The food we eat can have a significant impact on our metabolic health, particularly on blood glucose levels. Prolonged and excessive metabolic responses can lead to inflammation and disturbed insulin signalling, increasing the risk of chronic conditions such as obesity and type 2 diabetes.

While there are many contributing factors, cutting-edge research has put a spotlight on the gut microbiome as a key player in shaping these metabolic responses [1]. The food we eat plays a critical role in shaping the microbial environment by providing nutrients and compounds that interact with gut microbes, affecting our health positively or negatively.

By exploring the connections between the microbiome and metabolic health, we can learn dietary strategies to improve the way microbes and metabolism interact.

1. The molecules produced by gut microbes

You have probably heard of prebiotics and probiotics, but what about postbiotics?

The gut microbiome is like a pharmacy, capable of producing millions of substances that can affect human biology.

With a set of genes estimated to be 100 times more extensive than our own, the gut microbiome has the molecular instructions to create a vast range of compounds called postbiotics, which can cross the gut lining and interact with our receptor system. In other words, postbiotics are byproducts of gut microbes that our human cells can understand, and they can benefit our health by changing the way our cells and organs function.

  • Insulin signalling. Short-chain fatty acids (SCFAs) produced by certain gut microbes are linked to improved insulin signalling in healthy individuals, while impaired SCFA production increases the risk of type 2 diabetes [3]. Reduced levels of butyrate-producing bacteria, such as Roseburia intestinalis and Faecalibacterium prausnitzii, are common in the microbiomes of people with type 2 diabetes [4].
  • Appetite regulation. Research in mice suggests butyrate can control appetite and energy expenditure through its effect on gut-brain communication, leading to a reduction in food intake [5]. This helps prevent the overeating and metabolic inflammation that result from chronic overnutrition.
  • Gut barrier support. Butyrate and other SCFAs strengthen the gut barrier by activating genes that reinforce tight junctions, the proteins between intestinal cells that prevent gut contents from leaking into the body and triggering inflammation and metabolic dysfunction [6, 7].

How to produce more short-chain fatty acids

SCFAs such as butyrate help regulate insulin signalling, promote fullness, and strengthen the gut barrier. The best way to supercharge your microbiome to produce them is to eat fibre-rich foods: beans, legumes, fresh vegetables, nuts, seeds, fruit, and whole grains, which selectively encourage the growth of these beneficial bacteria. Supplementing with prebiotics such as chicory inulin can boost SCFAs further [8].

2. Reinforcing the gut barrier

Dysbiosis is an imbalance between good and bad bacteria, reduced microbial diversity, and a state where the activity of the microbiome does not support your health.

Dysbiotic microbiomes can cause leaky intestines by disrupting epithelial tight junctions, allowing bacterial components called endotoxins to seep into the bloodstream [9, 10]. High levels of endotoxaemia activate receptors on insulin target tissues, leading to inflammation that disrupts insulin signalling and drives insulin resistance, which increases the risk of developing type 2 diabetes [11].

How to prevent dysbiosis

Cultivating a healthy, diverse, stable gut microbiome is key to preventing leaky gut, metabolic endotoxaemia, and insulin resistance. Since unhealthy diets are the main cause of dysbiosis, opt for nutrient-dense whole foods over ultra-processed convenience foods. This encourages the growth of SCFA-producing microbes while preventing the colonisation of inflammatory bacteria.

3. Regulation of the gut mucosal lining

The inner lining of the gut is covered in a layer of mucus containing a protein called mucin. This gel-like coating reinforces the gut barrier and prevents microbes from causing inflammation [12].

Akkermansia muciniphila is a unique bacterium that thrives on this mucus layer. It digests mucin to generate acetate, an SCFA that nourishes other beneficial bacteria like the butyrate-producing F. prausnitzii [13]. This implies that mucosal, immune, and metabolic health are interconnected and depend on a well-balanced, synergistic microbial community.

In mouse models, A. muciniphila improved glucose homeostasis and reduced body fat mass. In humans, this species is more abundant in healthy individuals compared with prediabetic and type 2 diabetes patients [14, 15].

How to maintain your gut barrier

To increase the abundance of A. muciniphila, intermittent fasting can be effective, as it allows these microbes to access the mucus lining when no food is present [16]. Polyphenols, the natural compounds found in colourful fruits and vegetables, also positively impact A. muciniphila levels. Consuming dark leafy greens, beetroot, purple cabbage, and oranges will feed these species and enhance your mucosal immunity, gut health, and metabolic health.

Key takeaways

Changes to the gut microbiota can occur within days of dietary changes, so changing what you eat is probably the most effective way to reverse dysbiosis.
  • Include a large variety of plant-based dietary fibres to increase the population of SCFA-producing bacteria.
  • SCFAs such as butyrate improve insulin signalling, regulate appetite, and support gut health, all of which lead to better post-meal glucose responses and a reduced risk of metabolic disease.
  • Avoiding processed foods helps prevent dysbiosis, leaky gut, chronic inflammation, and insulin resistance.
  • Intermittent fasting and polyphenol-rich foods encourage the growth of mucin-loving bacteria, contributing to better gut and metabolic health.

Improving lifestyle factors such as sleep and stress can also benefit gut microbial composition, diversity, and overall health [18].

References

  1. link.springer.com/article/10.1007/s00125-018-4550-1
  2. gut.bmj.com/content/70/6/1174
  3. ncbi.nlm.nih.gov/pmc/articles/PMC6441384
  4. science.org/doi/10.1126/science.aao5774
  5. gut.bmj.com/content/67/7/1269.long
  6. link.springer.com/article/10.1007/s10620-012-2259-4
  7. journals.physiology.org/doi/full/10.1152/physiol.00041.2015
  8. cambridge.org/core/journals/british-journal-of-nutrition
  9. aspenjournals.onlinelibrary.wiley.com/doi/abs/10.1177/0148607111413772
  10. ncbi.nlm.nih.gov/pmc/articles/PMC3265717
  11. sciencedirect.com/science/article/abs/pii/S0271531712001595
  12. ncbi.nlm.nih.gov/pmc/articles/PMC5408367
  13. journals.asm.org/doi/pdf/10.1128/mbio.00770-17
  14. gut.bmj.com/content/64/6/872
  15. journals.plos.org/plosone/article?id=10.1371/journal.pone.0071108
  16. ncbi.nlm.nih.gov/pmc/articles/PMC6924600
  17. nature.com/articles/nature12820
  18. ncbi.nlm.nih.gov/pmc/articles/PMC6290721