Animal production has faced sanitary crises involving contamination of products by persistent organic pollutants (POP). In order to avoid the disposal of products originating from contaminated herd, innovative strategies aiming to hasten POP removal should be identified. The first step is to release POP from their storage site, the adipose tissue (AT), to the blood, in order to be metabolized or excreted. We hypothesized that POP would be released from AT to blood along with lipids, during body-fat mobilization over short- (1 h) or medium-term (1 wk) periods due to ?-agonist challenge or underfeeding, respectively. In order to test these hypotheses, 3 adult non-lactating Romane ewes were contaminated over 6 wk with a diet spiked with indicator polychlorobiphenyls (0.21 µg/kg BW/d of each PCB 28, 52, 101, 138, 153 and 180) and chlordecone (11.6 µg CLD/kg BW/d). Indicator PCB and CLD were chosen because of their high lipophilicity and contrasted distribution: mainly in AT fo r PCB, a nd in liver for CLD. Over the first 5 wk, diet met energy requirements, whereas during the 6th wk ewes were underfed (35% of energy requirements). ?-agonist challenges (4 nmol/kg BW of isoproterenol i.v.) performed at the end of wk 5 and 6 of the trial, induced fast (5-10 min) increase in plasma non-esterified fatty acid (NEFA) concentration (P = 0.05), but did not affect serum POP concentrations. Conversely, short-term (2-7 d) underfeeding increased NEFA, PCB 138, 153 and 180, and CLD (P < 0.01) in serum (x1.3-1.5 for POP, 0.11 to 0.17 ng/g after 7 d for PCB 180), without affecting PCB concentrations in AT and body fatness. These results suggest that POP are released from AT to blood through lipomobilisation in response to underfeeding, but not by acute lipolysis due to ?-agonist challenges.