Our Technology

Addressing Missing Dietary Nutrients in the GI Microbiome

Modern diets can contribute to poor digestive health.

A less rich, diverse GI microbiome is associated with unhealthy metabolic states. Contemporary diet choices contribute to GI dysbiosis, which is thought to be widespread.  Our products are designed to counteract this imbalance by providing missing dietary nutrients for the GI microbiota community. The goal is to:

  • Increase production of short chain fatty acids (SCFAs),
  • Prime the GI immune system and fortify the intestinal mucosal barrier, and
  • Reduce methane and hydrogen sulfide gas production that are associated with weight gain and intestinal permeability.*

* These statements have not been evaluated by the Food and Drug Administration.  The products of MicroBiome Therapeutics are not intended to diagnose, treat, cure or prevent any disease.

A GI Microbiome Modulator to Complement Lifestyle Change

Our first microbiome modulator is specifically formulated to deliver important nutrients to the GI microbiome. The aim is to nourish and nurture a healthy and diverse microbiota in those whose diets may have insufficient levels of prebiotic nutrients. It contains concentrated food-derived ingredients selected to expand and nurture the richness of the GI microbiome and is intended to be valuable both for individuals choosing to consume a healthier diet as well as for those maintaining their current dietary practices. This GI microbiome modulator was tested in two clinical trials that assessed a number of clinical outcomes (1,2).

Microbiome SCFA levels and Inulin

Short chain fatty acids (SCFAs) are small molecules that are produced in large quantities in the large intestine by groups of bacteria that feed on undigestible carbohydrates, such as inulin.  These undigestible carbohydrates pass through the small intestine unabsorbed into the blood, until they become in contact with the microbiota.  Collectively, prebiotics is a term used to describe these types of carbohydrates that are resistant to digestion.  These nutrients are only able to be metabolized (fermented) in the large intestine by the resident microbiota.  The byproducts of this microbial fermentation are SCFAs that lead to the secretion of certain peptide hormones (3,4,5). Some of these peptide hormones signal satiety while also decreasing gastric emptying and increasing insulin release (6).

Gut Permeability and Beta (ß)-Glucan

The physical barrier protecting cells of the intestines from being digested themselves is the mucus layer.  Mucus is largely composed of molecules that may also serve as nutrients for some of the microbiota. If low levels of prebiotic nutrients are present in the biome, such as during fasting or when following a carbohydrate restricted diet, microbiota may feed on components of mucus, reducing the protective GI barrier (7).  ß-glucan is a preferred food source for the microbiota and when added to the diet, serve to help protect the mucosal barrier.

If the physical GI barrier is compromised, the GI tract contains specialized immune systems to neutralize potentially harmful invaders.  The ability of the immune system to quickly recognize and respond to an invading pathogen is essential for controlling infection. One function of ß-glucan is to prime or ready the GI immune system to defend against pathogens if breaches in the mucosal barrier occur.

Oat β–glucans increase viscosity within the GI microbiome impairing the interaction of microbiota and toxins from engaging with the protective mucosal barrier of the intestines.

Methane and Hydrogen Sulfide in the Microbiome and Polyphenols

A byproduct produced by microbiota fermentation of prebiotic nutrients is hydrogen.  In turn, there are three groups of microbiota that may use this hydrogen to produce hydrogen sulfide, or methane, or acetate (9).  The methanogens that produce methane appear to favor fat absorption (10) and the sulfur reducing bacteria that produce hydrogen sulfide contribute to increased gut permeability and lower GI pathologies (9). Of these three groups, only the acetogens thrive on polyphenolic molecules like those found in blueberries (11).   Polyphenols stimulate a bloom in acetogens that use hydrogen to produce acetate (one of the SCFAs) in the large intestine (12). These SCFAs serve to stimulate release of satiety hormones.  Since only the acetogens are capable of feeding on polyphenolic molecules, they have a selective advantage over the other two hydrogenotrophs.

Bile Acids

Bile acids (BAs) are released from the gall bladder into the small intestine when fat is ingested.  BAs are toxic to some microbiota in the GI microbiome and to intestinal cells. Conversion of bile acids to bile salts is performed by groups of microbiota in the GI microbiome, a mechanism that reduces this BA toxicity (13). The presence of bile salts in the intestine is a process that can improve insulin sensitivity (14) and improve glucose tolerance (15).  The quantity of bile salt present is sensed by the intestine and regulated so that the liver does not overproduce bile acids, which could lead to diarrhea (16).  β–glucans have been shown to interact with bile salts in the small intestine (17), interfering with the bile acid sensing mechanism and resulting in overproduction of bile salts in the small intestine.  This produces positive effects in glucose regulation.  At the same time, the β–glucan-bile salt binding neutralizes the action in the large intestine, preventing diarrhea.

