Advantages of NMNH
NMNH: 1. “Bonzyme” Whole-enzymatic method, environmental-friendly, no harmful solvent residues manufacturing powder. 2. Bontac is a very first manufacture in the world to produce the NMNH powder on the level of high purity, stability. 3. Exclusive “Bonpure” seven-step purification technology, high purity（up to 99%) and stability of production of NMNH powder 4. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products of NMNH powder 5. Provide one-stop product solution customization service
Advantages of NADH
NADH: 1. Bonzyme whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Exclusive Bonpure seven-step purification technology, purity up higher than 98 % 3. Special patented process crystal form, higher stability 4. Obtained a number of international certifications to ensure high quality 5. 8 domestic and foreign NADH patents, leading the industry 6. Provide one-stop product solution customization service
Advantages of NAD
NAD: 1. “Bonzyme” Whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Stable supplier of 1000+ enterprises around the world 3. Unique “Bonpure” seven-step purification technology, higher product content and higher conversion rate 4. Freeze drying technology to ensure stable product quality 5. Unique crystal technology, higher product solubility 6. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products
Advantages of MNM
NMN: 1. “Bonzyme”Whole-enzymatic method, environmental-friendly, no harmful solvent residues 2. Exclusive“Bonpure”seven-step purification technology, high purity（up to 99.9%) and stability 3. Industrial leading technology: 15 domestic and international NMN patents 4. Self-owned factories and obtained a number of international certifications to ensure high quality and stable supply of products 5. Multiple in vivo studies show that Bontac NMN is safe and effective 6. Provide one-stop product solution customization service 7. NMN raw material supplier of famous David Sinclair team of Harvard University
We Have The Best Solutions for Your Business
Bontac Bio-Engineering (Shenzhen) Co., Ltd. (hereafter referred to as BONTAC) is a high-tech enterprise established in July 2012. BONTAC integrates R&D, production and sales, with enzyme catalysis technology as the core and coenzyme and natural products as main products. There are six major series of products in BONTAC, involving coenzymes, natural products, sugar substitutes, cosmetics, dietary supplements and medical intermediates.
As the leader of the global NMN industry, BONTAC has the first whole-enzyme catalysis technology in China. Our coenzyme products are widely used in health industry, medical & beauty, green agriculture, biomedicine and other fields. BONTAC adheres to independent innovation, with more than 170 invention patents. Different from the traditional chemical synthesis and fermentation industry, BONTAC has advantages of green low-carbon and high-value-added biosynthesis technology. What’s more, BONTAC has established the first coenzyme engineering technology research center at the provincial level in China which also is the sole in Guangdong Province.
In the future, BONTAC will focus on its advantages of green, low-carbon and high-value-added biosynthesis technology, and build ecological relationship with academia as well as upstream/downstream partners, continuously leading the synthetic biological industry and creating a better life for human beings.
What are the purposes of NMN supplements?
NMN supplements are mainly used to increase NAD+ levels to improve metabolic diseases and slow down the aging process.
Improve metabolic diseases: Studies have shown that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity.
Delay the aging process: NMN can increase the vitality of cells, improve the metabolic process of cells, and delay the aging process.
Protect DNA: NAD+ is an important metabolic substance in cells and participates in various biological processes such as cellular energy metabolism and DNA repair. Supplementing NMN can increase NAD+ levels and protect DNA.
Improves Athletic Capacity: NMN has been shown to improve athletic performance and increase fat burning ability
Improve neurodegenerative diseases: Studies have shown that NMN can improve neurodegenerative diseases, such as Alzheimer's disease
What NMN Supplements Do?
NMN supplements are mainly used to increase NAD+ levels to improve metabolic diseases and slow down the aging process.
Improve metabolic diseases: Studies have shown that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity.
Delay the aging process: NMN can increase the vitality of cells, improve the metabolic process of cells, and delay the aging process.
Protect DNA: NAD+ is an important metabolic substance in cells and participates in various biological processes such as cellular energy metabolism and DNA repair. Supplementing NMN can increase NAD+ levels and protect DNA.
Improves Athletic Capacity: NMN has been shown to improve athletic performance and increase fat burning ability
Improve neurodegenerative diseases: Studies have shown that NMN can improve neurodegenerative diseases, such as Alzheimer's disease
However, these studies were small, and NMN has not been shown to be effective in clinical trials, so further research is needed to determine the effectiveness of NMN supplements.
What diseases can NMN supplements treat?
