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Mechanisms of Action

Ankascin works by normalizing cellular mechanisms that are disrupted in the previous clinical studies.

High cholesterol, high blood pressure and high blood sugar are part of a group of related conditions called metabolic syndrome. This develops when the body loses the ability to properly manage its sources of energy, which are mostly fats and carbohydrates. Patients with this syndrome are at much higher risk for developing diabetes and cardiovascular disease. Many of the effects of metabolic syndrome are due to long-term inflammation and oxidative stress.


Figure 9. Dietary fat is digested into fatty acids, which are converted back tofat for long-term storage in the body. high fat levels increase the risk of developing metabolic syndrome and cardiovascular disease. Monascin andankaflavin decrease the production and storage of fat from fatty acids, directing them instead to production of energy.

However, both of which are reduced by monascin and ankaflavin. For instance, monascin reduces the production of inflammatory cytokines such as interleukin-6, interleukin-1β, and tumor necrosis factor α16. Monascin and ankaflavin also activate a cellular sensor of oxidative stress known as Nrf2; once activated, this sensor drives the production of many antioxidants to protect the body against damage16,17. Oxidation of cholesterol is an important first step in the production of plaques. By preventing this, monascin and ankaflavin reduce both inflammation and the increased blood pressure that normally develops with cardiovascular disease.

Ankascin has many ways of reducing LDL cholesterol, but among the most important of these is its ability to control how fat is made and used by the body. Dietary fat is digested into fatty acids, which the liver turns into cholesterol. It is for this reason that a high-fat diet, even if it is low in cholesterol, can increase your risk of cardiovascular disease. Ankascin reduces the conversion of fatty acids to cholesterol, by increasing their use in the production of energy. A diagram summarizing these effects is shown in Figure 9.

Monascin and ankaflavin prevent the development of metabolic syndrome by controlling blood sugar and the response of cells to insulin. Type 2 diabetes is common among patients with metabolic syndrome, and occurs when cells no longer respond to insulin by increasing their uptake of glucose23.

This results in dangerously high levels of blood glucose, which is responsible for the serious health problems associated with this disease. Insulin resistance is due, at least in part, to constant, high levels of inflammation, which directly blocks the cellular pathway necessary for cells to respond to insulin24.

Monascin acts to restore normal functioning of this pathway by reducing inflammation and its associated negative effects. Ankaflavin increases glucose uptake in the liver, increases insulin production by the pancreas, and decreases production of metabolites that increase the risk of diabetes25,26.

Monascin and ankaflavin also act to reduce the elevated blood pressure that occurs in hypertension. Chronic high blood pressure is associated with damaging changes in the structure of blood vessels, leading to a loss of elasticity and flexibility. Both Monascus metabolites use different mechanisms to prevent these alterations. Furthermore, treatment with monascin and ankaflavin lead to increased production of nitric oxide, which dilates the blood vessels and reduces blood pressure27.

Notably, nitroglycerin, which is one of the most important pharmaceuticals for the treatment of hypertension and heart attacks, functions through the same mechanism28. Monascin and ankaflavin also prevent the production of proteins that stiffen and inflame the blood vessels. Since inflamed blood vessels are also more likely to develop plaques, there is a two-fold effect of Ankascin here in reducing the risk of cardiovascular disease.

Moreover, unpublished data from Dr. Pan’s lab provides extra insight into the mechanism of action of ankaflavin in reducing blood pressure. The renin-angiotensin system is a signaling pathway used by the body to regulate blood volume29. Activation of this pathway increases salt and water retention, but also increases blood pressure. Consequently, the pathway is a major target of pharmaceuticals designed to treat hypertension. Ankaflavin counteracts this pathway and normalizes blood pressure, through several different mechanisms. First, it increases production of a hormone which directly opposes the activity of the renin-angiotensin system. Second, it blocks production of the hormone directly responsible for water and sodium retention by the kidneys. Finally, ankaflavin increases the activity of another pathway, the effect of which is to increase the production of nitric oxide, reduce inflammation and reactive oxygen species, reduce formation of blood clots, and to dilate blood vessels30.

By regulating the key cellular pathways involved in hypertension, ankaflavin successfully reverses the negative effects of lifestyle, genetics, and other factors that predispose individuals to cardiovascular disease.

Thus, by regulating the key cellular pathways involved in hypertension, ankaflavin successfully reverses the negative effects of lifestyle, genetics, and other factors that predispose individuals to cardiovascular disease.
It is clear that both monascin and ankaflavin have several beneficial activities in controlling cellular pathways that are affected in metabolic syndrome. Thus, dietary supplementation with Ankascin may support against symptoms of metabolic syndrome.

REFERENCES

16. Lee, B. H., Hsu, W. H., Huang, T., Chang, Y. Y., Hsu, Y. W. and Pan, T. M. (2013). Effects of monascin on anti- inflammation mediated by Nrf2 activation in advanced glycation end product-treated THP-1 monocytes and methylglyoxal-treated wistar rats. Journal of Agricultural and Food Chemistry 61: 1288–1298

17. Hsu, W.-H. H., Lee, B.-H. H., Huang, Y.-C. C., Hsu, Y.-W. W. and Pan, T.-M. M. (2012). Ankaflavin, a novel Nrf-2 activator for attenuating allergic airway inflammation. Free Radical Biology and Medicine 53: 1643–1651.

23. Taylor, R. (2013). Type 2 diabetes: etiology and reversibility. Diabetes Care 36: 1047–55.

24. Bastard, J.-P., Maachi, M., Lagathu, C., Kim, M. J., Caron, M., Vidal, H., Capeau, J. and Feve, B. (2006). Recent advances in the relationship between obesity, inflammation, and insulin resistance. European Cytokine Network 17: 4–12.

25. Lee, B. H., Hsu, W. H., Chang, Y. Y., Kuo, H. F., Hsu, Y. W. and Pan, T. M. (2012). Ankaflavin: A natural novel PPARγ agonist upregulates Nrf2 to attenuate methylglyoxal-induced diabetes in vivo. Free Radical Biology and Medicine      53: 2008–2016.

26. Gkogkolou, P. and Böhm, M. (2012). Advanced glycation end products: Key players in skin aging? Dermato-Endocrinology 4: 259–70.

27. Lee, B. H. and Pan, T. M. (2012). Benefit of Monascus-fermented products for hypertension prevention: A review. Applied Microbiology and Biotechnology 94: 1151–1161.

28. Lee, B. H. and Pan, T. M. (2012). Benefit of Monascus-fermented products for hypertension prevention: A review. Applied Microbiology and Biotechnology 94: 1151–1161.

29. Divakaran, S. and Loscalzo, J. (2017). The Role of Nitroglycerin and Other Nitrogen Oxides in Cardiovascular Therapeutics. Journal of the American College of Cardiology 70: 2393–2410.

30. Patel, V. B., Zhong, J.-C., Grant, M. B. and Oudit, G. Y. (2016). Role of the ACE2/Angiotensin 1-7 Axis of the Renin-Angiotensin System in Heart Failure. Circulation Research 118: 1313–1326

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