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Anti-aging has always been a very hot topic.
In view of everyone’s pursuit of anti-aging, various skin care products and health care products that promote this effect are very popular.
Nicotinamide mononucleotide (NMN) is one of the "leading By".
In human cells, there is a natural molecule-nicotinamide adenine dinucleotide (NAD+), which is essential for regulating cell aging and maintaining normal functions of the body.
With age, NAD+ levels will gradually Decline indicates that the body is gradually aging [1].
It has also been found in mice that insufficient NAD+ is associated with obesity and aging-related metabolic abnormalities [2-4].
NMN is the precursor molecule of NAD+ and the key rate-limiting factor for NAD+ synthesis.
NMN supplementation in obese mice can increase NAD+ levels, improve glucose tolerance, insulin sensitivity and pancreatic β-cell function [5-7], and long-term supplementation of NMN can alleviate age-related insulin resistance [8].
Although good curative effects have been achieved in mice, and some NMN-related products are also on the market in the United States and other countries, in fact, the efficacy of supplementing NMN in humans has not been verified.
Picture from Pixabay.
com In today’s "Science" magazine, the results of the first NMN clinical trial were published [9].
Researchers at the University of Washington School of Medicine found that for postmenopausal prediabetic women, NMN can improve skeletal muscle Insulin sensitivity also improves the expression of genes related to muscle structure and remodeling.
However, NMN failed to lower blood sugar and blood pressure, improve blood lipid profile, increase insulin sensitivity in the liver, nor reduce liver fat or reduce the levels of some inflammatory markers observed in mouse experiments.
The trial included 25 postmenopausal prediabetic women with a BMI of 25.
3-39.
1kg/m², 13 of whom took 250mg of NMN orally every day and the other 12 took a placebo.
The trial lasted for 10 weeks.
After 10 weeks of treatment, the concentration of some NMN metabolites in the blood of the NMN group increased, and the basal NAD+ level in peripheral blood mononuclear cells also increased.
These changes did not occur in the placebo group.
The changes in plasma NMN metabolite concentration (A) and basal NAD+ level in peripheral blood mononuclear cells (B) were taken 1.
5 hours after the last dose of the participant’s quadriceps muscle samples, although the NAD+ and NAD+ levels in the muscle tissues of the two groups Nicotinamide levels did not change, but the levels of N-methyl-nicotinamide, methyl-2-pyridone-5-hydroxyamine and N-methyl-4-pyridone-5-hydroxyamine in the NMN group increased, indicating NMN treatment increases NAD+ turnover in the muscles.
Participants' body fat mass, lean mass, abdominal fat volume, liver triglyceride levels, blood glucose, blood pressure, insulin, free fatty acids, lipids, adipocytokines and leptin levels, as well as basal glucose levels and fatty acid metabolism dynamics There was no change after treatment in the two groups.
In addition, hepatic insulin sensitivity and adipose tissue insulin sensitivity did not differ between the two groups before and after treatment.
The researchers also found that after insulin injection in the NMN group, the phosphorylation of kinases AKT and mTOR in the muscle, and the levels of total AKT and mTOR protein were higher than those before NMN treatment, but there was no such change in the placebo group.
AKT and mTOR are key factors for insulin signaling to regulate glucose uptake and muscle remodeling.
The results of this in vitro experiment are consistent with their observations of muscle insulin sensitivity in participants treated with NMN or placebo.
RNA sequencing of the quadriceps samples showed that before treatment, the baseline conditions were compared with those after insulin injection.
The placebo group and NMN group had 21 and 15 differentially expressed genes, respectively.
After treatment, these two The numbers have become 5 and 308.The number of differentially expressed genes in the placebo group (left) and NMN group (right) in the basic situation and after insulin injection.
The NMN group has the most abundant genes in the platelet-derived growth factor (PDGF) binding pathway.
After insulin injection, The expression of PDGF receptor β and skeletal muscle pericyte markers (CD90 and CD109) increased significantly.
Downstream targets of PDGF signaling, such as COL1A1, COL5A1 and COL6A1, also increased their expression after NMN treatment.
