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


METHODS
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.


METHODS
The study was conducted at the clinical research center of the German Space Agency.


METHODS
Nine healthy young volunteers participated.


METHODS
Energy intake was calibrated to physical activity and decreased by about 20% in hypocaloric conditions.


METHODS
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-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).


CONCLUSIONS
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.
Bosutti
Alessandra
A
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. biolo@units.it.
Malaponte
Grazia
G
Zanetti
Michela
M
Castellino
Pietro
P
Heer
Martina
M
Guarnieri
Gianfranco
G
Biolo
Gianni
G
D000328:Adult; D002097:C-Reactive Protein / Q000032:analysis*; D031204:Caloric Restriction; D006801:Humans; D007249:Inflammation / Q000517:prevention & control*; D016753:Interleukin-10 / Q000097:blood / Q000235:genetics; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D009043:Motor Activity; D012333:RNA, Messenger / Q000032:analysis; D000683:Serum Amyloid P-Component / Q000032:analysis*; D000099153:Pentraxins
D002097:C-Reactive Protein; D016753:Interleukin-10; D015850:Interleukin-6; D012333:RNA, Messenger; D000683:Serum Amyloid P-Component; D000099153:Pentraxins