OBJECTIVE: Epidemiological studies show the association of sleep restriction (SR) with obesity and insulin resistance. Experimental studies are limited to the concurrent or short-term effects of SR. Here, we examined the late effects of SR regarding weight gain and metabolic alterations induced by a high-fat diet (HFD). METHODS: C57BL/6 mice were subjected to a multiple platform method of SR for 15 days, 21 h daily, followed by 6 weeks of a 30% HFD. RESULTS: Just after SR, serum insulin and resistin concentrations were increased and glycerol content decreased. In addition, resistin, TNF-α, and IL-6 mRNA expression were notably increased in epididymal fat. At the end of the HFD period, mice previously submitted to SR gained more weight (32.3 ± 1.0 vs. 29.4 ± 0.7 g) with increased subcutaneous fat mass, had increments in the expression of the adipogenic genes PPARγ, C/EBPα, and C/EBPβ, and had macrophage infiltration in the epididymal adipose tissue. Furthermore, enhanced glucose tolerance and insulin resistance were also observed. CONCLUSIONS: The consequences of SR may last for a long period, characterizing SR as a predisposing factor for weight gain and insulin resistance. Metabolic changes during SR seem to prime adipose tissue, aggravating the harmful effects of diet-induced obesity.
OBJECTIVE: Epidemiological studies show the association of sleep restriction (SR) with obesity and insulin resistance. Experimental studies are limited to the concurrent or short-term effects of SR. Here, we examined the late effects of SR regarding weight gain and metabolic alterations induced by a high-fat diet (HFD). METHODS: C57BL/6 mice were subjected to a multiple platform method of SR for 15 days, 21 h daily, followed by 6 weeks of a 30% HFD. RESULTS: Just after SR, serum insulin and resistin concentrations were increased and glycerol content decreased. In addition, resistin, TNF-α, and IL-6 mRNA expression were notably increased in epididymal fat. At the end of the HFD period, mice previously submitted to SR gained more weight (32.3 ± 1.0 vs. 29.4 ± 0.7 g) with increased subcutaneous fat mass, had increments in the expression of the adipogenic genes PPARγ, C/EBPα, and C/EBPβ, and had macrophage infiltration in the epididymal adipose tissue. Furthermore, enhanced glucose tolerance and insulin resistance were also observed. CONCLUSIONS: The consequences of SR may last for a long period, characterizing SR as a predisposing factor for weight gain and insulin resistance. Metabolic changes during SR seem to prime adipose tissue, aggravating the harmful effects of diet-induced obesity.
Authors: Edson M de Oliveira; Thais P Ascar; Jacqueline C Silva; Silvana Sandri; Silene Migliorini; Ricardo A Fock; Ana Campa Journal: Diabetologia Date: 2016-04-28 Impact factor: 10.122
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