NMN (Nicotinamide Mononucleotide) is a substance similar to vitamin B3, which can produce NAD+ (a key metabolic intermediate) in the body. Therefore, studies have shown that NMN may help improve aging-related health issues such as metabolism, immunity, cell repair, brain health, and more.
Currently, NMN supplements are mainly used to treat the following diseases:
Aging-related metabolic disorders such as diabetes, obesity, high cholesterol, etc.
Aging-related neurodegenerative diseases, such as Alzheimer's disease.
Aging-associated immune decline.
Aging-related cardiovascular disease.
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Frequently Asked Question
Do you have any question?
NMN supplements may cause side effects such as upset stomach, diarrhea, and nausea. There is also research showing that NMN supplements may affect insulin sensitivity and insulin levels, so people with diabetes should consult their doctor before taking them.
NMN supplements have not yet undergone large-scale clinical trials to verify their effectiveness. Currently, research on NMN supplements is mainly focused on animal and in vitro experiments. These studies show that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity, and can delay the aging process.
The long-term health effects of NMN supplementation are not well studied. Existing studies mainly focus on animal and in vitro experiments, which show that NMN can improve the symptoms of metabolic diseases such as diabetes, fatty liver and obesity, and can delay the aging process. However, the results of these studies do not represent the long-term effects of NMN on human health.
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Unraveling Impacts of Ginsenoside Rg3 Treatment on IL-1β-induced Injury of NPCs
Introduction Intervertebral disc degeneration (IDD) is a frequently seen orthopedic disease, which is accompanied with excessive apoptosis of nucleus pulposus cells (NPCs) and degeneration of extracellular matrix (ECM), with main symptoms of pain and numbness in the waist, legs and feet, as well as inflammation on and around the surface of bone tissues. Strikingly, ginsenoside Rg3, the main active ingredient of ginseng, has been attested to exhibit anti-catabolic and anti-apoptotic effects in IL-1β-treated human NPCs and IDD rats by inactivating the p38 MAPK pathway. The risk factors for IDD IDD is generally associated with risk factors such as aging, excessive exercise, working environment, and genetics. As one ages, the amount of water in the body and in the intervertebral discs will be reduced accordingly. Intervertebral discs that lack moisture will lose their elastic function and become hard. Once there is any stimulation or pressure, the intervertebral disc may crack, leading to intervertebral disc injury. For instance, the mechanical trauma caused by excessive exercise and work may accelerate the fragility of disc and exacerbate IDD. Anti-catabolic and anti-apoptotic effects of ginsenoside Rg3 in IL-1β-treated human NPCs and IDD rats Ginsenoside Rg3 plays an anti-apoptotic role in IL-1β-treated human NPCs and IDD rats, as evidenced by the down-regulation of pro-apoptosis protein Bax and up-regulation of anti-apoptosis protein Bcl-2 in IL-1β-stimulated NPCs and IDD model rats. Besides, ginsenoside Rg3 represses ECM degradation in IL-1β-stimulated NPCs and intervertebral disc tissues of IDD rats, as attested by the decreased expression of ECM degradation-related factors MMPs (MMP2 and MMP3) and ADAMTSs (Adamts4, and Adamts5). Ginsenoside Rg3 exhibits anti-catabolic and anti-apoptotic effects in IL-1β-treated human NPCs. Ginsenoside Rg3 reduces apoptosis and catabolism in IDD rats. Alleviation of ginsenoside Rg3 in IDD via p38 MAPK pathway Ginsenoside Rg3 can alleviate NPC degeneration, recover the arrangement of annulus fibrous, and preserve more proteoglycan matrix via inactivating p38 MAPK pathway. In vitro, the fluorescence intensity of p38 is enhanced in IL-1β-stimulated NPCs, yet ginsenoside Rg3 offsets this promoting effect. In vivo, the phosphorylated p38 level is elevated in NPCs and the intervertebral disc tissues of IDD rats, while ginsenoside Rg3 works inversely. Ginsenoside Rg3 suppresses the IL-1β-stimulated p38 MAPK pathway in human NPCs Ginsenoside Rg3 inactivates the p38 MAPK pathway in IDD rats. Conclusion The anti-catabolic and anti-apoptotic effects of ginsenoside Rg3 in IL-1β treated human disc nucleus pulposus cells and in a rat model of disc degeneration are accomplished by inactivating the MAPK pathway, providing new clues on the treatment of IDD. Reference Chen J, Zhang B, Wu L, et al. Ginsenoside Rg3 exhibits anti-catabolic and anti-apoptotic effects in IL-1β treated human disc nucleus pulposus cells and in a rat model of disc degeneration by inactivating the MAPK pathway. Cell Mol Biol. 2024;70(1):233-238. doi:10.14715/cmb/2024.70.1.32 BONTAC Ginsenosides BONTAC has been dedicated to the R&D, manufacture and sale of raw materials for coenzyme and natural products since 2012, with self-owned factories, over 170 global patents as well as strong R&D team. BONTAC has rich R&D experience and advanced technology in the biosynthesis of rare ginsenosides Rh2/Rg3, with pure raw materials, higher conversion rate and higher content (up to 99%). One-stop service for customized product solution is available in BONTAC. With unique Bonzyme enzymatic synthesis technology, both S-type and R-type isomers can be accurately synthesized here, with stronger activity and precise targeting action. Our products are subjected to strict third-party self-inspection, which are worth of trustworthy. Disclaimer This article is based on the reference in the academic journal. The relevant information is provided for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC. Under no circumstances will BONTAC be responsible or liable in any way for any claims, damages, losses, expenses or costs resulting or arising directly or indirectly from your reliance on the information and material on this website.
