# Impact of Acute (Poly)Phenol-Rich Sugarcane Extract Consumption on Postprandial Glycemic Response in Healthy Adults: A Randomized Crossover Study

**Authors:** Ulluwis H. A. J. Hewawansa, Elizabeth Barber, Michael J. Houghton, Rizliya Visvanathan, Luca Nicolotti, Ricardo J. S. Costa, Gary Williamson

PMC · DOI: 10.3390/foods15040631 · 2026-02-10

## TL;DR

This study found that sugarcane extract had minor effects on blood sugar and insulin levels in healthy people, with some enzyme activity changes.

## Contribution

The study explores the acute effects of sugarcane (poly)phenol-rich extract on postprandial glucose and insulin responses in healthy adults.

## Key findings

- PRSE had minor impact on postprandial glucose and insulin levels in healthy volunteers.
- Low-dose PRSE delayed insulin peak by 30 minutes without altering HOMA-IR.
- PRSE inhibited α-glucosidases in vitro but enhanced α-amylase activity.

## Abstract

Background: Effects on insulin sensitivity and postprandial glycemia through enzyme inhibition and regulation of glucose transport have been extensively researched; however, the role of sugarcane (poly)phenols remain underexplored. Methods: In a randomized, placebo-controlled, single-blinded crossover study, 12 healthy participants consumed a bread-based meal containing 50 g of carbohydrates, supplemented with either 0.5% or 5% liquid PRSE or sugar-balanced controls. Glucose and plasma insulin levels were assessed over 180 min. The extract was evaluated for its inhibitory effect on human α-amylases (salivary and pancreatic) and α-glucosidases (sucrase, maltase, and isomaltase) utilizing solid PRSE. Results: The postprandial glucose and insulin responses to bread sandwiches in healthy volunteers remained unchanged by both PRSE dosages. High-dose treatment reduced the Matsuda index by 9.8%, perhaps due to a subtle alteration in whole-body insulin sensitivity. Low-dose intervention postponed the insulin peak by 30 min without altering HOMA-IR. In vitro, PRSE diminished sucrase activity by 67% (IC50 = 425.8 ± 18.7 µg/mL) and lowered maltase and isomaltase activity by 40% (IC25 = 876.3 ± 131 and 960.6 ± 95.2 µg/mL, respectively). It enhanced the activity of human salivary and pancreatic α-amylases. Conclusion: In healthy people, acute PRSE supplementation had a minor impact on postprandial glucose and insulin levels. Low-dose PRSE postponed the insulin peak, whereas high-dose PRSE reduced Matsuda index potentially via α-amylase activation, suggesting a modest alteration in whole-body insulin sensitivity without significantly changing the glucose or insulin response. In vitro, PRSE exhibited modest inhibition of human α-glucosidases.

## Linked entities

- **Proteins:** LOC102577737 (uncharacterized LOC102577737), LOC4341824 (probable alpha-glucosidase Os06g0675700)
- **Chemicals:** glucose (PubChem CID 5793), insulin (PubChem CID 70678557)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, SI (sucrase-isomaltase) [NCBI Gene 6476], SLC2A4 (solute carrier family 2 member 4) [NCBI Gene 6517] {aka GLUT4}, AMY2A (amylase alpha 2A) [NCBI Gene 279] {aka AMY2, PA}
- **Diseases:** injury to (MESH:D014947), metabolic syndrome (MESH:D024821), impaired glucose homeostasis (MESH:D044882), diabetic (MESH:D003920), colon adenocarcinoma (MESH:D003110), metabolic diseases (MESH:D008659), insulin secretory defect (MESH:D008579), carbohydrate malabsorption (MESH:D008286), MI (MESH:C566784), Insulin Resistance (MESH:D007333), gastrointestinal conditions (MESH:D005767), type 2 diabetes (MESH:D003924), impaired glucose tolerance (MESH:D018149)
- **Chemicals:** 4-hydroxybenzaldehyde (MESH:C011483), sugar (MESH:D000073893), salicylic acid (MESH:D020156), gallic acid (MESH:D005707), methanol (MESH:D000432), acetonitrile (MESH:C032159), monosaccharide (MESH:D009005), lactose (MESH:D007785), 3-coumaric acid (MESH:C043332), Nobiletin (MESH:C008661), polyols (MESH:C024617), Maltoheptaose (MESH:C031146), EDTA (MESH:D004492), methane (MESH:D008697), butter (MESH:D002079), vanillin (MESH:C100058), phenolic acids (MESH:C017616), ferulic acid (MESH:C004999), disaccharide (MESH:D004187), streptozotocin (MESH:D013311), Apigenin (MESH:D047310), water (MESH:D014867), Phenol (MESH:D019800), metformin (MESH:D008687), Blood Glucose (MESH:D001786), isomaltose (MESH:D007534), 4-hydroxybenzoic acid (MESH:C038193), gentisic acid (MESH:C010925), oligosaccharide (MESH:D009844), sodium (MESH:D012964), acarbose (MESH:D020909), CFEs (-), maltose (MESH:D008320), alloxan (MESH:D000496), starch (MESH:D013213), carbohydrate (MESH:D002241), chloroform (MESH:D002725), sucrose (MESH:D013395), fructose (MESH:D005632), (poly)phenol (MESH:D059808), tricin (MESH:C017769), cobalt (MESH:D003035), neochlorogenic acid (MESH:C473200), Glucose (MESH:D005947), chlorogenic acid (MESH:D002726), flavonoids (MESH:D005419), calcium (MESH:D002118), luteolin (MESH:D047311), caffeic acid (MESH:C040048), hydrogen (MESH:D006859)
- **Species:** Saccharomyces cerevisiae (baker's yeast, species) [taxon 4932], Saccharum officinarum (noble cane, species) [taxon 4547], Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]
- **Cell lines:** TC7 — Homo sapiens (Human), Colon carcinoma, Cancer cell line (CVCL_S881), Caco-2 — Homo sapiens (Human), Colon adenocarcinoma, Cancer cell line (CVCL_0025), Caco-2/TC7 — Homo sapiens (Human), Colon adenocarcinoma, Cancer cell line (CVCL_0233)

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12939605/full.md

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Source: https://tomesphere.com/paper/PMC12939605