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Recently, reductions in nicotinamide adenine dinucleotide (NAD^⁺) associated with aging and metabolic diseases have gained considerable attention, as they are implicated in abnormalities of lipid metabolism and obesity. Previous studies have shown that supplementation with nicotinamide mononucleotide (NMN), a key intermediate in NAD^⁺ biosynthesis, exerts anti‑aging, anti‑obesity, and anti‑diabetic effects in animal models; however, these findings were based on administration via drinking water or intraperitoneal administration. Evidence regarding the effectiveness of NMN when incorporated directly into the diet has remained limited.

A research group led by Dr. Bungo Shirouchi (Department of Nutrition Science, Faculty of Nursing and Nutrition, University of Nagasaki) reported for the first time that dietary NMN reduces body fat mass and hypertriglyceridemia in obese diabetic db/db mice.

In this study, five‑week‑old male db/db mice were pair‑fed for 4 weeks with either a control diet—based on the standard AIN‑76 formulation and modified to induce early onset of lipid abnormalities by including 7% corn oil and 0.1% cholesterol—or an NMN‑supplemented diet containing 0.5% NMN. Metabolic parameters were evaluated to assess the effects of dietary NMN.

The NMN group exhibited a significant reduction in the Lee index (an obesity indicator) and body fat accumulation. Dietary NMN also attenuated hepatic triglyceride (TG) accumulation and significantly suppressed elevations in plasma TG levels.

Respiratory gas analysis indicated that dietary NMN intake significantly enhanced energy expenditure by suppressing carbohydrate oxidation and increasing fat oxidation.

Furthermore, hepatic fatty acid synthase (FAS) activity was significantly reduced, while carnitine palmitoyltransferase (CPT) activity was significantly increased. These changes suggest that reduced fatty acid synthesis and enhanced β‑oxidation contributed to lower hepatic TG content and, consequently, to the suppression of plasma TG elevation.

The study also evaluated T‑cadherin—known as an adiponectin‑binding protein and target of adiponectin action—and found that dietary NMN significantly increased plasma concentrations of soluble T‑cadherin isoforms (100 kDa and 130 kDa). A significant positive correlation was observed between plasma adiponectin and soluble T‑cadherin. These findings suggest that dietary NMN enhances hepatic fatty acid β‑oxidation, likely through reduced malonyl‑CoA levels mediated by increased adiponectin.

This study provides important new evidence that dietary NMN preferentially promotes fat oxidation and increases energy expenditure. Further investigations in diet‑induced obesity models and human clinical studies are expected to inform future nutritional interventions.

Please refer to the following publication for more details.

Bungo Shirouchi et al.
Dietary Nicotinamide Mononucleotide, a Key NAD⁺ Intermediate, Alleviates Body Fat Mass and Hypertriglyceridemia by Enhancing Energy Expenditure with Promotion of Fat Oxidation and Hepatic Lipolysis and Suppressing Hepatic Lipogenesis in db/db Mice
Metabolites. 2025; 15(5):333.

We offer a wide range of ELISA kits for lipid metabolism research and also provide testing services.

■T-Cadherin
T-Cadherin (T-cad) is a protein that binds to Adiponectin (APN), an adipocyte-secreted factor. APN binds to and accumulates in aorta, heart, skeletal muscle, and mesenchymal stem cells. Through this interaction, it is thought to promote exosome production and exert a protective effect on organ tissues. In humans, single nucleotide polymorphisms (SNPs) near the T‑Cadherin gene are strongly associated with impaired glucose tolerance and increased cardiovascular disease risk.
Recently, three soluble forms of T‑Cadherin—130 kDa, 100 kDa, and 30 kDa—were identified in human blood. These soluble isoforms correlate with multiple clinical parameters in patients with type 2 diabetes, and the 130‑kDa and 100‑kDa forms decrease rapidly during the acute phase of myocardial infarction, suggesting their potential utility as biomarkers.
In addition, soluble T-Cadherin has been found to promote the proliferation of pancreatic beta cells and prevent the decline in insulin secretory capacity, and its function as a humoral factor is also in focus.

We hope this information will be useful for your research.
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