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Diurnal Variation and Impairment of Postprandial Glucose-Insulin Responses and Lipid Rhythms in Simulated Shift Work
Ameena M Khan Sullivan1, Cheryl M Isherwood1, Hana Hassanin2,3
1Section of Chronobiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK.
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.
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