How does prebiotic supplements help with insulin sensitivity? 8 Mechanisms

Prebiotics have been shown to have potential benefits for improving insulin sensitivity and glucose control in both healthy individuals and those with various metabolic disorders. Here are a few mechanisms why prebiotic can help:

1. Prebiotics can stimulate the production of short-chain fatty acids (SCFAs), which can improve insulin sensitivity. SCFAs are produced by the fermentation of prebiotics by gut bacteria, and have been shown to increase insulin sensitivity in both humans and animals (1, 2).
2. Prebiotics can increase the abundance of beneficial gut bacteria, such as Bifidobacteria and Akkermansia muciniphila, which have been associated with improved insulin sensitivity. These bacteria may help to regulate gut barrier function, reduce inflammation, and improve glucose metabolism (3, 4).
3. Prebiotics may improve gut barrier function, which can reduce inflammation and improve insulin sensitivity. A healthy gut barrier helps to prevent the entry of harmful bacteria and toxins into the bloodstream, which can contribute to inflammation and insulin resistance (5).
4. Prebiotics may help to reduce inflammation in the gut and throughout the body, which can improve insulin sensitivity. Chronic inflammation is a key contributor to insulin resistance, and prebiotics have been shown to reduce inflammatory markers in both humans and animals (6, 7).
5. Prebiotics may help to regulate the release of gut hormones, such as GLP-1 and PYY, which can improve insulin sensitivity. These hormones play a role in regulating glucose metabolism and appetite, and prebiotics have been shown to increase their production in both humans and animals (8, 9).
6. Prebiotics may improve lipid metabolism, which can improve insulin sensitivity. Studies have shown that prebiotics can reduce levels of triglycerides and cholesterol, which are risk factors for insulin resistance and type 2 diabetes (10, 11).
7. Prebiotics may improve mitochondrial function, which can improve insulin sensitivity. Mitochondria are the energy-producing organelles in cells, and dysfunction in these organelles has been linked to insulin resistance. Prebiotics have been shown to improve mitochondrial function in animal studies (12).
8. Prebiotics may improve liver function, which can improve insulin sensitivity. The liver plays a key role in glucose metabolism, and dysfunction in this organ can contribute to insulin resistance. Prebiotics have been shown to improve liver function in animal studies (13).

References:

1. Cani PD, et al. Gut microbiota fermentation of prebiotics increases satietogenic and incretin gut peptide production with consequences for appetite sensation and glucose response after a meal. Am J Clin Nutr. 2009 Nov;90(5):1236-43.
2. Chambers ES, et al. Effects of targeted delivery of propionate to the human colon on appetite regulation, body weight maintenance and adiposity in overweight adults. Gut. 2019 Aug;68(8):1741-1750.
3. Dao MC, et al. Akkermansia muciniphila and improved metabolic health during a dietary intervention in obesity: relationship with gut microbiome richness and ecology. Gut. 2016;65:426-436.
4. Everard A, et al. Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity. Proc Natl Acad Sci USA. 2013;110:9066-9071.
5. Cani PD, et al. Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability. Gut. 2009;58:1091-1103.
6. Everard A, et al. Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity. Proc Natl Acad Sci USA. 2013
7. Cani, P. D., Lecourt, E., Dewulf, E. M., Sohet, F. M., Pachikian, B. D., Naslain, D., ... & Delzenne, N. M. (2009). Gut microbiota fermentation of prebiotics increases satietogenic and incretin gut peptide production with consequences for appetite sensation and glucose response after a meal. The American Journal of Clinical Nutrition, 90(5), 1236-1243. https://doi.org/10.3945/ajcn.2009.28095
8. Delzenne, N. M., Cani, P. D., Daubioul, C., & Neyrinck, A. M. (2005). Impact of inulin and oligofructose on gastrointestinal peptides. British Journal of Nutrition, 93(S1), S157-S161. https://doi.org/10.1079/BJN20041352
9. Cani, P. D., Dewulf, E. M., & Delzenne, N. M. (2009). Inulin-type fructans modulate gastrointestinal peptides involved in appetite regulation (glucagon-like peptide-1 and ghrelin) in rats. British Journal of Nutrition, 101(4), 514-521. https://doi.org/10.1017/S0007114508020302
10. Dewulf, E. M., Cani, P. D., Claus, S. P., Fuentes, S., Puylaert, P. G., Neyrinck, A. M., ... & Delzenne, N. M. (2013). Insight into the prebiotic concept: lessons from an exploratory, double blind intervention study with inulin-type fructans in obese women. Gut, 62(8), 1112-1121. https://doi.org/10.1136/gutjnl-2012-303304
11. Everard, A., Cani, P. D., & Delzenne, N. M. (2014). Gut microbiota and related metabolic disorders. Digestive Diseases, 32(3), 481-489. https://doi.org/10.1159/000357853
12. Amar, J., Burcelin, R., Ruidavets, J. B., Cani, P. D., Fauvel, J., Alessi, M. C., ... & Bingham, A. (2008). Energy intake is associated with endotoxemia in apparently healthy men. The American Journal of Clinical Nutrition, 87(5), 1219-1223. https://doi.org/10.1093/ajcn/87.5.1219
13. Cani, P. D., Amar, J., Iglesias, M. A., Poggi, M., Knauf, C., Bastelica, D., ... & Delzenne, N. M. (2007). Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes, 56(7), 1761-1772. https://doi.org/10.2337/db06-1491