The gut microbiome and blood sugar: what bacteria have to do with insulin
Trillions of bacteria in the large intestine work on what digestion leaves behind. What they produce reaches all the way into glucose metabolism — through a mechanism that is now well described.
Translated from the German original. In case of doubt, the German version applies.
The microbiome is a topic surrounded by marketing noise. Between probiotic advertising and stool-test offers, what is actually supported gets lost. Yet there is a well-studied pathway that can be used in practice — and it has nothing to do with expensive products.
The mechanism: short-chain fatty acids
Fibre consists of carbohydrates the small intestine cannot break down. It reaches the large intestine undigested — and that is where the real work begins. Bacteria ferment it, producing short-chain fatty acids: mainly acetate, propionate and butyrate.
These fatty acids are not waste products but signalling molecules. They bind to receptors in the gut wall and trigger the release of GLP-1 and peptide YY — the same satiety and blood-sugar hormones that modern diabetes medications target. Butyrate additionally serves the cells of the gut lining as their main energy source and strengthens the barrier function of the gut wall.
The cycle in one sentence
Fibre feeds the bacteria → bacteria produce short-chain fatty acids → these trigger GLP-1 and improve insulin sensitivity → the gut barrier becomes more stable and low-grade inflammation decreases.
What the studies show
A randomised trial published in Science is particularly instructive here. Participants with type 2 diabetes received a deliberately high-fibre diet. The result: specific bacterial strains that produce short-chain fatty acids increased — and where this group was more diverse and more abundant, HbA1c improved more markedly. This was mediated in part by increased GLP-1 production.
At the same time, bacteria producing metabolically unfavourable compounds declined. So this is not simply about “more good bacteria” but about a shift in the whole ecosystem.
Meta-analyses of randomised trials confirm the direction: fermentable fibres — inulin, resistant starch, beta-glucan, arabinoxylan — reduce fasting glucose, HbA1c and insulin-resistance indices, and dampen inflammatory markers.
What follows in practice
The good news: the effective lever is not expensive. It is food, not capsules.
- Variety beats quantity. Different types of fibre feed different bacteria. Pulses, vegetables, nuts, seeds and wholegrains complement each other.
- Use resistant starch. It forms when starchy foods are cooked and cooled again — cooled potatoes or yesterday’s pulses are a simple example.
- Increase gradually. Suddenly doubling fibre intake reliably causes bloating. The bacterial community needs weeks to adapt.
- Drink enough. Fibre binds water; without sufficient fluid the effect on digestion reverses.
What I observe
The clearest effect I see in my CGM is not the next morning’s reading but the shape of the curve after a meal: with a high fibre share it rises more gently and falls more evenly. The peak is lower, even though the amount of carbohydrate is comparable.
Note: Single-case observation (n = 1) from my own CGM data. Not transferable and no substitute for medical advice.
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Sources
Sources as of: 22 Jul 2026.
- Randomised trial: a deliberately high-fibre diet promotes specific SCFA-producing bacteria; better HbA1c outcomes mediated via GLP-1. Science (2018) (opens in a new window)
- Review of short-chain fatty acids as the link between microbiome and glucose metabolism. PMC (opens in a new window)
- Relationship between gut microbiota, short-chain fatty acids and type 2 diabetes; the role of dietary fibre. Acta Diabetologica / PMC (opens in a new window)
- Systematic review and meta-analysis: effect of dietary fibre on microbiota, lipid profile and inflammatory markers in type 2 diabetes. PMC (opens in a new window)