Allulose at 10g cuts postprandial glucose by 28%

Your blood sugar after a bowl of rice doesn't just depend on the rice. What you drink alongside it turns out to matter quite a bit. A paper published today in Nutrients adds fresh human data to that picture, though with caveats large enough to affect how much weight you put on the numbers. 1

The study tested four low-digestible carbohydrates (LDCs) — allulose, 1-kestose, resistant maltodextrin (RD), and fructo-oligosaccharide powder (FOP) — co-consumed with a carbohydrate-heavy reference meal. Each LDC produced a distinct acute metabolic response. Allulose produced the strongest glycemic signal: a 28% reduction in postprandial glucose incremental area under the curve (iAUC — the total glucose exposure above fasting baseline over 180 minutes) and a 29% reduction in insulin iAUC compared to the reference meal alone.

The study design

Noh et al. ran two separate acute crossover investigations, both conducted at the Glycemic Index Research Service (SUGiRS) at the University of Sydney. 1

Study 1 (n=10 healthy adults, age 27.4 ± 8.3 years, BMI 22.1 ± 1.9): tested allulose, 1-kestose, and RD as standalone drinks — each dissolved in 250 mL water at 25 g total carbohydrate — against a 25 g glucose control. Blood glucose was tracked for 120 minutes. All three LDCs held blood sugar near baseline, significantly below the glucose control (p < 0.05 for each), confirming that these compounds are genuinely low-glycemic on their own.

Study 2 (n=10 adults with elevated fasting glucose of 5.6–6.1 mmol/L, age 39.4 years, BMI 22.7) moved to a real-meal context: steamed Jasmine rice, peas, and soy sauce providing 77.8 g of available carbohydrate and 1,646 kJ. Each of the four LDCs was tested at 10 g dissolved in 250 mL water, consumed alongside the meal. Blood glucose, insulin, active GLP-1 (glucagon-like peptide-1), and subjective satiety were measured over 180 minutes. The design was single-blind and randomized; participants served as their own controls.

Both studies followed ISO 26642:2010 methodology — the standard protocol for glycemic index testing — and received ethics approval from the University of Sydney Human Research Ethics Committee.

Study design overview for both investigations. 1

What each LDC did — and didn't do

The four compounds produced strikingly different acute profiles, which is the most useful clinical takeaway from this paper. 1

LDC (10 g dose)	Glucose iAUC change	Insulin iAUC change	GLP-1 effect	Satiety effect
Allulose	−28% (163 vs. 227 mmol·min/L, p=0.0029)	−29% (13,956 vs. 19,797 pmol·min/L, p=0.0029)	+12% tAUC (p=0.042)	Not significant
1-Kestose	−18% (186 vs. 227 mmol·min/L, p=0.0195)	−16% (16,642 vs. 19,797 pmol·min/L, p=0.0098)	Not significant	Not significant
Resistant maltodextrin	Not significant (217 vs. 227)	Not significant (17,319 vs. 19,797)	Not significant	Significant increase (p=0.042)
FOP	Not significant (207 vs. 227)	Not significant (18,747 vs. 19,797)	Not significant	Not significant

Several things in this table deserve attention.

Allulose's glucose effect was detectable within the first 30 minutes: the reference meal alone raised blood sugar by Δ3.23 ± 0.20 mmol/L at that timepoint, whereas the meal plus allulose raised it by only Δ2.27 ± 0.23 mmol/L (p = 0.0061). The attenuation continued at 45 minutes (Δ2.05 ± 0.31 mmol/L, p = 0.0257). 1

1-kestose's benefit did not appear at any individual time point — it only emerged as a cumulative area reduction. The authors suggest this reflects "a more gradual and sustained attenuation of postprandial glycemia rather than an acute inhibitory effect," possibly through subtle modulation of intestinal transit time. 1

Resistant maltodextrin stands apart: it was the only LDC to significantly increase subjective satiety across the 30–180 minute measurement window (p = 0.042), and the authors attribute this to its high water-holding capacity as a soluble fiber — physical gastric distension rather than hormonal signaling. 1

FOP's null result on all outcomes is consistent with its biology: as a prebiotic fiber, it requires prolonged intake and gut fermentation to produce short-chain fatty acids, which are what eventually stimulate GLP-1. One meal's worth of FOP does nothing detectable acutely.

www.mdpi.com

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How allulose actually works

Allulose (also called D-psicose) is a rare sugar found naturally in small amounts in figs, raisins, and wheat. 1 It has about 70% the sweetness of sucrose but contributes only ~0.4 kcal/g because most of it passes through the small intestine unabsorbed.

The dual mechanism behind its glycemic effect has been characterized in prior research. Allulose competitively inhibits SGLT1 and GLUT2 — two intestinal glucose transporters — blocking a portion of glucose absorption at the gut wall. Simultaneously, it appears to stimulate GLP-1 secretion from enteroendocrine L-cells in the small intestine. GLP-1 slows gastric emptying and augments the glucose-dependent phase of insulin secretion. In this study, that GLP-1 signal was a 12% increase in tAUC over 180 minutes (8,136 ± 1,319 vs. 7,244 ± 1,151 pg·min/mL, p = 0.042). 1

The authors note that this physiological GLP-1 elevation is not equivalent to the receptor activation produced by GLP-1 receptor agonist drugs like semaglutide (Ozempic/Wegovy) — the magnitude differs by orders of magnitude, and the mechanism is nutritional, not pharmacological.

