Context: Energy balance and physical activity potentially influence systemic inflammation. Objective: Our objective was to test the hypothesis that moderate energy restriction may prevent activation of inactivity-induced inflammatory response. Design: Participants were studied four times at the end of 14-d periods of experimental bed rest or controlled ambulation, after receiving eucaloric or hypocaloric diets. Setting: The study was conducted at the clinical research center of the German Space Agency. Subjects: Nine healthy young volunteers participated. Interventions: Energy intake was calibrated to physical activity and decreased by about 20% in hypocaloric conditions. Main Outcome Measures: Changes in body fat by dual-energy x-ray absorptiometry as well as plasma inflammatory markers and cytokine mRNA levels in blood cells were measured. Results: Fat mass did not change significantly in eucaloric conditions and decreased in hypocaloric periods (-1.0 ± 0.3 and -1.0 ± 0.3 kg in ambulatory and bed rest, respectively). Bed rest in eucaloric conditions increased plasma C-reactive protein (CRP) (+143 ± 53%) and both the ratios between plasma IL-6 and IL-10 (4 ± 1 times) and white blood cell IL-6 and IL-10 mRNAs (5 ± 1 times). Energy restriction prevented bed-rest-mediated increases in CRP and the IL-6 to IL-10 ratio. Bed rest increased (P = 0.03) long pentraxin-3 (PTX3) plasma concentration, without significant activity-bydiet interaction. In all conditions (n = 36), CRP and PTX3 were inversely correlated (r = -0.61; P < 0.001). Changes in fat mass, leptin, and IL-6 directly correlated with CRP and inversely correlated with PTX3. IL-10 inversely correlated with CRP and directly correlated with PTX3 (r = 0.52; P < ;0.01). Conclusions: Calorie restriction prevents the inflammatory response induced by 14 d of bed rest. Wesuggest an inverse regulation of CRP and PTX3 in response to changes in energy balance. Copyright © 2008 by The Endocrine Society.

Calorie restriction modulates inactivity-induced changes in the inflammatory markers c-reactive protein and pentraxin-3

CASTELLINO, Pietro;
2008-01-01

Abstract

Context: Energy balance and physical activity potentially influence systemic inflammation. Objective: Our objective was to test the hypothesis that moderate energy restriction may prevent activation of inactivity-induced inflammatory response. Design: Participants were studied four times at the end of 14-d periods of experimental bed rest or controlled ambulation, after receiving eucaloric or hypocaloric diets. Setting: The study was conducted at the clinical research center of the German Space Agency. Subjects: Nine healthy young volunteers participated. Interventions: Energy intake was calibrated to physical activity and decreased by about 20% in hypocaloric conditions. Main Outcome Measures: Changes in body fat by dual-energy x-ray absorptiometry as well as plasma inflammatory markers and cytokine mRNA levels in blood cells were measured. Results: Fat mass did not change significantly in eucaloric conditions and decreased in hypocaloric periods (-1.0 ± 0.3 and -1.0 ± 0.3 kg in ambulatory and bed rest, respectively). Bed rest in eucaloric conditions increased plasma C-reactive protein (CRP) (+143 ± 53%) and both the ratios between plasma IL-6 and IL-10 (4 ± 1 times) and white blood cell IL-6 and IL-10 mRNAs (5 ± 1 times). Energy restriction prevented bed-rest-mediated increases in CRP and the IL-6 to IL-10 ratio. Bed rest increased (P = 0.03) long pentraxin-3 (PTX3) plasma concentration, without significant activity-bydiet interaction. In all conditions (n = 36), CRP and PTX3 were inversely correlated (r = -0.61; P < 0.001). Changes in fat mass, leptin, and IL-6 directly correlated with CRP and inversely correlated with PTX3. IL-10 inversely correlated with CRP and directly correlated with PTX3 (r = 0.52; P < ;0.01). Conclusions: Calorie restriction prevents the inflammatory response induced by 14 d of bed rest. Wesuggest an inverse regulation of CRP and PTX3 in response to changes in energy balance. Copyright © 2008 by The Endocrine Society.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11769/52990
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