent applications. Its proprietary crystal technology provides higher solubility for $\text{NAD}^+$ raw material products, achieving a purity of over 99%. Combined with freeze-drying technology, product stability is further optimized. Moreover, BONTAC's $\text{NAD}^+$ is produced using a 100% enzymatic method, making it eco-friendly with zero harmful solvent residues.
Additionally, BONTAC is a high-quality NMN raw material supplier to Prof. David Sinclair's Anti-Aging Laboratory at Harvard University. It is a drafter of Chinese group standards for NMN product specifications and testing methods, as well as the first in China and the only provincial-level Coenzyme Engineering Technology Research Center in Guangdong Province.
(Image 1: Study paper header titled "Nicotinamide Mononucleotide (NMN) Works in Type 2 Diabetes through Unexpected Effects in Adipose Tissue, Not by Mitochondrial Biogenesis")
(Image 2: Diagram showing organ-specific effects of NMN in high-fat diet (HFD) mice)
Figure 1. NMN acts on type 2 diabetes through unexpected effects in adipose tissue, rather than mitochondrial biogenesis.
Biological Background of NMN
NMN is a naturally occurring substance found in all living organisms. It serves as a direct precursor to $\text{NAD}^+$ (Nicotinamide Adenine Dinucleotide), a key molecule in cellular energy metabolism. As humans age, $\text{NAD}^+$ levels in the body gradually decline. Because NMN can elevate $\text{NAD}^+$ levels, it is considered to have potential for anti-aging and for treating various diseases.
(Image 3: Summary diagram of health benefits of restoring $\text{NAD}^+$ levels via NMN supplementation in mouse models and published human clinical trials)
Figure 2. Health benefits of restoring $\text{NAD}^+$ levels through NMN supplementation.
NMN and Type 2 Diabetes
Glucose metabolism is a fundamental process essential for mammalian energy homeostasis, coordinated through complex interactions among various organs and tissues. Among them, the liver, muscle, adipose tissue, and brain are the primary target tissues that consume glucose.Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease characterized by insulin resistance and elevated blood glucose levels. Because impaired glucose uptake is a hallmark of T2DM, previous studies have shown that NMN can improve age-related diseases—including type 2 diabetes—by boosting $\text{NAD}^+$ levels. However, how NMN influences diabetes treatment at the molecular level has not been fully clarified.
In this new study, researchers used a comprehensive proteomic approach to investigate the effects of NMN across different tissues in a mouse model of type 2 diabetes. They found that NMN treatment significantly improved glucose uptake capacity in mice, but this effect was not achieved through the conventional mitochondrial biogenesis pathway.
(Image 4: Diagrams and graphs showing mouse muscle and liver insulin resistance pathways, along with IPGTT glucose levels before and after NMN treatment)
Figure 3. NMN significantly improves blood glucose uptake in HFD mice, but not through insulin resistance pathways in muscle or liver.
NMN and Adipose Tissue
The most striking finding of the study is that NMN exerts its effects primarily through adipose tissue rather than muscle tissue. The researchers discovered that NMN treatment increased protein synthesis and degradation in adipose tissue, as well as the expression of UCP1 (a protein that promotes thermogenesis). This helps convert glucose into heat rather than increasing energy storage through mitochondrial biogenesis.
(Image 5: Enrichment charts, gene network diagrams, and histological tissue stainings for PRAT and EAT in HFD vs. HFD+NMN mice)
Figure 4. NMN stimulates adipocyte proliferation by upregulating the mTOR pathway.
NMN and Liver / Brain Cells
In addition, the study found that NMN downregulated spliceosome-related proteins in liver and muscle cells, which may lead to a slight decrease in protein synthesis efficiency. In the brain, NMN increased ketone body production, downregulated components of mitochondrial oxidative phosphorylation and the tricarboxylic acid (TCA) cycle, and induced fasting-like effects.(Image 6: Heatmaps, gene networks, and enrichment charts for differential protein expression in mouse brain)
Figure 5. Significant changes induced by NMN treatment in the brain proteome of HFD mice.
Overall, this study not only deepens our understanding of NMN's mechanisms of action, but also provides new perspectives for future diabetes research. As research continues to advance, we look forward to NMN playing a greater role in clinical settings and bringing new hope to patients with diabetes.
BONTAC NMN
Supplier to David Sinclair's Anti-Aging LaboratoryBONTAC owns its manufacturing facility and holds multiple international certifications, including SELF GRAS, FSSC 22000, FDA, DMF, HALAL, and KOSHER, serving as a stable supplier to more than 100 enterprise clients globally. BONTAC has accumulated 173 domestic and international patent applications. Its proprietary crystal technology provides higher solubility for $\text{NAD}^+$ raw material products, achieving a purity of over 99%. Combined with freeze-drying technology, product stability is further optimized. Moreover, BONTAC's $\text{NAD}^+$ is produced using a 100% enzymatic method, making it eco-friendly with zero harmful solvent residues.
Additionally, BONTAC is a high-quality NMN raw material supplier to Prof. David Sinclair's Anti-Aging Laboratory at Harvard University. It is a drafter of Chinese group standards for NMN product specifications and testing methods, as well as the first in China and the only provincial-level Coenzyme Engineering Technology Research Center in Guangdong Province.
