期刊
PLOS ONE
卷 13, 期 9, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0200817
关键词
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资金
- Aarhus University, Denmark
- Ministry of Food, Agriculture and Fisheries of Denmark [3304-FSE-06-0505-01]
- Department of Clinical Medicine, Aarhus University [1727-210320]
- A.P. Moller Foundation for the Advancement of Medical Science [10-12]
- Danish Council for Research and Innovation [0603-00479B]
Insulin resistance is a well-known physiological adaptation to prolonged fasting in healthy skeletal muscle. Obesity is associated with insulin resistance and metabolic inflexibility in skeletal muscle, and a pronounced increase in the risk of metabolic complications. Under the hypothesis that the metabolic traits of insulin resistance associated with prolonged fasting are different from insulin resistance associated with obesity, we examined nine obese and nine lean participants during 12 and 72h of fasting, respectively. Insulin resistance in obese participants was associated with impaired insulin signaling, and reduced levels of glucose-6-phosphate and TCA-cycle intermediates. 72h of fasting in lean participants reduced insulin-stimulated glucose uptake to levels similar to obese participants fasted for 12h. This was associated with increased lipid oxidation, but not accumulation of diacylglycerol or acyl-carnitines and impairment of insulin signaling. Prolonged fasting was associated with pronounced increases in beta-hydroxybutyrate and beta- hydroxybutyrylcarnitine levels in skeletal muscle suggesting augmented ketone body metabolism. Fasting induced insulin resistance may be a consequence of substrate competition. The underlying mechanism behind insulin resistance in obesity is thus not comparable to the physiological adaptations in skeletal muscle induced by prolonged fasting in lean participants.
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