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Date: Sep 29,2025
[Article guide] A Science clinical trial shows that daily NMN supplementation improved skeletal muscle insulin sensitivity in overweight or obese postmenopausal women with prediabetes. By boosting NAD⁺ turnover and enhancinginsulin pathways, NMN demonstrated safe, meaningful metabolic benefits. Leadsynbio shares such findings to promote healthier aging through science-based innovation.

Obesity and Diabetes: A Growing Concern

Obesity is a serious health condition—both a disease itself and a major contributor to multiple metabolic disorders. Among these, diabetes is one of the most common complications.   

       In China, ~500 million people are prediabetic → ~1 in 3 adults is at risk of developing diabetes.
       Key mechanism: Insulin resistance is a primary driver of prediabetes.


What is Insulin Resistance?

Insulin resistance (↓ insulin sensitivity) occurs when cells respond poorly to insulin.

       Glucose uptake is impaired → blood sugar rises
       Can progress to type 2 diabetes if unchecked      

Visual cue: Insulin resistance → “key not fitting the lock” → glucose can’t enter cells efficiently.


NMN Enhances Skeletal Muscle Insulin Sensitivity

Study Overview

       Type: Randomized, double-blind, 10-week human clinical trial
       Participants: 25 postmenopausal women with prediabetes (BMI 25.3–39.1 kg/m²)
       Intervention:
                            NMN group: 250 mg/day (n=13)
                            Placebo group: (n=12)

Outcome measures:

       Body composition
       Skeletal muscle insulin sensitivity & signaling
       Muscle NAD⁺ levels & gene expression profiles

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NMN Increases NAD⁺ Turnover

       Peripheral blood mononuclear cell NAD⁺ levels ↑ in NMN group vs placebo
       Muscle NAD⁺ and nicotinamide: unchanged
       Downstream NAD⁺ metabolites ↑suggests enhanced NAD⁺ turnover

Visual cue: NMN → NAD⁺ “recycling speed ↑” → better metabolic efficiency

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NMN Improves Muscle Insulin Sensitivity

       Muscle biopsies analyzed for:
                                                         Glucose uptake capacity
                                                         Insulin signaling: phosphorylation at AKT T308, S473, and mTOR S2448
       Result: NMN group showed significant increases → enhanced muscle insulin sensitivity

Visual cue: Muscle cells respond better to insulin → glucose uptake ↑

插图2

Effects on Skeletal Muscle Biology

       RNA sequencing of quadriceps muscle → identified differentially expressed genes (DEGs)
       PDGF (platelet-derived growth factor) pathway: highest DEG enrichment post-insulin injection (↑60-fold)
       Downstream targets of PDGFRB & PDGF signaling ↑ → supports insulin signaling enhancement
       PDGF pathway previously linked to AKT phosphorylation ↑

Visual cue: NMN → PDGF pathway activation → insulin signaling ↑


Clinical Significance

       NMN supplementation (250 mg/day) enhances skeletal muscle insulin signaling
       Improves insulin sensitivity in overweight/obese postmenopausal women with prediabetes
       Effectiveness comparable to:
                                                    10% body weight loss
                                                    12-week troglitazone treatment
       Demonstrates clinically meaningful improvement in muscle insulin response

Key takeaway: NMN could be a promising strategy for metabolic health support.

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References

1.Li Y, Teng D, Shi X, et al. Prevalence of diabetes recorded in China using 2018 diagnostic criteria from the American Diabetes Association: national cross sectional study. BMJ. 2020;369:m997.

2.Mihoko Yoshino et al. Science. Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. DOI:10.1126/science.abe9985

3.M. Razmara, C. H. Heldin, J. Lennartsson, Platelet-derived growth factor-induced Akt phosphorylation requires mTOR/Rictor and phospholipase C-γ1, whereas S6 phosphorylation depends on mTOR/Raptor and phospholipase D. Cell Commun. Signal. 11, 3 (2013).

 

Disclaimer: This article is intended for educational purposes and does not constitute medical or commercial advice. Information is derived from publicly available sources. Any reproduction, publication, or citation requires prior written consent from Leadsynbio.





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