How does NMN achieve its weight loss effect?

Recently, a research team from the Graduate School of Integrative Pharmacy and Nutrition at Shizuoka University in Japan found that the use of Nicotinamide Mononucleotide (NMN) can effectively promote weight loss in animals on a high-fat diet in just 8 weeks.

The study first made mice gain weight on a high-fat diet and then added NMN to the diet. To compare the effects, they set up two control groups: one on a regular diet and the other on a pure high-fat diet. It was found that after 8 weeks, mice that continued to eat a high-fat diet and took NMN lost weight. These mice had significantly reduced subcutaneous adipose tissue (sWAT), however, their epididymal adipose tissue (eWAT, a type of visceral fat), did not change significantly in volume.

Mice treated with NMN on a high-fat diet had significantly lower body weight for eight weeks

Visceral fat and subcutaneous fat are two different types of fat. In the human body, the growth of visceral fat is mainly achieved through the expansion of fat cell volume and the acceleration of lipid production; while the increase of subcutaneous fat is mainly through the expansion of fat cell volume. The researchers measured the size of adipocytes in mice and found that the volume of adipocytes was significantly reduced after NMN treatment. The discovery sheds new light on how NMN helps people on a high-fat diet lose weight, providing new insights into the relationship between food, weight and health.

Histological examination showed that adipocytes in subcutaneous adipose tissue were reduced by NMN treatment

The mechanism of NMN promoting fat breakdown

NMN helps to reduce body weight, reduce subcutaneous fat content and reduce the size of fat cells, but how exactly does it work? The researchers explored this further, first by measuring the size of fat cells, which affects the rate at which fat is made and broken down. The results showed that the effect of NMN can improve the hypertrophy of adipocytes and significantly reduce the volume of adipocytes in mice.

Next, the researchers tried to further explore how NMN affects the rate of fat production and breakdown, and the relationship between the two, and they hoped to find an effective weight loss strategy in this way. They chose 3T3-L1 adipocytes, an in vitro model commonly used in adipocyte biology, and treated them with NMN. They found that after 4 days of 0.5 mM NMN treatment, fat accumulation in mouse adipocytes was significantly reduced, while cell viability was not affected.

Treatment with 0.5 mM NMN for four days significantly reduces lipid accumulation in differentiated 3T3-L1

In addition, the researchers also measured the glycerol content in the culture medium of 3T3-L1 adipocytes after NMN treatment. Glycerol is an important product of fat catabolism. They found that after NMN treatment, the content of glycerol increased, which means that NMN treatment can speed up the rate of fat breakdown.

Increased release of glycerol from 3T3-L1 differentiated adipocytes treated with NMN for 24 hours

To get a more complete picture of NMN's role in influencing fat production and breakdown, the researchers also examined the expression of four genes involved in fat production and breakdown. They found that after treating differentiated 3T3-L1 adipocytes with NMN for 24 hours, the expression level of lipolysis-related protein Atgl (fat triglyceridease) was increased, while the expression of genes related to lipogenesis (Srebf1c and Pparγ) was not No significant changes occurred. These findings provide new ideas for better understanding and utilization of NMN's potential in weight loss and regulation of lipogenesis and breakdown.

The expression level of Atgl was increased after treatment with NMN for 24 hours

Atgl is recognized as a key enzyme leading the process of fat degradation, responsible for catalyzing the initial stage of the process of fat degradation. The function of this enzyme is to convert intracellular triglycerides into diacylglycerols and free fatty acids, thereby initiating the degradation of fats. Previous scientific findings have shown that Atgl activity is inversely correlated with fat content, i.e. Atgl activity is reduced in white adipose tissue in obese animals and humans. In mouse models, systemic or specific deletion of Atgl leads to increased fat content.

New scientific findings reveal that NMN has the ability to induce fat degradation by increasing the activity of Atgl enzyme in adipocytes. However, how NMN specifically regulates Atgl expression remains an unsolved question. In-depth studies have found that NMN treatment can significantly increase the expression of Sirt1 protein in 3T3-L1 adipocytes and increase the phosphorylation level of AMPK.

NMN increases the expression of Sirt1 in 3T3-L1 adipocytes

AMPK, full name AMP-activated protein kinase, is an important molecule that regulates energy metabolism. Scientific evidence shows that Sirt1 mediates the activation of AMPK by enhancing the activity of its upstream kinase LKB1, which is achieved through the deacetylation of LKB1. To confirm whether NMN regulates fat degradation through the Sirt1-AMPK signaling pathway, the researchers used inhibitors of AMPK.

The results of the study showed that the expression of Atgl was not significantly increased in the AMPK inhibitor-treated group compared with the control group using only NMN, and the fat content of the mice was not significantly changed. This finding suggests that NMN cannot effectively increase the expression of Atgl when the AMPK signaling pathway is inhibited. These findings suggest that NMN regulates the expression of Atgl through the Sirt1-AMPK signaling pathway, and the AMPK signaling pathway is a key link in the fat-reducing effect of NMN.

Decreased mRNA expression and AMPK phosphorylated Atgl content of 3T3-L1 differentiated 3T3-L1 treated with NMN

Tag: NMN

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