This study was designed to investigate postprandial responses to a mix
ed meal in simulated shift work conditions. Nine normal health subject
s (six males and three females) were studied on two occasions at the s
ame clock time (1330 h) after consuming test meals, first in their nor
mal environment and secondly after a 9 h phase advance (body clock tim
e 2230 h). Plasma glucose, insulin, glucose-dependent insulinotropic p
olypeptide (GIP), glucagon-like peptide-1 (GLP-1), triacylglycerol (TA
G) and non-esterified fatty acids (NEFAs) were determined at intervals
for 6 h after each test meal. Postprandial. plasma glucose, insulin,
GIP and GLP-1 profiles were evaluated by calculating areas under the c
urve (AUG) for the first 2 h and the last 4 h of the sampling together
with total AUC. Significantly higher postprandial glucose responses (
total AUC) were observed after the phase shift than before (AUC 0-360
min, 2.01 (1.51-2.19) vs 1.79 (1.56-2.04) mmol/l.min; P<0.02; mean (ra
nge)). No significant difference was observed wh en the first 2 h of e
ach response was compared, but significantly higher glucose levels wer
e observed in the last 4 h of the study after the phase shift than bef
ore (AUC 120-360 min, 1.32 (1.08-1.42) vs 1.16 (1.00-1.28) mmol/l.min;
P<0.05). Similar results were obtained for insulin (AUG 0-360 min, 81
.72 (30.75-124.97) vs 58.98 (28.03-92.57) pmol/l.min; P<0.01; AUC 120-
360 min, 40.73 (16.20-65.25) vs 25.71 (14.25-37.33) pmol/l.min; P<0.02
). No differences were observed in postprandial plasma GIP and GLP-1 r
esponses before and after the phase shift. Postprandial circulating li
pid levels were affected by phase shifting. Peak plasma TAG levels occ
urred 5 h postprandially before the phase shift. Postprandial rises in
plasma TAG were significantly delayed after the phase shift and TAG l
evels continued to rise throughout the study. Plasma postprandial NEFA
levels fell during the first 3 h both before and after the phase shif
t. Their rate of return to basal levels was significantly delayed afte
r the phase shift compared with before. This study demonstrates that a
simulated phase shift can significantly alter pancreatic B-cell respo
nses and postprandial glucose and lipid metabolism.