This 2023 rodent study compared a high-fat high-sugar diet’s deleterious effects with adding ten bioactive dietary fibers vs. adding the weight-loss pill Orlistat vs. a normal diet:

“Different dietary fibers supplementation improved obesity in rats with diversely positive responses, improvement of dyslipidemia, serum hormone, serum metabolome, and gut microbiota disorders.

Model group ate 66.5% normal chow diet, 10% lard, 20% sucrose, 2.5% cholesterol and 1% sodium cholate. Normal group ate normal chow.

Treatment groups ate high-fat high-sugar diet plus 270 mg/kg each of either barley β-glucan, glucomannan, arabinoxylan, inulin, guar gum, xanthan gum, carrageenan, apple pectin, arabinogalactan, or xylan dietary fibers. Orlistat (Y) supplementation was equivalent to 120 mg taken 3 times per day for 70 kg humans.

We found that supplementation with β-glucan, arabinoxylan, xanthan gum, guar gum, apple pectin, carrageenan, inulin, and xylan significantly reduced body weight and dyslipidemia, whereas glucomannan and arabinogalactan did not. Apple pectin, β-glucan and arabinoxylan improved the most biomarkers (15, 17 and 18 kinds) relevant to obesity.

Most dietary fibers improved physiological indicators which have a risk with obesity, including accumulation of body fat, dyslipidemia, glucose metabolic abnormality, oxidative stress, and adipocytokines secreted by adipose tissue, while β-glucan reversed almost all physiological indicators. Consequently, intake of β-glucan could be considered as therapy for obesity management induced by high fat diet.”

https://www.sciencedirect.com/science/article/abs/pii/S0268005X23001637 “Different dietary fibers unequally remodel gut microbiota and charge up anti-obesity effects” (not freely available). Thanks to Dr. Jiajia Wen for providing a copy.

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A human equivalent to this study’s 270 mg/kg daily dietary fiber intake is (270 mg x .162) x 70 kg = 3062 mg. I eat > 4 grams of oat β-glucan daily, and much less than that of orange pectin. No human will eat > 10 grams of inulin every day without having severe gastrointestinal adverse effects.

I didn’t curate this study’s gut microbiota findings because it used fecal samples. Per Measuring gut microbiota, Part 1 and Part 2, fecal microbiota don’t adequately represent gut microbiota in either the entire gastrointestinal tract, or in any section of it.

Replicating other studies’ fecal microbiota findings doesn’t advance science when these don’t define subjects’ gastrointestinal tract situations. More work is needed to improve methods of investigating gut microbiota.