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Later eating start time associated with worse glycaemic parameters and higher body fat in prediabetes.

Later eating start time associated with worse glycaemic parameters and higher body fat in prediabete…
Photo by Sasun Bughdaryan / Unsplash
Key Takeaway
Note that later eating start times associate with worse glycaemic metrics in prediabetes, but causality remains unproven.

This observational study evaluated 297 individuals with prediabetes, defined as impaired fasting glucose or impaired glucose tolerance. The cohort had a mean age of 59.5 years and a mean BMI of 31.3 kg/m2. The primary exposure was the timing of the eating start (ES), compared against an earlier eating start time. Outcomes included various glycaemic parameters and measures of body composition.

The analysis revealed that each later hour of eating start was associated with higher fasting insulin (0.88 mU/l per hour; 95% CI, 0.13 to 1.64 mU/l) and higher 120-minute insulin (16.17 mU/l per hour; 95% CI, 5.91 to 26.44 mU/l). Additionally, AUC insulin increased by 1061 mU/l*min per hour (95% CI, 357 to 1764 mU/l*min), while HOMA-IR rose by 0.30 units per hour (95% CI, 0.10 to 0.50). Conversely, the Matsuda insulin sensitivity index decreased by 0.15 units per hour (95% CI, -0.28 to -0.02).

Regarding body composition, individuals with a later eating start exhibited increased body fat percentage (0.81% per hour; 95% CI, 0.27 to 1.34%). No associations were found for visceral fat or liver fat. No adverse events or discontinuations were reported, as tolerability data were not collected. The study was supported by the Deutsche Forschungsgemeinschaft and other German research bodies.

Key limitations include the observational nature of the design, which precludes causal inference regarding eating timing and metabolic outcomes. The study phase was not reported, and follow-up duration was not specified. While earlier eating start times may relate to improved glucose metabolism and lower progression risk, clinicians should interpret these findings as associations rather than definitive clinical recommendations for dietary timing interventions.

Study Details

EvidenceLevel 5
PublishedApr 2026
View Original Abstract ↓
BackgroundPrediabetes is associated with an increased risk of progression to type 2 diabetes. While dietary interventions in prediabetes traditionally focus primarily on energy and macronutrient intake, the role of eating timing has recently been highlighted. This study aimed to examine the relationships between eating timing pattern and glycaemic parameters in prediabetes. Methods297 individuals with prediabetes, i.e. impaired fasting glucose or impaired glucose tolerance (age 59.5 y, BMI 31.3 kg/m2), underwent detailed metabolic phenotyping including an oral glucose tolerance test and magnetic resonance imaging/spectroscopy. Parameters of temporal eating pattern (eating timing, daily calorie distribution, and meal number) were extracted from four-day food records. Eating start (ES) was defined as the start of the first caloric event of the day. ResultsAmong eating timing parameters, ES showed the most associations with glycaemic traits. Each later hour of ES was associated with a 0.88 mU/l higher fasting insulin (95% CI, 0.13 to 1.64 mU/l), a 16.17 mU/l higher 120 min insulin (95% CI, 5.91 to 26.44 mU/l), a 1061 mU/l*min higher AUC insulin (95% CI, 357 to 1764 mU/l*min),a 0.30 units higher HOMA-IR (95% CI, 0.10 to 0.50), and a -0.15 units lower Matsuda insulin sensitivity index (95% CI, -0.28 to -0.02) after adjustment for age, sex, and daily energy intake, as well as food composition. Glycemic associations remained after additional adjustment for body fat percentage, which was increased in individuals with later ES (0.81% per ES hour; 95% CI, 0.27 to 1.34%). No associations of eating timing with visceral or liver fat were found. ConclusionLate ES is associated with estimates of hyperinsulinemia and lower insulin sensitivity in prediabetes, independent of energy intake, food composition, and body fat. Earlier ES might relate to improved glucose metabolism and lower the risk of progression to diabetes. FundingThis work was supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation, RA 3340/4-1 to OP-R, project number 530918029). The DZD is funded by the German Federal Ministry for Education and Research (BMBF, funding code 01GI0925). KM was supported by the Competence Cluster Nutrition Research Berlin-Potsdam, funded by the Federal Ministry of Education and Research (BMBF, funding code 01EA1408) and by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) - TRR 412/1 - project number 535081457. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=79 SRC="FIGDIR/small/25342809v2_ufig1.gif" ALT="Figure 1"> View larger version (24K): [email protected]@1dad8eborg.highwire.dtl.DTLVardef@d73fb7org.highwire.dtl.DTLVardef@19829a9_HPS_FORMAT_FIGEXP M_FIG C_FIG
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