Targeting NAD+ Salvage Pathway as a Potential Approach to Combat Obesity
Introduction Mar 4th is determined as the World Obesity Day. World Obesity Federation, UNICEF and WHO have hosted a global youth-led webinar to talk about obesity & youth. The obesity crisis has gradually attracted much attention. The latest report by the Lancet suggests that one billion people are bothered by obesity (2022), with 650 million adults, 340 million adolescents and 39 million children. Recently, etiological studies and interventions for obesity have been progressively focused on the central nervous system, with an attempt to curb the onset of obesity at its source. Notably, targeting NAD+ salvage pathway in hypothalamic astrocytes may be a potential approach to combat obesity. The association of hypothalamic astrocytes and obesity The hypothalamus functions as the appetite regulation center, which receives and integrates the neuroendocrine factors produced by the central nervous system and peripheral tissues to promote or suppress appetite, so as to affect body weight. Noteworthily, aypothalamic astrocytes can apparently decrease glucose clearance and increase plasma insulin levels, playing an essential role in modulating energy metabolism, which are expected to be a new target for obesity treatment. Alleviation of high-fat diet (HFD)-induced obesity by repressing astrocyte NAD+ salvage pathway Under conditions of excessive fat intake, the NAD+ salvage pathway is specifically activated in hypothalamic astrocytes, which restrains the energy expenditure (EE) and fat oxidation in adipose tissues by downregulating sympathetic nerve innervation, eventually resulting in the accumulation of adipose tissue fat and the development of obesity. CD38 as a downstream mediator of astrocyte inflammation induced by the NAD+ salvage pathway. CD38 functions downstream of the NAD+ salvage pathway in hypothalamic astrocytes burdened with excess fat. CD38 knockdown in arcuate nucleus astrocytes diminishes the weight gain, reduces fat mass, increases EE, and lowers RER during HFD consumption. Cd38 depletion in hypothalamic astrocytes may improve hypothalamic inflammation by increasing NAD+ level. Hypothalamic inflammation can not only lead to energy imbalances, but also exacerbate central insulin resistance and leptin resistance, which can lead to the accumulation of fat in peripheral tissues. The role of nicotinamide phosphoribosyltransferase (NAMPT)–NAD+–CD38 axis in obesity In mammals, the salvage pathway represents the primary means of maintaining cellular NAD+ level. A crucial step in the NAD+ salvage pathway is catalyzed by NAMPT. In response to fat overload, the activation of the astrocytic NAMPT-NAD+-CD38 axis induces pro-inflammatory responses in the hypothalamus, eliciting aberrantly activated basal Ca2+ signals and compromised Ca2+ responses to metabolic hormones such as insulin, leptin, and glucagon-like peptide 1, ultimately resulting in dysfunctional hypothalamic astrocytes and contribute to the development of obesity. Conclusion Mechanically, inhibition of hypothalamic astrocytic NAD+ salvage pathway, along with its downstream CD38, mitigates hypothalamic inflammation and attenuates the development of HFD-induced obesity in male mice. Reference Park, J.W., Park, S.E., Koh, W. et al (2024). Hypothalamic astrocyte NAD+ salvage pathway mediates the coupling of dietary fat overconsumption in a mouse model of obesity. Nat Commun 15, 2102. https://doi.org/10.1038/s41467-024-46009-0 BONTAC NAD BONTAC has been dedicated to the R&D, manufacture and sale of raw materials for coenzyme and natural products since 2012, with self-owned factories, over 170 global patents as well as strong R&D team. BONTAC has rich R&D experience and advanced technology in the biosynthesis of NAD and its precursors (eg. NMN and NR). There are various types of NAD to be selected, encompassing NAD ER Grade (endoxin removal), NAD Grade I (IVD/dietary supplement/cosmetics raw powder), NAD Grade II (API/intermediates) and NAD Grade IV (if any higher requirement on the solubility), which can be provided in the form of lyophilized powder or crystalline powder. The purity of BONTAC NAD can reach above 98%. Disclaimer This article is based on the reference in the academic journal. The relevant information is provided for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC. BONTAC holds no responsibility for any claims, damages, losses, expenses or costs resulting or arising directly or indirectly from your reliance on the information and material on this website.
