TY - JOUR
T1 - Impaired postprandial fullness in Type 2 diabetic subjects is rescued by acute exercise independently of total and acylated ghrelin
AU - Knudsen, Sine H
AU - Karstoft, Kristian
AU - Solomon, Thomas
PY - 2013/9/1
Y1 - 2013/9/1
N2 - Knudsen SH, Karstoft K, Solomon TP. Impaired postprandial fullness in Type 2 diabetic subjects is rescued by acute exercise independently of total and acylated ghrelin. J Appl Physiol 115: 618-625, 2013. First published June 20, 2013; doi:10.1152/japplphysiol.00204.2013.-Ghrelin levels are suppressed in obese subjects and subjects with Type 2 diabetes mellitus (T2DM). Exercise-stimulated decreases in plasma ghrelin are a proposed mediator of exercise-induced satiety in healthy subjects. However, exercise-induced satiety and the impact of impaired ghrelin levels in obesity-related disease are poorly understood. Therefore our objective was to investigate exercise-induced postprandial satiety and ghrelin responses in overweight subjects with T2DM (N = 8) and healthy controls (N = 7). Visual analog scale satiety questionnaires (assessing hunger, thirst, food that could be eaten, nausea, and fullness) and circulating levels of glucose, insulin, and total and acylated ghrelin were measured at baseline and in response to a 75 g oral glucose load, provided immediately after an aerobic exercise bout (1 h at 50% Wmax) or no exercise (rest trial), on two separate occasions. Baseline levels of total (284.4 ± 15.9 and 397.6 ± 35.2 pmol/l) and acylated ghrelin (7.9 ± 1.0 and 13.7 ± 1.2 pmol/l) were lower in subjects with T2DM compared with healthy subjects (P < 0.05). In the rest trial, post- vs. preprandial feeling of fullness increased in healthy subjects but decreased in subjects with T2DM (healthy vs. T2DM; P < 0.05). Exercise increased postprandial fullness in the T2DM group (P < 0.05), while plasma ghrelin levels were unaffected. Our data suggest that the presence of T2DM likely drives suppressed ghrelin levels and poor appetite regulation, but a single exercise bout is sufficient to restore oral glucose-induced fullness independently of ghrelin.
AB - Knudsen SH, Karstoft K, Solomon TP. Impaired postprandial fullness in Type 2 diabetic subjects is rescued by acute exercise independently of total and acylated ghrelin. J Appl Physiol 115: 618-625, 2013. First published June 20, 2013; doi:10.1152/japplphysiol.00204.2013.-Ghrelin levels are suppressed in obese subjects and subjects with Type 2 diabetes mellitus (T2DM). Exercise-stimulated decreases in plasma ghrelin are a proposed mediator of exercise-induced satiety in healthy subjects. However, exercise-induced satiety and the impact of impaired ghrelin levels in obesity-related disease are poorly understood. Therefore our objective was to investigate exercise-induced postprandial satiety and ghrelin responses in overweight subjects with T2DM (N = 8) and healthy controls (N = 7). Visual analog scale satiety questionnaires (assessing hunger, thirst, food that could be eaten, nausea, and fullness) and circulating levels of glucose, insulin, and total and acylated ghrelin were measured at baseline and in response to a 75 g oral glucose load, provided immediately after an aerobic exercise bout (1 h at 50% Wmax) or no exercise (rest trial), on two separate occasions. Baseline levels of total (284.4 ± 15.9 and 397.6 ± 35.2 pmol/l) and acylated ghrelin (7.9 ± 1.0 and 13.7 ± 1.2 pmol/l) were lower in subjects with T2DM compared with healthy subjects (P < 0.05). In the rest trial, post- vs. preprandial feeling of fullness increased in healthy subjects but decreased in subjects with T2DM (healthy vs. T2DM; P < 0.05). Exercise increased postprandial fullness in the T2DM group (P < 0.05), while plasma ghrelin levels were unaffected. Our data suggest that the presence of T2DM likely drives suppressed ghrelin levels and poor appetite regulation, but a single exercise bout is sufficient to restore oral glucose-induced fullness independently of ghrelin.
U2 - 10.1152/japplphysiol.00204.2013
DO - 10.1152/japplphysiol.00204.2013
M3 - Journal article
C2 - 23788577
SN - 8750-7587
VL - 115
SP - 618
EP - 625
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 5
ER -