Type II diabetes (T2DM) is currently one of the most serious health crises. According to today's incidence, by 2045, the incidence of the disease will exceed 50%. Although there are more than 10 different foods and drugs used to treat type 2 diabetes in the United States, and more than 7,000 clinical trials are currently screening new drug candidates, it seems more practical to find more effective and less effective natural alternative drugs .
Recently, "Science" published an article on the clinical research of NMN(β-Nicotinamide mononucleotide, CAS No.: 1094-61-7). Scientists studied the NMN effects of insulin sensitivity, insulin signal transduction and tissue remodeling in skeletal muscle of 25 postmenopausal overweight or obese pre-diabetic women after NMN supplementation.
Type II diabetes is the result of systemic insulin resistance, and its biological response to normal or elevated insulin levels is weakened, resulting in insensitivity to insulin intervention and glucose metabolism. In order to maintain normal blood sugar levels, pancreatic beta cells secrete more insulin, which leads to compensatory hyperinsulinemia, leading to type II diabetes, which is a vicious circle.
NAD (Nicotinamide adenine dinucleotide, NAD+, NADH) is one of the most abundant metabolites in the human body, and it is an auxiliary substrate for many enzymes. NAD can be used to regulate the citric acid cycle, cytosolic glycolysis, gluconeogenesis, glycogen metabolism and mitochondrial fatty acid oxidation. NAD homeostasis is closely related to mitochondrial dysfunction, insulin resistance and obesity. NMN supplementation can alleviate insulin resistance related to NAD biosynthesis. NMN improves the glucose tolerance of the age-induced T2DM mouse model. Because NAD and its metabolites play an important role in the insulin sensitivity and glucose tolerance of rodents.
Giving human NMN for 10 weeks can increase muscle insulin sensitivity, but the insulin sensitivity of liver and adipose tissue assessed by hyperinsulinemic glucose clamp is not affected. Study participants who received NMN had no changes in muscle NAD levels, but NMN metabolites increased after NMN treatment, indicating an increase in NAD turnover. The observed increase in muscle glucose treatment was approximately 25%, but this was due to an increase in the NAD dose. RNA sequencing of the quadriceps muscle samples showed that the platelet-derived growth factor (PDGF) binding pathway in the treatment group was abundant, indicating that the muscle is involved in NMN-mediated insulin sensitivity.
This study provides important data for the safety and effectiveness of NMN supplementation in humans. Although NMN has a long way to go as a new drug candidate for the treatment of type II diabetes, this study paves the way for the development of new NMN drugs for diabetes and guides the direction of scientific research.
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