The Nuanced Role of NADPH in the Complex Landscape of Metabolic Disorders
1.Introduction Nicotinamide adenine dinucleotide phosphate hydrogen (NADPH), also known as reduced coenzyme II, is a critical cofactor in cellular antioxidant systems and lipid synthesis, which links insulin resistance and ferroptosis of pancreatic β cells in the context of metabolic disorders such as diabetes mellitus, playing a central role in maintaining metabolic homeostasis. 2. Biological role of NADPH NADPH functions as a coenzyme essential to cellular metabolism, playing pivotal roles in various critical biological processes, such as ROS scavenging, ROS production, fatty acid synthesis and cholesterol synthesis. 3. Biosynthetic pathway of NADPH Cellular production of NADPH is facilitated through several pathways, including the pentose phosphate pathway, the citric acid cycle, and fatty acid metabolism. The dynamic equilibrium between NADPH synthesis and consumption is essential for preserving cellular redox balance and enabling a host of biosynthetic reactions. 4. The role of NADPH in insulin secretion from pancreatic β-Cells Both redox reaction and metabolic signaling can modulate insulin secretion from pancreatic β-cells, where NADPH plays a central role. It can not only serves as a metabolic coupling factor, but also acts as a custodian of β-cell integrity, delicately managing the interplay between metabolic inputs and insulin output. 5. The interaction between insulin resistance and NADPH A substantial body of evidence reveals that NADPH is critical for the regulation of oxidative stress and inflammatory responses, the main contributors to the pathogenesis of insulin resistance. Specifically, NADPH is implicated in ROS production via NOX and is also utilized in the synthesis of new fatty acids, which contributes to the development of insulin resistance, particularly in the context of obesity-induced chronic inflammation. 6. The impact of NADPH upon the ferroptosis in the context of diabetes In pancreatic β cells, the elevated blood sugar and pro-inflammatory cytokines can trigger oxidative stress and iron accumulation to promote lipid peroxidation, thereby facilitating the ferroptosis. In return, the ferroptosis can reduce insulin secretion and beta cell mass, which is contributive to the progression of diabetes. In general, NADPH plays a dual role in ferroptosis. On the one hand, it can promote ROS generation via NOX. On the other hand, it can support antioxidant defense through glutathione regeneration. In the context of diabetes, NADPH may predominantly fuel processes leading to ferroptosis, mainly due to the enhanced activity and affinity of NOX, which however requires further research for verification. 7. Conclusion NADPH has a critical role in the complex landscape of metabolic disorders, particularly insulin resistance and ferroptosis. Regulating NADPH-related pathways may open up new opportunities for the treatment of metabolic disorders. Reference Moon, Dong-Oh. “NADPH Dynamics: Linking Insulin Resistance and β-Cells Ferroptosis in Diabetes Mellitus.” International journal of molecular sciences vol. 25,1 342. 26 Dec. 2023, doi:10.3390/ijms25010342 Production advantages and features of BONTAC NADPH BONTAC has rich R&D experience and advanced technology in the biosynthesis of NADPH. Bonzyme whole-enzymatic method is adopted, which is environmental-friendly, with no harmful solvent residues. The purity of NADPH can reach up to 95%, which is benefited from the exclusive Bonpure seven-step purification technology. BONTAC has self-owned factories and has obtained a number of international certifications, where high quality and stable supply of products can be ensured. BONTAC has four domestic and foreign NADPH patents, leading the industry. Disclaimer This article is based on the reference in the academic journal. The relevant information is provide for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The views expressed in this article do not represent the position of BONTAC. Under no circumstances will BONTAC be held responsible or liable in any way for any claims, damages, losses, expenses, costs or liabilities whatsoever (including, without limitation, any direct or indirect damages for loss of profits, business interruption or loss of information) resulting or arising directly or indirectly from your reliance on the information and material on this website.