These results indicate that NMN increases myogenic cell population and enhances PDGF signal transduction in skeletal muscle.
Since PDGF signaling, especially PDGF receptor β, can enhance insulin-stimulated AKT phosphorylation and glucose transport in skeletal muscle and various other types of cells.
Therefore, as previously observed, after insulin injection in the NMN group, insulin-stimulated AKT phosphorylation The increase in chemical and glucose uptake may be mediated by PDGF receptor β.
Overall, the results of this test show that for overweight or obese postmenopausal women, supplementation of NMN for 10 weeks can increase muscle insulin signaling and muscle insulin sensitivity, and increase the turnover of NAD+ in skeletal muscle.
In other words, the role of NMN is mainly aimed at insulin sensitivity in muscles, and does not affect other important factors related to insulin resistance, including insulin sensitivity in liver and adipose tissue, abdominal adipose tissue volume, intrahepatic triglyceride content and fasting blood glucose Wait.
The corresponding author of the study, Professor Samuel Klein, said that although their test results suggest that NMN is beneficial to the insulin sensitivity of skeletal muscle, it is not enough to support any clinical recommendations, because generally speaking, if a therapy can improve skeletal muscle For insulin sensitivity, other metabolic health indicators will also be improved accordingly, but their test did not show this [10].
They believe that more research is needed to determine whether NMN has a clinical effect on the prevention or control of prediabetes or diabetes, and they are currently conducting another trial that also includes male participants to evaluate NMN.
Singularity is hiring everyone! Everybody Hi~! We need fresh blood to inject new energy into the singularity.
Come on, become the singularity cake and do a new job with us! These are the little friends we are currently looking for~ If you want to create and innovate with the singularity cakes, come join us.
Please send your resume and work (if any) to: hr@geekheal.
com or you can directly add to the WeChat (geekheal-xintan) of Geekheal-xintan for communication.
When adding friends, please note: recruitment + position + professional field.
We are waiting for you at Singularity.
References: [1] Braidy N, Guillemin GJ, Mansour H, et al.
Age related changes in NAD+ metabolism oxidative stress and Sirt1 activity in wistar rats[J].
PloS one, 2011, 6(4): e19194.
[2 ] Imai S, Yoshino J.
The importance of NAMPT/NAD/SIRT1 in the systemic regulation of metabolism and ageing[J].
Diabetes, Obesity and Metabolism, 2013, 15(s3): 26-33.
[3] Verdin E.
NAD+ in aging, metabolism, and neurodegeneration[J].
Science, 2015, 350(6265): 1208-1213.
[4] McReynolds MR, Chellappa K, Baur J A.
Age-related NAD+ decline[J].
Experimental gerontology, 2020, 134: 110888.
[5] Yoshino J, Mills KF, Yoon MJ, et al.
Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet-and age-induced diabetes in mice[J].
Cell metabolism, 2011 , 14(4): 528-536.
[6] Stromsdorfer KL, Yamaguchi S, Yoon MJ, et al.
NAMPT-mediated NAD+ biosynthesis in adipocytes regulates adipose tissue function and multi-organ insulin sensitivity in mice[J].
Cell reports, 2016, 16(7): 1851-1860.
[7] Uddin GM, Youngson NA, Sinclair DA, et al.
Head to head comparison of short-term treatment with the NAD+ precursor nicotinamide mononucleotide (NMN) and 6 weeks of exercise in obese female mice[J].
Frontiers in pharmacology, 2016, 7: 258.
[8] Mills KF, Yoshida S, Stein LR, et al.
Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice[J].
Cell metabolism, 2016, 24(6): 795-806.
[9] https://science.
sciencemag.
org/content/early/2021/04/21/science.
abe9985[10] https://medicine.
wustl.
edu/news/anti-aging-compound-that-improves-metabolic-health-in-mice- improves-muscle-glucose-metabolism-in-people/The author of this article | Ying Yuyanedu/news/anti-aging-compound-that-improves-metabolic-health-in-mice-improves-muscle-glucose-metabolism-in-people/ author of this article | Ying Yuyan
In view of everyone’s pursuit of anti-aging, various skin care products and health care products that promote this effect are very popular.
