TY - JOUR
T1 - THU308 Metabolic And Neuroendocrine Adaptability Following One Night Of Partial Sleep Restriction In Dutch Males
AU - Pelsma, Iris
AU - van den Berg, Rosa
AU - Kooijman, Sander
AU - Snel, Marieke
AU - Zhu, Gewei
AU - Moore, Alison
AU - Pople, Jenny
AU - Lavrijsen, Sjan
AU - Birch-Machin, Mark
AU - Bhogal, Ranjit
AU - El ghalbzouri, Abdoelwaheb
AU - Martinez-Tellez, Borja
AU - Giesbrecht, Timo
AU - Kersten, Sander
AU - van Weeghel, Michiel
AU - Cornelis meijer, Onno
AU - Pereira Arias, Alberto
AU - Gunn, David
AU - Rensen, Patrick
AU - Biermasz, Nienke
PY - 2023/10/5
Y1 - 2023/10/5
N2 - Introduction: Chronic and acute short sleep associate with many adverse effects. Metabolic and neuroendocrine effects during the day following short sleep, however, are unknown. Methods: Randomized cross-over study using short sleep (4h) vs normal sleep (8h) in 31 males (31 years (IQR 23-47, BMI 26.0±4.2 kg/m2 (range 20.1-35.0). Glucose, lipid, incretin, ACTH, and cortisol levels, as well as respiratory exchange ratio (RER; indirect calorimetry) were assessed following standardized mixed meals. RNAseq of morning skeletal muscle biopsies and pathway analysis on differentially expressed genes was performed. Results: Short sleep increased fasting free fatty acids (0.34 mmol/L (IQR 0.26 - 0.38) vs 0.47 mmol/L (IQR 0.38 - 0.70), P<0.0001). Cortisol levels peaked upon early wake-up, which eliminated a peak at normal wake-up. Morning postprandial glucose peaked later (time P<0.001, levels P=0.106, pattern P=0.031), whilst insulin was unaffected. Afternoon postprandial insulin was lowered (time P<0.001, levels P=0.044, pattern P=0.419), whilst glucose was unaffected. Morning and afternoon postprandial TC, and LDL-c were lowered (morning: TC, time P<0.0001, levels P=0.009, pattern P=0.289; LDL-c, time P<0.001, levels P=0.038, pattern P=0.797; afternoon: TC, time P<0.001, levels P=0.007, pattern P=0.92; LDL-c, time P<0.001, levels P=0.055, pattern P=0.991). Pathway analysis of muscle revealed increased fatty acid oxidation (FAO), reflected by increased Oxidative Phosphorylation and Mitochondrial Dysfunction pathways, accompanied by lowered fasting RER (0.87 (IQR 0.86 - 0.92) vs 0.86 (IQR 0.84 - 0.87), P=0.0033). Conclusions: Acute partial sleep restriction subtly and temporarily changed glucose dynamics (morning), and insulin levels (afternoon), and lowered TC and LDL-c levels in the morning and afternoon, with concurrent increased FAO and mitochondrial dysfunction pathways in skeletal muscle, and calorimetric shifting from glucose towards lipid oxidation (fasted and postprandial), potentially highlighting increased delipidation of chylomicrons following sleep restriction.
AB - Introduction: Chronic and acute short sleep associate with many adverse effects. Metabolic and neuroendocrine effects during the day following short sleep, however, are unknown. Methods: Randomized cross-over study using short sleep (4h) vs normal sleep (8h) in 31 males (31 years (IQR 23-47, BMI 26.0±4.2 kg/m2 (range 20.1-35.0). Glucose, lipid, incretin, ACTH, and cortisol levels, as well as respiratory exchange ratio (RER; indirect calorimetry) were assessed following standardized mixed meals. RNAseq of morning skeletal muscle biopsies and pathway analysis on differentially expressed genes was performed. Results: Short sleep increased fasting free fatty acids (0.34 mmol/L (IQR 0.26 - 0.38) vs 0.47 mmol/L (IQR 0.38 - 0.70), P<0.0001). Cortisol levels peaked upon early wake-up, which eliminated a peak at normal wake-up. Morning postprandial glucose peaked later (time P<0.001, levels P=0.106, pattern P=0.031), whilst insulin was unaffected. Afternoon postprandial insulin was lowered (time P<0.001, levels P=0.044, pattern P=0.419), whilst glucose was unaffected. Morning and afternoon postprandial TC, and LDL-c were lowered (morning: TC, time P<0.0001, levels P=0.009, pattern P=0.289; LDL-c, time P<0.001, levels P=0.038, pattern P=0.797; afternoon: TC, time P<0.001, levels P=0.007, pattern P=0.92; LDL-c, time P<0.001, levels P=0.055, pattern P=0.991). Pathway analysis of muscle revealed increased fatty acid oxidation (FAO), reflected by increased Oxidative Phosphorylation and Mitochondrial Dysfunction pathways, accompanied by lowered fasting RER (0.87 (IQR 0.86 - 0.92) vs 0.86 (IQR 0.84 - 0.87), P=0.0033). Conclusions: Acute partial sleep restriction subtly and temporarily changed glucose dynamics (morning), and insulin levels (afternoon), and lowered TC and LDL-c levels in the morning and afternoon, with concurrent increased FAO and mitochondrial dysfunction pathways in skeletal muscle, and calorimetric shifting from glucose towards lipid oxidation (fasted and postprandial), potentially highlighting increased delipidation of chylomicrons following sleep restriction.
U2 - 10.1210/jendso/bvad114.743
DO - 10.1210/jendso/bvad114.743
M3 - Abstract
SN - 2472-1972
VL - 7
JO - Journal of the Endocrine Society
JF - Journal of the Endocrine Society
IS - Supplement_1
M1 - A401
ER -