Declines in plasma erythritol levels and improvements in insulin sensitivity and glucose metabolism: POUNDS lost trial.

Authors

Yoriko Heianza, Jennifer C Rood, Catherine M Champagne, Frank B Hu, George A Bray, Frank M Sacks, Lu Qi

Published in

International journal of obesity (2005). Jul 21, 2026. Epub Jul 21, 2026.

Abstract

Erythritol is a non-nutritive sweetener that is also endogenously produced from glucose. We investigated whether declines in plasma erythritol and other sugar alcohols (polyols) in response to weight-loss dietary interventions were significantly associated with long-term improvements in glucose metabolism and insulin sensitivity.
Plasma erythritol, mannitol/sorbitol, and arabitol/xylitol were repeatedly measured among adults with overweight or obesity who participated in the POUNDS Lost trial (n = 802 at baseline and n = 664 at 6 months). We analyzed associations of changes in erythritol, mannitol/sorbitol, and arabitol/xylitol from baseline to 6 months with changes in homeostasis model assessment of insulin resistance (HOMA-IR), fasting insulin, fasting glucose, and HbA1c at 6 months and 2 years of intervention.
Plasma erythritol levels were positively related to HOMA-IR, fasting insulin, and glycemic markers at baseline. Greater declines in plasma erythritol in response to the interventions were associated with greater reductions in HOMA-IR (p < 0.001) and fasting insulin (p < 0.001) at 6 months. Similar associations were found for changes in arabitol/xylitol, but not for mannitol/sorbitol. Every 1 SD reduction in plasma erythritol during the initial 6-month period was related to long-term (2-year) decreases in log-transformed HOMA-IR (β [SE] -0.07 [0.02], p = 0.008) and glycemic markers (β -1.0 [0.44] mg/dL, p = 0.025 for fasting glucose; β -0.05% [0.02%], p = 0.019 for HbA1c).
Declines in plasma erythritol may be related to long-term improvements in insulin sensitivity and glycemic status during weight-loss dietary interventions in adults with overweight or obesity.

PMID:
42477477
Bibliographic data and abstract were imported from PubMed on 21 Jul 2026.

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