If we went back to the beginning of our story—meaning the story of humanity—we’d remember a very important detail: man and woman were both made from the dust of the earth.

One of the vital parts of soil that makes it a living, thriving, life-supporting entity is its microbial content. And so it is with us, today. Though far removed from Eden, remnants of Eve’s legacy have been passed down through the generations—our internal microbiome. You see, it is from mom that the microbes have been passed down. We are inoculated at birth. Specific microbes living in our intestinal tract produce butyrate and other short-chain fatty acids as a result of breaking down fiber from the food we eat. These short-chain fatty acids behave as powerful signaling molecules with system-wide communication. Isn’t it amazing that this miniscule substance, produced in the dark dungeon of our large intestine, can be so influential?

While we’re focused on butyrate, we should note that short-chain fatty acids in general exert anti-obesity and anti-diabetic effects. The prevalence of both obesity and type 2 diabetes can probably serve as a clue that in seeking for answers to these global problems we would be wise to spend some time considering what is going on (or should be going on) in the gut. Butyrate performs many roles, including protecting us from insulin resistance, weight gain, and fatty liver.

There may be multiple ways it exerts this protection. Some researchers say that butyrate “may epigenetically regulate gene expression in different diseases, including obesity and metabolic syndrome.”1 Others see a pathway for butyrate’s impact through our energy production plants in the liver, and still others observe that butyrate stimulates the release of the GLP-1 hormone from intestinal cells. GLP-1 is a target for some diabetes medications.

An experiment was conducted in which three groups of mice were fed a high-fat diet and compared with a control group. Mice given the high-fat diet gained weight, developed insulin resistance, and increased levels of serum triglycerides, cholesterol, and liver enzymes—a marker of fatty liver progression. In contrast, the mice given supplemental butyrate or a butyrate derivative along with the high-fat diet experienced significantly reduced weight gain, liver enzymes, and blood lipids compared with the high-fat group who didn’t receive the butyrate or butyrate derivative. The same kind of benefit was seen with serum proinflammatory markers. These markers were elevated in the high-fat diet group but reduced in the supplemented animals. Similarly, mice on the high-fat diet experienced elevated blood sugar levels, while the group that ate the high-fat diet and the butyrate supplements had much lower levels. The mice “exhibited improved tolerance to glucose at all time points.”2

We’re not mice. I know. And this was only one study. But there are others that show the association between what is going on in the gut with butyrate production and conditions such as type 2 diabetes. Several human cohorts around the world reveal a decrease of butyrate-producing bacteria in obese individuals with pre-diabetes and type 2 diabetes.3

For example, a Dutch study showed association between improved glucose tolerance and increased potential for butyrate production. A group of Danes diagnosed with prediabetes had a lower abundance of butyrate-producing bacteria compared with age and sex-matched individuals with normal glucose regulation.  Addressing an altered gut microbiome and reduced butyrate production in a prediabetic state might just be an excellent place to implement therapeutic options in the quest to prevent a diabetes diagnosis.

What strategy could we implement to support a healthier microbiome and optimal butyrate production? The best place to begin would be the diet. Consuming a diet rich in a diversity of whole plant-based foods has been found to support a robust microbiome. The fibers in these foods provide substrate for butyrate-producing bacteria to thrive on. Of course, medications, mood, and Monsanto shouldn’t be ignored as potential contributors, as well. Experimentation with the probiotic strain VSL#3 has shown that this probiotic may improve diabetes by enhancing butyrate levels. But for now, the take home message is don’t forget whole, plant-based foods.

I can almost hear you saying, “Risë!  All that science and biology to get to that conclusion?”

Yep.

1. https://diabetesjournals.org/diabetes/article/66/5/1405/40728/Butyrate-Regulates-Liver-Mitochondrial-Function

2. Ibid.

3. https://pubmed.ncbi.nlm.nih.gov/34737725/

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