The prevalence of obesity has increased rapidly during recent years and has reached epidemic proportions. As a result, the scientific community is interested in active biomolecules which are naturally present in plants and foodstuffs and may be useful in body weight management. In recent years, polyphenols have made up one of the most frequently studied groups among these molecules. Numerous studies have been carried out on animals to analyse the potential anti-obesity effects of resveratrol, a non-flavonoid polyphenol, and a general consensus concerning the body-fat-lowering effect of this compound exists. By contrast, studies in humans have been few so far. Moreover, in these studies, the effectiveness of resveratrol is low. The aims of the present review are to summarize the results reported so far on this topic and to justify the differences observed between animals and humans. It seems that the reduced response to resveratrol in humans cannot be attributed to the use of lower doses in humans because the doses that induce body-fat-lowering effects in rodents are in the same range as those used in human studies. With regard to the experimental period length, treatments were longer in animal studies than in human studies. This can be one of the reasons contributing to the reduced responses observed in humans. Moreover, animals used in the reported studies are young while volunteers participating in human studies are adults, suggesting that resveratrol may be more efficient in young individuals. In addition to differences in the experimental designs, metabolic differences between animals and human cannot be discarded.

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1 The e ect of trichloroethanol (TCEt), the active metabolite of chloral hydrate, on the intracellular concentration of calcium ([Ca 2+ ] i ) was investigated in rat submandibular glands (RSMG) acini loaded with fura-2. 2 TCEt (1 ± 10 mM) increased the [Ca 2+ ] i independently of the presence of calcium in the extracellular medium. Dichloroethanol (DCEt) and monochloroethanol (MCEt) reproduced the stimulatory e ect of TCEt but at much higher concentrations (about 6 fold higher for DCEt and 20 fold higher for MCEt). 3 TCEt mobilized an intracellular pool of calcium, which was depleted by a pretreatment with thapsigargin, an inhibitor of the sarcoplasmic and endoplasmic reticulum calcium-dependent ATPases, but not with FCCP, an uncoupler of mitochondria. 4 TCEt 10 mM inhibited by 50% the thapsigargin-sensitive microsomal Ca 2+ -ATPase. DCEt 10 mM and MCEt 10 mM inhibited the ATPase by 20 and 10%, respectively. 5 TCEt inhibited the increase of the [Ca 2+ ] i and the production of inositol phosphates in response to carbachol, epinephrine and substance P. 6 TCEt inhibited the uptake of calcium mediated by the store-operated calcium channel (SOCC). 7 ATP and Bz-ATP increased the [Ca 2+ ] i in RSMG acini and this e ect was blocked by extracellular magnesium, by Coomassie blue and by oxydized ATP (oATP). 8 TCEt potentiated the increase of the [Ca 2+ ] i and of the uptake of extracellular calcium in response to ATP and Bz-ATP. 9 TCEt had no e ect on the uptake of barium and of ethidium bromide in response to purinergic agonists. 10 These results suggest that TCEt, at sedative concentrations, exerts various e ects on the calcium regulation: (1) it mobilizes a thapsigargin-sensitive intracellular pool of calcium in RSMG acini; (2) it inhibits the uptake of calcium via the SOCC; (3) it inhibits the activation by G protein-coupled receptors of a polyphosphoinositide-speci®c phospholipase C. It does not interfere with the activation of the ionotropic P2X receptors. 11 The use of chloral hydrate should be avoided in studies exploring the in vivo responses to sialagogues.