Metabolic Health

3 Surprising Connections Between Your Microbiome, Diet, and Metabolic Health

5 minutes read

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 signaling, increasing the risk of chronic conditions such as obesity and Type 2 diabetes (T2D). 

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].

So, what has the science brought to light so far?

The gut is home to a vast community of microorganisms that make up the gut microbiome. Each person's microbiome is unique and influenced by various factors such as genetics and environmental exposures — including the mode of delivery during childbirth or the time spent outdoors in nature.

The food we eat plays a critical role in shaping the microbial environment by providing nutrients and compounds that interact with the 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 release of molecules produced by gut microbes

You’ve 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 [2]. With a set of genes estimated to be 100 times more extensive than our own, the gut microbiome has an array of molecular instructions creating a vast range of molecules 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 can benefit our health by changing the way our cells and organs function.

  • Insulin signaling. SCFAs produced by certain gut microbes are linked to improved insulin signaling in healthy individuals, while impaired SCFA production and absorption increase the risk of T2D [3]. Reduced levels of butyrate-producing bacteria, such as Roseburia intestinalis and Faecalibacterium prausnitzii, are common in the microbiomes of individuals with T2D [4]. That is to say, lower levels of SCFA-producing bacteria may disrupt insulin signaling and increase insulin resistance. 
  • Appetite regulation. Research in mice suggests that butyrate can control appetite and energy expenditure through its effect on gut-brain communication, leading to a reduction in food intake [5]. This prevents overeating and disease-causing metabolic inflammation that results from chronic overnutrition. Put another way, butyrate may play a role in regulating feelings of hunger and satiety, reducing the likelihood of eating too much, which protects metabolic health.  
  • Gut barrier support. The cells lining the intestine (called epithelial cells) act as the first line of defense by maintaining gut integrity and preventing foreign substances from entering the body. Butyrate and other SCFAs can strengthen the gut barrier by activating genes that reinforce tight junctions — the proteins between the intestinal cells that prevent gut contents from leaking into the body — leading to inflammation and metabolic dysfunction [6, 7].

How you can produce more short-chain fatty acids

SCFAs, such as butyrate, are crucial for metabolic health. They help regulate insulin signaling, promote feelings of fullness and reduce overeating, and strengthen the gut barrier, preventing inflammation and metabolic issues. The best way to supercharge your gut microbiome to produce SCFAs is to eat fiber-rich foods, such as beans, legumes, fresh vegetables, nuts, seeds, fruit, and whole grains, as these selectively encourage the growth of these beneficial bacteria. Alternatively, supplementing with prebiotics, such as chicory inulin, can boost SCFAs further [8].

2. Reinforcing the integrity and reducing the permeability of the gut barrier

Dysbiosis is defined as an imbalance between “good” and “bad” bacteria, reduced gut microbial diversity, and a condition where the activity of the microbiome does not support your health. 

Dysbiotic microbiomes can cause leaky intestines by disrupting epithelial tight junctions (again, the proteins that prevent leaking), allowing bacterial components called endotoxins to seep into the bloodstream [9, 10]. High levels of endotoxemia activate receptors on insulin target tissues, leading to inflammation that disrupts insulin signaling, and leads to insulin resistance, which increases the risk of developing T2D [11].

How you can prevent dysbiosis in the gut

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

3. Regulation of the gut mucosal lining

As we’ve learned, the gut barrier is crucial for maintaining optimal health. However, it is less known that the inner lining of the gut is covered in a layer of mucus that contains 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 the protein mucin to generate acetate, an SCFA that nourishes other beneficial bacteria, like butyrate-producing F.prausnitzii [13]. This mutualistic relationship implies that mucosal, immune, and metabolic health are interconnected and depend on a well-balanced synergistic microbial community. In other words, a healthy microbiome depends on the collaboration and teamwork of individual microbes to create a balanced ecosystem that benefits the gut, immune system, and metabolism.

In mice models, A.muciniphila resulted in improved glucose homeostasis and a reduction in body fat mass, while in humans this species was more abundant in healthy individuals compared to prediabetic and T2D patients [14, 15].

How you can 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 there is no food present, which promotes the production of SCFAs [16]. Additionally, polyphenols, which are natural compounds found in colorful fruits and vegetables, have been shown to positively impact A.muciniphila levels in the gut. Consuming foods like dark leafy greens (spinach and kale), beetroot, purple cabbage, and oranges will feed these species and enhance your mucosal immunity, gut health, and metabolic health.

Key Takeaways

The structure and function of the gut microbiome are closely related to metabolic health. However, this connection is complex, and various interactions are at play. Changes to the gut microbiota can occur within days of dietary changes, meaning changing what you eat is probably the most effective way to reverse dysbiosis, repopulate the microbiota, heal the gut barrier, and strengthen the mucosal layer [17]. Additionally, improving lifestyle factors such as sleep and stress can benefit gut microbial composition, diversity, and overall health [18].

To sum up, here is what we’ve learned about the microbiome-metabolic health connection:

  • Include a large variety of plant-based dietary fibers to increase the population of SCFA-producing bacteria.
  • SCFAs such as butyrate can improve insulin signaling, regulate appetite, and support gut health, all of which lead to better postprandial (post-meal) glucose responses and a reduced risk of metabolic disease. 
  • Avoiding processed foods will help to prevent dysbiosis, leaky gut, chronic inflammation, and insulin resistance.
  • Intermittent fasting and including polyphenol-rich food will encourage the growth of mucin-loving bacteria contributing to better gut and metabolic health.

References:

  1. https://link.springer.com/article/10.1007/s00125-018-4550-1
  2. https://gut.bmj.com/content/70/6/1174
  3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6441384/
  4. https://www.science.org/doi/10.1126/science.aao5774
  5.  https://gut.bmj.com/content/67/7/1269.long
  6. https://link.springer.com/article/10.1007/s10620-012-2259-4
  7. https://journals.physiology.org/doi/full/10.1152/physiol.00041.2015?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org
  8. https://www.cambridge.org/core/services/aop-cambridge-core/content/view/B5897AC48DE5977ABA96D98D1A52B8A9/S0007114508019880a.pdf/div-class-title-effect-of-inulin-on-the-human-gut-microbiota-stimulation-of-span-class-italic-bifidobacterium-adolescentis-span-and-span-class-italic-faecalibacterium-prausnitzii-span-div.pdf
  9. https://aspenjournals.onlinelibrary.wiley.com/doi/abs/10.1177/0148607111413772
  10.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3265717/
  11.  https://www.sciencedirect.com/science/article/abs/pii/S0271531712001595?via%3Dihub
  12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5408367/
  13.  https://journals.asm.org/doi/pdf/10.1128/mbio.00770-17
  14.  https://gut.bmj.com/content/64/6/872
  15. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0071108
  16. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6924600/
  17. https://www.nature.com/articles/nature12820
  18. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6290721/

Written by: Natalie Falshaw, MSc
Reviewed by: Emily Johnson, MSc RD

Table of Contents

  • 1. The release of molecules produced by gut microbes
  • 2. Reinforcing the integrity and reducing the permeability of the gut barrier
  • 3. Regulation of the gut mucosal lining
  • Key Takeaways

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