The insulin iAUC reduction of 29% is likely a downstream consequence of the glucose reduction rather than a direct insulinotropic effect — as the authors put it, "a direct consequence of the reduced glycemic stimulus, consistent with the glucose-dependent nature of insulin secretion." 1

Plasma glucose time-course in Study 2: reference meal (black), allulose (green), 1-kestose (blue), RD (red), FOP (purple). Allulose significantly attenuated glucose at 30 and 45 minutes. 1

How this fits the prior evidence on allulose

Tani et al. (2023, PLOS ONE) conducted a systematic review and meta-analysis of 8 RCTs with 145 participants and found allulose at ≤10 g per meal significantly reduced postprandial blood glucose AUC (SMD = −0.26, p = 0.03, I² = 0%). 2 That corresponds to roughly a 13–14% relative iAUC reduction — smaller than the 28% in Noh et al. 2026, though Tani's pooled estimate spans multiple study designs, carbohydrate loads, and populations.

The FDA granted allulose GRAS status (notices GRN #647, #693, #828) and in 2019 finalized guidance exempting it from "Total Sugars" and "Added Sugars" on Nutrition Facts labels, reflecting that its metabolic handling differs from conventional sugars. 1

The consistency of the glycemic signal across independent research groups gives the allulose finding more credibility than the single paper here warrants alone.

Limitations and a conflict of interest that changes the reading

This section is not a formality — it affects how much weight you should place on the 28% figure. 1

Funding and authorship: The study was funded by Samyang Corporation, the South Korean manufacturer of all four test compounds (allulose under the Nexweet® brand, resistant maltodextrin as Fiberest® HF, and crystalline 1-kestose). Six of the nine authors are Samyang employees with affiliations in Food R&D. The authors disclose that "the funder was involved in the study design and manuscript preparation." Two additional authors (F.A. and K.L.) work at SUGiRS, the commercial glycemic testing service where the study was conducted — a service that depends on industry contracts. The only author without a disclosed financial conflict is the corresponding author, Sanguine Byun at Yonsei University.

This does not mean the data are wrong. The measurements — blood glucose, insulin, GLP-1 — are objective and hard to manipulate in an obvious way. But funder involvement in study design and manuscript preparation is a known source of reporting bias (selective outcome emphasis, endpoint choice, framing of results). Readers should treat the effect sizes as hypothesis-generating rather than definitive, and weight them against the independent Tani 2023 meta-analysis above.

Sample size: Both studies enrolled n=10 participants. With this sample size, the study is underpowered to detect small effects, estimate effect sizes precisely, or identify subgroup differences. The significant p-values are real, but the 95% confidence intervals — which are not fully reported in the summary — will be wide. The pilot scale is appropriate for an exploratory study but requires replication in adequately powered independent trials.

Single-blind design: Participants could not be blinded to the test compound (they tasted the drinks), which may introduce expectation effects on subjective outcomes like satiety. Glycemic measurements are less susceptible to this.

Acute design only: No data exist from this study on chronic consumption, cumulative glycemic effects over weeks, gut microbiome modulation, or effects in people with diagnosed type 2 diabetes. The study's findings are acute snapshots.

Interindividual variability: The elevated-fasting-glucose population in Study 2 (n=10) spanned a narrow range (5.6–6.1 mmol/L). Effects in people with normal fasting glucose, frank insulin resistance, or type 2 diabetes are not characterized here.

The authors themselves call this an "exploratory investigation" and recommend "larger, double-blind, randomized controlled trials with subgroup analyses stratified by metabolic phenotype."

journals.plos.org

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The recommendation

The evidence does not support treating allulose as a therapeutic intervention for blood sugar management. What the data do support — consistent across this paper and the Tani 2023 meta-analysis — is that 10 g of allulose consumed with a carbohydrate-heavy meal produces a meaningful and reproducible reduction in postprandial glucose and insulin excursions in healthy and pre-diabetic adults.

The practical implication depends on who you are:

Health-conscious adults eating high-glycemic-index staples (white rice, bread, pasta) as dietary staples: adding 10 g of allulose to your cooking water or stirring it into a pre-meal drink is a low-cost, low-risk intervention with a replicated acute glycemic signal. Allulose is widely available as a baking and cooking sugar substitute; 10 g is approximately 2 teaspoons.
Clients with pre-diabetes or metabolic syndrome (the population closest to Study 2's participants): the glycemic benefit is consistent, but the COI and sample size issues mean this should supplement — not replace — evidence-based dietary strategies (carbohydrate moderation, fiber intake, meal timing, weight management).
Those primarily interested in satiety management: allulose is not the tool for that goal based on this data. Resistant maltodextrin (found in commercial fiber supplements and functional foods) is the better-supported option for acute fullness.
Anyone drawn to 1-kestose or FOP for acute glycemic control: the evidence does not support those uses. Both show either marginal or null acute effects; their value, if any, is chronic and prebiotic.

For dietitians advising clients who ask about allulose: the product exists, the regulatory approvals are real, the glycemic mechanism is biologically plausible and replicated in multiple independent studies. The study quality ceiling is still relatively low. Until an adequately powered, manufacturer-independent double-blind RCT is published, this is a reasonable but cautious option — worth discussing, not prescribing.

Cover image: AI-generated illustration.