Nicotinamide mononucleotide (NMN) is one of the "leading By".
In human cells, there is a natural molecule-nicotinamide adenine dinucleotide (NAD+), which is essential for regulating cell aging and maintaining normal functions of the body.
With age, NAD+ levels will gradually Decline indicates that the body is gradually aging [1].
It has also been found in mice that insufficient NAD+ is associated with obesity and aging-related metabolic abnormalities [2-4].
NMN is the precursor molecule of NAD+ and the key rate-limiting factor for NAD+ synthesis.
NMN supplementation in obese mice can increase NAD+ levels, improve glucose tolerance, insulin sensitivity and pancreatic β-cell function [5-7], and long-term supplementation of NMN can alleviate age-related insulin resistance [8].
Although good curative effects have been achieved in mice, and some NMN-related products are also on the market in the United States and other countries, in fact, the efficacy of supplementing NMN in humans has not been verified.
Picture from Pixabay.
com In today’s "Science" magazine, the results of the first NMN clinical trial were published [9].
Researchers at the University of Washington School of Medicine found that for postmenopausal prediabetic women, NMN can improve skeletal muscle Insulin sensitivity also improves the expression of genes related to muscle structure and remodeling.
However, NMN failed to lower blood sugar and blood pressure, improve blood lipid profile, increase insulin sensitivity in the liver, nor reduce liver fat or reduce the levels of some inflammatory markers observed in mouse experiments.
The trial included 25 postmenopausal prediabetic women with a BMI of 25.
3-39.
1kg/m², 13 of whom took 250mg of NMN orally every day and the other 12 took a placebo.
The trial lasted for 10 weeks.
After 10 weeks of treatment, the concentration of some NMN metabolites in the blood of the NMN group increased, and the basal NAD+ level in peripheral blood mononuclear cells also increased.
These changes did not occur in the placebo group.
The changes in plasma NMN metabolite concentration (A) and basal NAD+ level in peripheral blood mononuclear cells (B) were taken 1.
5 hours after the last dose of the participant’s quadriceps muscle samples, although the NAD+ and NAD+ levels in the muscle tissues of the two groups Nicotinamide levels did not change, but the levels of N-methyl-nicotinamide, methyl-2-pyridone-5-hydroxyamine and N-methyl-4-pyridone-5-hydroxyamine in the NMN group increased, indicating NMN treatment increases NAD+ turnover in the muscles.
Participants' body fat mass, lean mass, abdominal fat volume, liver triglyceride levels, blood glucose, blood pressure, insulin, free fatty acids, lipids, adipocytokines and leptin levels, as well as basal glucose levels and fatty acid metabolism dynamics There was no change after treatment in the two groups.
In addition, hepatic insulin sensitivity and adipose tissue insulin sensitivity did not differ between the two groups before and after treatment.
The researchers also found that after insulin injection in the NMN group, the phosphorylation of kinases AKT and mTOR in the muscle, and the levels of total AKT and mTOR protein were higher than those before NMN treatment, but there was no such change in the placebo group.
AKT and mTOR are key factors for insulin signaling to regulate glucose uptake and muscle remodeling.
The results of this in vitro experiment are consistent with their observations of muscle insulin sensitivity in participants treated with NMN or placebo.
RNA sequencing of the quadriceps samples showed that before treatment, the baseline conditions were compared with those after insulin injection.
The placebo group and NMN group had 21 and 15 differentially expressed genes, respectively.
After treatment, these two The numbers have become 5 and 308.The number of differentially expressed genes in the placebo group (left) and NMN group (right) in the basic situation and after insulin injection.
The NMN group has the most abundant genes in the platelet-derived growth factor (PDGF) binding pathway.
After insulin injection, The expression of PDGF receptor β and skeletal muscle pericyte markers (CD90 and CD109) increased significantly.
Downstream targets of PDGF signaling, such as COL1A1, COL5A1 and COL6A1, also increased their expression after NMN treatment.
