Diurnal Variation and Impairment of Postprandial Glucose-Insulin Responses and Lipid Rhythms in Simulated Shift Work.

Authors

Ameena M Khan Sullivan, Cheryl M Isherwood, Hana Hassanin, Debra J Skene, Daan R van der Veen

Published in

Nutrition bulletin. Jun 21, 2026. Epub Jun 21, 2026.

Abstract

Shift work is associated with insulin resistance, dyslipidaemia and metabolic syndrome, but how consecutive meals at the same clock times differentially shape postprandial metabolism in day- and night-shifts remains unclear. This study used a unique simulated shift work intervention with four consecutive meals and high-resolution sampling to examine interactions of endogenous rhythms and behavioural timing on postprandial metabolism. Nine healthy non-shift-worker participants (age 21-33 years, 3 females) completed a strictly-controlled laboratory protocol with a day-shift followed by two night-shifts of 10-h delayed sleep and mealtimes. Participants consumed four identical, isoenergetic, mixed-composition meals per shift. Three of four mealtimes (08:00, 18:00, 22:00) were fixed across conditions; the first and last meals were 1 h after waking and before bedtime. Plasma glucose, insulin, triglycerides, HDL-cholesterol and total cholesterol were measured hourly, with continuous interstitial glucose monitoring. Subjective hunger and appetite were assessed throughout. Plasma lipid rhythms shifted with the 10-h delay in sleep-wake times: acrophases delayed ~10-13 h and amplitudes lowered 46%-54% (all p < 0.01). Night-shifts elevated postprandial glucose (+165 mmol/L·min, 95% CI 1.05-34.31, p = 0.05) and insulin (+7678.7 mmol/L·min, 95% CI 3671.02-11686.38, p < 0.01). Time-of-day effects persisted irrespective of shift, with 18:00 meals producing the highest glycaemic responses (+261 mmol/L·min, 95% CI 124.37-398.01, p < 0.01). Insulin dynamics did not fully compensate for elevated glycaemia in night-shifts, indicating lower glucose tolerance and insulin sensitivity. Mistimed meals suggest a mechanism by which circadian disruption may increase metabolic disease risk.

PMID:
42324738
Bibliographic data and abstract were imported from PubMed on 22 Jun 2026.

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