Recommended Dietary Fiber Intake

Dietary fiber is a term used to collectively describe all carbohydrates that are not digested in the human GI tract.   The American Diabetes Association recommends 14g total dietary fiber per 1,000 kcal consumed for children, adolescents, adults and elderly persons (18). The average daily caloric consumption for adults is 2,000 kcal, translating to 28g of recommended daily fiber. Soluble fiber, especially ß-glucan, has been sufficiently studied for the FDA to authorize a health claim that foods containing 0.75g to 1.7g per serving can reduce the risk of heart disease (19). Soluble and fermentable inulin is linked to laxation and an increase in the water content of stool. The greater the amount of added dietary fiber, the more defecation frequency is normalized to one bowel movement daily (20).

Although the health consequences of consuming sufficient quantities of dietary fiber are established by the American Diabetes Association, recent discoveries of microbiome function will undoubtedly expand our understanding of the nutritional biology of prebiotics.


  1. Burton JH, et al. Addition of a gastrointestinal microbiome modulator to metformin improves metformin tolerance and fasting glucose levels.    J Diabetes Sci and Technol. 9(4):808-14.
  2. Rebello C J, et al. A gastrointestinal microbiome modulator improves glucose tolerance in overweight and obese subjects: A randomized controlled pilot trial. 2015.  J Diabetes Complications 29(8):1272-6.
  3. Buchholz AC, Schoeller DA. Is a calorie a calorie?  Am J Clin Nutr 79(suppl): 899s-906s.
  4. Covington DK, et al. The G-protein-coupled receptor 40 family (GPR40-GPR43) and its role in nutrient sensing. 2006. Biochem Soc Trans. 34:770-773
  5. Karaki S, et al. Short-chain fatty acid receptor, GPR43, is expressed by enteroendocrine cells and mucosal mast cells in rat intestine. 2006. Cell Tissue Res. 324:353-360.
  6. Sandoval DA, D’Alessio DA. Physiology of proglucagon peptides: role of glucagon and GLP-1 in health and disease. 2015. Physiol Rev. 95:513–548.
  7. Brockhausen I. Mucin-type O-glycans in human colon and breast cancer: glycodynamics and functions. 2006. EMBO Reports 7:599-604.
  8. Koropatkin NM, Cameron EA, Martens EC. How glycan metabolism shapes the human gut microbiota. 2012. Nat Rev Microbiol 10(5):323-335.
  9. Nakamura N, et al. Mechanisms of microbial hydrogen disposal in the human colon and implications for health and disease. 2010. Annu Rev Food Sci Technol 1:363-395.
  10. Samuel BS, Gordon JI. A humanized gnotobiotic mouse model of host–archaeal– bacterial mutualism. 2006. Proc Natl Acad Sci U S A; 103:10011-10016.
  11. Rodriquez-Mateos A, et al. Procyanidin, anthocyanin, and chlorogenic acid contents of highbush and lowbush blueberries. 2012. J Agric Food Chem. 60:5772-5778.
  12. Bain J, et al. Dissecting the in vivo metabolic potential of two human gut acetogens. 2010. J Biol Chem; 285: 22082-22090
  13. Ridlon JM, Kang DJ, Hylemon PB. Bile salt biotransformations by human intestinal bacteria. 2006. J Lipid Res 47(2):241-259.
  14. Fang S, et al. Intestinal FXR agonist promotes adipose tissue browning and reduces obesity and insulin resistance. 2015. Nat Med. 21:159–165.
  15. Schaap FG. Role of fibroblast growth factor 19 in the control of glucose homeostasis. 2012. Curr Opin Clin Nutr Metab Care. 15:386–391.
  16. Walters JRF. Bile acid diarrhea and FGF19: new views on diagnosis, pathogenesis and therapy 2014. Nat. Rev. Gastroenterol. Hepatol.11;426–434
  17. Mikkelsen MS, et al. Probing interactions between ß-glucan and bile salts at atomic detail by 1H-13C NMR assays. J Agric Food Chem 62(47):11472-11478.
  18. Slavin JL. Position of the American Dietetic Association: Health Implications of Dietary Fiber. 2008. J Am Diet Assoc 108:1716-1731.
  19. US Department of Health and Human Services, Food and Drug Administration. Food labeling; health claims; soluble dietary fiber from certain foods and coronary heart disease. 2006. Final rule. 71 Federal Register 29248-29250.
  20. Haack VS, et al. Increasing amounts of dietary fiber provided by foods normalizes physiologic response of the large bowel without altering calcium balance or fecal steroid excretion. 1998. Am J Clin Nutr. 68: 615-622.