Bosutti Alessandra, Malaponte Grazia, Zanetti Michela, Castellino Pietro, Heer Martina, Guarnieri Gianfranco, Biolo Gianni
Department of Clinical, Technological, and Morphological Sciences, Division of Internal Medicine, University of Trieste, Clinica Medica, Ospedale di Cattinara, Strada di Fiume 447, Trieste 34149, Italy.
J Clin Endocrinol Metab. 2008 Aug;93(8):3226-9. doi: 10.1210/jc.2007-1684. Epub 2008 May 20.
Energy balance and physical activity potentially influence systemic inflammation.
Our objective was to test the hypothesis that moderate energy restriction may prevent activation of inactivity-induced inflammatory response.
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.
The study was conducted at the clinical research center of the German Space Agency.
Nine healthy young volunteers participated.
Energy intake was calibrated to physical activity and decreased by about 20% in hypocaloric conditions.
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.
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-by-diet 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).
Calorie restriction prevents the inflammatory response induced by 14 d of bed rest. We suggest an inverse regulation of CRP and PTX3 in response to changes in energy balance.
能量平衡和身体活动可能会影响全身炎症反应。
我们的目的是检验适度能量限制可能预防因不活动引起的炎症反应激活这一假设。
在接受等热量或低热量饮食后,对参与者在14天的实验性卧床休息或可控行走期结束时进行了4次研究。
该研究在德国航天局的临床研究中心进行。
9名健康年轻志愿者参与。
根据身体活动量校准能量摄入,在低热量条件下减少约20%。
通过双能X线吸收法测量身体脂肪的变化,以及血细胞中血浆炎症标志物和细胞因子mRNA水平。
在等热量条件下,脂肪量无显著变化,在低热量期减少(行走和卧床休息时分别减少-1.0±0.3和-1.0±0.3千克)。在等热量条件下卧床休息会使血浆C反应蛋白(CRP)升高(+143±53%),以及血浆IL-6与IL-10的比值(4±1倍)和白细胞IL-6与IL-10 mRNA升高(5±1倍)。能量限制可预防卧床休息介导的CRP和IL-6与IL-10比值升高。卧床休息会使长五聚蛋白3(PTX3)血浆浓度升高(P = 0.03),饮食与活动之间无显著交互作用。在所有条件下(n = 36),CRP与PTX3呈负相关(r = -0.61;P < 0.001)。脂肪量、瘦素和IL-6的变化与CRP呈正相关,与PTX3呈负相关。IL-10与CRP呈负相关,与PTX3呈正相关(r = 0.52;P < 0.01)。
热量限制可预防14天卧床休息引起的炎症反应。我们认为CRP和PTX3会因能量平衡变化而产生反向调节。