L-tryptophan supplementation was given to manipulate the long-term sequelae of early-life programming by undernutrition. We found that the effects of this Tofacitinib dietary intervention can be monitored non invasively by circadian sampling of blood Dglucose. Expressions of PERIOD1 protein by synchronized primary cell lines established from young rats were altered according to diet and L-tryptophan supplementation. However the capacity of colonization at seeding and the adhesion potentials of primary cells were clearly altered in rats born from mothers fed on dietary protein restriction, irrespectively of the supplementation with L-tryptophan. The body weight means 
of low-protein groups in our experiment remain lower than control groups until the end of the observation period, but, the weight of visceral fat of undernourished offspring was similar to control group at the end of experiment. L-tryptophan supplementation between D-12 and D-21 did not alter the catchup growth nor the absolute food consumption of male offspring from weaning to the end of growth period. The daily food intake of rat pups measured between Day 39 and Day-42 showed that the food consumption of the LP group is lower than the CP group irrespectively of a supplementation by Ltryptophan. These observations on nursing rats with offspring are similar to results obtained in lactating sows. In addition, the relative food intake was higher for the LP group during the night cycle but the relative intakes of both groups were similar during the light cycle. These data are consistent with the temporary hyperphagy that we previously demonstrated in undernourished rat pups. A daily bolus of L-tryptophan between D-12 and D-21 did alter the level of D-glucose both in LPT and CPT groups. Our D-glucose profiles displayed a maximum BYL719 around 16 h Zeitgeber time like the profiles obtained on plasma D-glucose titration. However a significant circadian rhythm of Dglucose oscillation was only obtained with the control-fed group receiving a perinatal bolus of L-tryptophan. Results shown on Figures 3 and 5 suggest that there are a long-term effect of tryptophan supplementation on rats enduring perinatal undernutrition as well as on control-fed rats. As shown on Figure 4, we found a significant difference on the cycle of food intake during 4 consecutive days of observations on rats exposed to perinatal undernutrition and receiving a daily bolus of L-tryptophan. These results are suggesting that our supplementation triggered discrete phenotypic alterations. We think that our results indicate that milk formulas designed to improve sleep-wake cycles of babies have to be tested on rat models under several conditions of feeding to check for global phenotypic consequences. Beside oral gavage, Ltryptophan supplementation has to be tested from birth in formulated milk by using gastrostomized rat pups or with subcutaneous or intraperitonal injections. In any case, subsequently to our experiment, testing formula fortified with Ltryptophan on cerebellum gene expression of nursing rat neonates is clearly insufficient. To explore whether our supplementation with L-tryptophan interacted with the influence of perinatal undernutrition on male somatic cells, we have selected primary cells from the tip of the tail of every rat. We have tested the capacity of these primary cells to adhere and colonize plastics and the diversity of phenotypes selected from the biopsies.