||Chronic exposure to light at night, as in shift work, alters biological clocks (chronodisruption), impacting negatively pregnancy outcome in human. Actually, the interaction of maternal and fetal circadian systems could be a key factor determining a fitting health in adult. We propose that chronic photoperiod shifts (CPS) during pregnancy, alter maternal circadian rhythms, and impair circadian physiology in the adult offspring, increasing health risks. Pregnant rats were exposed to normal photoperiod (12h-light/12h-dark) or to CSP until 85 gestation. The effects of gestational CPS were evaluated on the mother and adult offspring. In the mother we measured rhythms of heart-rate, body temperature and activity through gestation, and daily rhythms of plasma variables: melatonin, corticosterone, aldosterone and markers of renal function; at 18 days of gestation. In adult offspring, we measured rhythms of clock gene expression in the suprachiasmatic nucleus (SCN), locomotor activity, body temperature, heart rate, blood pressure, plasma variables, glucose tolerance and corticosterone response to adrenocorticotropic hormone (ACTH). CPS altered all maternal circadian rhythms; lengthened gestation and increased newborn weight. The adult CPS offspring presented normal rhythms of clock gene expression in the SCN, locomotor activity and body temperature. However, the daily rhythm of plasma melatonin was absent, and corticosterone, aldosterone, renal markers, blood pressure and heart-rate rhythms were altered. Moreover, CPS offspring presented decreased glucose tolerance and abnormal corticosterone response to ACTH. Altogether, these data shows that gestational CPS induced long-term effects on the offspring circadian system, wherein a normal SCN coexists with altered endocrine, cardiovascular and metabolic function.