Based on the 2025 Nature Metabolism study: “Dietary fiber–adapted gut microbiome clears dietary fructose and reverses hepatic steatosis” by Jung et al.
If you asking what would be equivalent dose for humans comparing to the dose used in mice in the study I cited, the answer is that we do not know. Inulin is not approved by FDA as a medication; therefore such precise studies were not conducted to my knowledge. Inulin is regulated as a supplement, so less stringent criteria are applied to its use. Many consumer and professional resources recommend about 5–10 g/day, often split into 1–2 doses. Most guidance emphasizes starting low (2–3 g/day) and increasing gradually to minimize gas, bloating, or abdominal discomfort.
Do not forget, that food is always best source of nutrients. Many commonly eaten plant foods contain inulin, especially certain roots, bulbs, and whole grains:
Chicory root (often used to make “chicory coffee” or as chicory root fiber in foods)
Jerusalem artichoke (sunchoke)
Dandelion greens and dandelion root
Yacón root
Dahlia tubers and salsify (less common but very rich)
Garlic, onions, leeks, shallots, spring onions
Asparagus
Bananas (especially slightly green)
Jicama
Wheat and wheat bran; smaller amounts in barley, rye, and oats
This is a really elegant example of “food as metabolic engineering”, not just calories. Clinically, the gut–liver axis is where I see so much hidden pathology show up (NAFLD, high TGs, post-meal fatigue), and your explanation makes the mechanism intuitive: once fructose load exceeds small-intestinal handling capacity, the liver becomes the overflow tank, driving de novo lipogenesis, oxidative stress, and insulin resistance. What’s especially intriguing here is the training concept: inulin doesn’t “block sugar”, it reshapes microbial capacity so more fructose is cleared upstream before it reaches the liver. That’s a very different mental model than restriction-only approaches and it helps explain why consistent fiber patterns can change someone’s metabolic trajectory over months.
Two physician-level caveats for our longevity-focused readers:
1. This is strong mechanistic evidence (and very plausible), but it’s still largely mouse-to-human translation, so outcomes in people will depend on baseline diet, microbiome, and metabolic status.
2. Inulin can be symptom-provoking in IBS/FODMAP-sensitive folks; titrate slowly, start low, and “foods first” (onions/garlic/leeks/asparagus/Jerusalem artichoke) before jumping to higher-dose supplements.
Hopeful, practical, and a great reminder that improving sugar tolerance often starts with feeding the microbes that protect the liver, not just chasing willpower.
Whats the dosage for human equivalent of inulin
If you asking what would be equivalent dose for humans comparing to the dose used in mice in the study I cited, the answer is that we do not know. Inulin is not approved by FDA as a medication; therefore such precise studies were not conducted to my knowledge. Inulin is regulated as a supplement, so less stringent criteria are applied to its use. Many consumer and professional resources recommend about 5–10 g/day, often split into 1–2 doses. Most guidance emphasizes starting low (2–3 g/day) and increasing gradually to minimize gas, bloating, or abdominal discomfort.
Do not forget, that food is always best source of nutrients. Many commonly eaten plant foods contain inulin, especially certain roots, bulbs, and whole grains:
Chicory root (often used to make “chicory coffee” or as chicory root fiber in foods)
Jerusalem artichoke (sunchoke)
Dandelion greens and dandelion root
Yacón root
Dahlia tubers and salsify (less common but very rich)
Garlic, onions, leeks, shallots, spring onions
Asparagus
Bananas (especially slightly green)
Jicama
Wheat and wheat bran; smaller amounts in barley, rye, and oats
Another super article, much info that is useful
Thank You.
This is a really elegant example of “food as metabolic engineering”, not just calories. Clinically, the gut–liver axis is where I see so much hidden pathology show up (NAFLD, high TGs, post-meal fatigue), and your explanation makes the mechanism intuitive: once fructose load exceeds small-intestinal handling capacity, the liver becomes the overflow tank, driving de novo lipogenesis, oxidative stress, and insulin resistance. What’s especially intriguing here is the training concept: inulin doesn’t “block sugar”, it reshapes microbial capacity so more fructose is cleared upstream before it reaches the liver. That’s a very different mental model than restriction-only approaches and it helps explain why consistent fiber patterns can change someone’s metabolic trajectory over months.
Two physician-level caveats for our longevity-focused readers:
1. This is strong mechanistic evidence (and very plausible), but it’s still largely mouse-to-human translation, so outcomes in people will depend on baseline diet, microbiome, and metabolic status.
2. Inulin can be symptom-provoking in IBS/FODMAP-sensitive folks; titrate slowly, start low, and “foods first” (onions/garlic/leeks/asparagus/Jerusalem artichoke) before jumping to higher-dose supplements.
Hopeful, practical, and a great reminder that improving sugar tolerance often starts with feeding the microbes that protect the liver, not just chasing willpower.