Anu Sharma1, Marcello C Laurenti2, Chiara Dalla Man2, Ron T Varghese1, Claudio Cobelli2, Robert A Rizza1, Aleksey Matveyenko3, Adrian Vella4. 1. Endocrine Research Unit, Department of Endocrinology, Diabetes and Nutrition, Mayo Clinic College of Medicine, 200 First St SW, 5-194 Joseph, Rochester, MN, 55905, USA. 2. Department of Information Engineering, University of Padua, Padua, Italy. 3. Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA. 4. Endocrine Research Unit, Department of Endocrinology, Diabetes and Nutrition, Mayo Clinic College of Medicine, 200 First St SW, 5-194 Joseph, Rochester, MN, 55905, USA. vella.adrian@mayo.edu.
Abstract
AIMS/HYPOTHESIS: Shift-work is associated with circadian rhythm disruption and an increased risk of obesity and type 2 diabetes. We sought to determine the effect of rotational shift-work on glucose metabolism in humans. METHODS: We studied 12 otherwise healthy nurses performing rotational shift-work using a randomised crossover study design. On each occasion, participants underwent an isotope-labelled mixed meal test during a simulated day shift and a simulated night shift, enabling simultaneous measurement of glucose flux and beta cell function using the oral minimal model. We sought to determine differences in fasting and postprandial glucose metabolism during the day shift vs the night shift. RESULTS:Postprandial glycaemic excursion was higher during the night shift (381±33 vs 580±48 mmol/l per 5 h, p<0.01). The time to peak insulin and C-peptide and nadir glucagon suppression in response to meal ingestion was also delayed during the night shift. While insulin action did not differ between study days, the beta cell responsivity to glucose (59±5 vs 44±4 × 10-9 min-1; p<0.001) and disposition index were decreased during the night shift. CONCLUSIONS/ INTERPRETATION:Impaired beta cell function during the night shift may result from normal circadian variation, the effect of rotational shift-work or a combination of both. As a consequence, higher postprandial glucose concentrations are observed during the night shift.
RCT Entities:
AIMS/HYPOTHESIS: Shift-work is associated with circadian rhythm disruption and an increased risk of obesity and type 2 diabetes. We sought to determine the effect of rotational shift-work on glucose metabolism in humans. METHODS: We studied 12 otherwise healthy nurses performing rotational shift-work using a randomised crossover study design. On each occasion, participants underwent an isotope-labelled mixed meal test during a simulated day shift and a simulated night shift, enabling simultaneous measurement of glucose flux and beta cell function using the oral minimal model. We sought to determine differences in fasting and postprandial glucose metabolism during the day shift vs the night shift. RESULTS: Postprandial glycaemic excursion was higher during the night shift (381±33 vs 580±48 mmol/l per 5 h, p<0.01). The time to peak insulin and C-peptide and nadir glucagon suppression in response to meal ingestion was also delayed during the night shift. While insulin action did not differ between study days, the beta cell responsivity to glucose (59±5 vs 44±4 × 10-9 min-1; p<0.001) and disposition index were decreased during the night shift. CONCLUSIONS/ INTERPRETATION: Impaired beta cell function during the night shift may result from normal circadian variation, the effect of rotational shift-work or a combination of both. As a consequence, higher postprandial glucose concentrations are observed during the night shift.
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