These results indicate that NMN increases myogenic cell population and enhances PDGF signal transduction in skeletal muscle.
Since PDGF signaling, especially PDGF receptor β, can enhance insulin-stimulated AKT phosphorylation and glucose transport in skeletal muscle and various other types of cells.
Therefore, as previously observed, after insulin injection in the NMN group, insulin-stimulated AKT phosphorylation The increase in chemical and glucose uptake may be mediated by PDGF receptor β.
Overall, the results of this test show that for overweight or obese postmenopausal women, supplementation of NMN for 10 weeks can increase muscle insulin signaling and muscle insulin sensitivity, and increase the turnover of NAD+ in skeletal muscle.
In other words, the role of NMN is mainly aimed at insulin sensitivity in muscles, and does not affect other important factors related to insulin resistance, including insulin sensitivity in liver and adipose tissue, abdominal adipose tissue volume, intrahepatic triglyceride content and fasting blood glucose Wait.
The corresponding author of the study, Professor Samuel Klein, said that although their test results suggest that NMN is beneficial to the insulin sensitivity of skeletal muscle, it is not enough to support any clinical recommendations, because generally speaking, if a therapy can improve skeletal muscle For insulin sensitivity, other metabolic health indicators will also be improved accordingly, but their test did not show this [10].
They believe that more research is needed to determine whether NMN has a clinical effect on the prevention or control of prediabetes or diabetes, and they are currently conducting another trial that also includes male participants to evaluate NMN.
Singularity is hiring everyone! Everybody Hi~! We need fresh blood to inject new energy into the singularity.
Come on, become the singularity cake and do a new job with us! These are the little friends we are currently looking for~ If you want to create and innovate with the singularity cakes, come join us.
Please send your resume and work (if any) to: hr@geekheal.
com or you can directly add to the WeChat (geekheal-xintan) of Geekheal-xintan for communication.
When adding friends, please note: recruitment + position + professional field.
We are waiting for you at Singularity.
References: [1] Braidy N, Guillemin GJ, Mansour H, et al.
Age related changes in NAD+ metabolism oxidative stress and Sirt1 activity in wistar rats[J].
PloS one, 2011, 6(4): e19194.
[2 ] Imai S, Yoshino J.
The importance of NAMPT/NAD/SIRT1 in the systemic regulation of metabolism and ageing[J].
Diabetes, Obesity and Metabolism, 2013, 15(s3): 26-33.
[3] Verdin E.
NAD+ in aging, metabolism, and neurodegeneration[J].
Science, 2015, 350(6265): 1208-1213.
[4] McReynolds MR, Chellappa K, Baur J A.
Age-related NAD+ decline[J].
Experimental gerontology, 2020, 134: 110888.
[5] Yoshino J, Mills KF, Yoon MJ, et al.
Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet-and age-induced diabetes in mice[J].
Cell metabolism, 2011 , 14(4): 528-536.
[6] Stromsdorfer KL, Yamaguchi S, Yoon MJ, et al.
NAMPT-mediated NAD+ biosynthesis in adipocytes regulates adipose tissue function and multi-organ insulin sensitivity in mice[J].
Cell reports, 2016, 16(7): 1851-1860.
[7] Uddin GM, Youngson NA, Sinclair DA, et al.
Head to head comparison of short-term treatment with the NAD+ precursor nicotinamide mononucleotide (NMN) and 6 weeks of exercise in obese female mice[J].
Frontiers in pharmacology, 2016, 7: 258.
[8] Mills KF, Yoshida S, Stein LR, et al.
Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice[J].
Cell metabolism, 2016, 24(6): 795-806.
[9] https://science.
sciencemag.
org/content/early/2021/04/21/science.
abe9985[10] https://medicine.
wustl.
edu/news/anti-aging-compound-that-improves-metabolic-health-in-mice- improves-muscle-glucose-metabolism-in-people/The author of this article | Ying Yuyanedu/news/anti-aging-compound-that-improves-metabolic-health-in-mice-improves-muscle-glucose-metabolism-in-people/ author of this article | Ying Yuyan
