As research on the gut microbiome progresses, new types of bacteria beyond the mainstays Bifidobacterium and Lactobacillus are emerging as targets to enhance microbial health. Chief among this list is Akkermansia, a genus represented by the single species Akkermansia muciniphilia in humans. This R&D deep dive delves into the fascinating world of Akkermansia, exploring its beneficial role in gut barrier function and modulating human weight and metabolism.1 In addition, sufferers of disorders like obesity, Type 2 Diabetes, IBD and IBS have recorded depleted levels of Akkermansia.2 Prepare to uncover the science behind this remarkable bacterium and learn why it may just be one of the most important inhabitants of the gut, and most talked above microbe of this decade.

What is Akkermansia muciniphila?

Akkermansia is a genus of mucin-feeding bacteria that lives in the human intestines.3 Unlike many other gut residents, Akkermansia has the unique ability to utilize mucin—the main component of mucus—as its primary nutrient source.4 This not only helps regulate the thickness of the mucus layer, which is crucial for gut barrier function, but also impacts various other physiological processes.5

Akkermansia muciniphila in Health

Akkermansia is increasingly recognized for its beneficial impacts on overall health and metabolism. It plays a pivotal role in maintaining gut barrier integrity and modulating the immune system.6 Studies have positively linked levels of Akkermansia to improved metabolic profiles like beneficial glucose metabolism, insulin signaling, and body weight, enhanced gut health, and even reduced risk factors for obesity and diabetes.7-10 Furthermore, interventions that increase Akkermansia levels also tend to increase levels of GLP-1.11,12 The bacterium’s ability to influence systemic health illustrates the importance of microbial balance in homeostasis and disease prevention.13

Akkermansia muciniphila and Health Challenges

Shifts in the levels of Akkermansia can influence health status. Research indicates that decreased populations of this bacterium are associated with several conditions characterized by increased intestinal permeability and inflammation.14 For instance, lower levels of Akkermansia have been observed in individuals with certain metabolic disorders and gut-related challenges, highlighting its role in maintaining a healthy gut microbiome.15

Research

While previous studies show that Akkermansia growth is associated with host health benefits, the magnitude of Akkermansia increase tends to be modest.16 Solnul®’s Low Dose Clinical Study revealed the highest reported increase in Akkermansia levels in a human clinical study17 These findings suggest that increasing Akkermansia levels via prebiotic fiber supplementation with Solnul® supports these bacteria in a health promoting context. Formulators seeking to develop products for improved barrier function and leaky gut, and metabolic improvements like weight loss and blood glucose management can complement their formulations with Solnul®, thereby supporting endogenous Akkermansia.18

Global Trends

The future holds promising developments for the application of Akkermansia in health and nutrition management. As global trends lean towards personalized medicine, and with nearly one-third of Americans projected to use GLP-1s (semaglutide weight-loss drugs like Ozempic and Wegovy) by 2028,19 the importance of natural GLP-1 boosters and companion products that enhance Akkermansia cannot be overstated.20 Its potential in improving gut health and systemic functions makes it efforts to stimulate the activity or enhance the abundance of this genus a significant point of interest in the nutraceutical industry globally.

Publication

Resistant potato starch supplementation reduces serum histamine levels in healthy adults with links to attenuated intestinal permeability

Webinar

Leaky Gut: Can Resistant Starch Enhance Gut Barrier Function?

References

1. Everard et al. 2013. PNAS; Plovier et al. 2017. Nat Med; Depommier et al. 2019. Nat Med
2. Png et al. 2010. Am J Gastroenterol; Everard et al. 2013. PNAS; Halmos et al. 2015. Gut; Halmos et al. 2016. Clin Transl Gastroenterol
3. Derrien et al. 2017. Microbial Pathogenesis. 1(1):1-10.
4. Belzer and de Vos. 2012. ISME Journal. 6(8):1449-1458.
5. Everard et al. 2013. Proceedings of the National Academy of Sciences. 110(22):9066-9071.
6. Plovier et al. 2017. Nature Medicine. 23(1):107-113.
7. Everard et al. 2013. Proc Natl Acad Sci USA. 110(22):9066-71.
8. Schneeberger et al. 2015. Sci Rep. 5:16643.
9. Plovier et al. 2017. Nat Med. 23(1):107-113.
10. Dao et al. 2016. Gut. 65(3):426-436.
11. Tachon et al. 2013. FEMS Microbiol Ecol. 83(2):299-309.
12. Reid et al. 2016. Eur J Nutr. 55(8):2399-2409.
13. Cani and de Vos. 2017. Frontiers in Microbiology. 8:1765.
14. Schneeberger et al. 2014. Cell Metabolism. 20(5):658-670.
15. Collado et al. 2016. European Journal of Clinical Nutrition. 70(7):765-771.
16. Blatchford et al. 2017. J Nutr Sci; Hibberd et al. 2019. Benef Microbes; Medina-Vera et al. 2019. Diabetes Metab
17. Bush et al. 2023. Nutrients. 15(7):1582.
18. Bush et al. 2023. J Funct Food. 108:105740
19. Goldman Sachs, February 2024
20. Zhang et al. 2020. Trends in Food Science & Technology. 99:610-621.


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