Gestational Chronodisruption Impairs Circadian Physiology in Rat Male Offspring, Increasing the Risk of Chronic Disease

Nov 2, 2016Endocrinology

Disrupting Day-Night Signals During Pregnancy Changes Body Clocks and Raises Chronic Disease Risk in Male Rat Offspring

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Abstract

Chronic photoperiod shift during pregnancy lengthened gestation and increased newborn weight.

Maternal circadian rhythms in heart rate, body temperature, and activity were altered by chronic photoperiod shift.
Adult offspring exhibited normal rhythms of clock gene expression in the suprachiasmatic nucleus, but daily plasma melatonin rhythm was absent.
Corticosterone, aldosterone, renal markers, blood pressure, and heart rate rhythms were disrupted in adult offspring.
CPS offspring showed decreased glucose tolerance and an abnormal corticosterone response to ACTH.
These findings suggest gestational chronic photoperiod shift may induce long-term effects on offspring circadian systems and associated health risks.

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Chronic exposure to light at night, as in shift work, alters biological clocks (chronodisruption), negatively impacting pregnancy outcome in humans. Actually the interaction of maternal and fetal circadian systems could be a key factor determining a fitting health in adults. We propose that chronic photoperiod shift (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 (12 h light, 12 h dark) or to CPS until 85% of 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 the clock gene expression in the suprachiasmatic nucleus (SCN), locomotor activity, body temperature, heart rate, blood pressure, plasma variables, glucose tolerance, and corticosterone response to 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 an abnormal corticosterone response to ACTH. Altogether these data show that gestational CPS induced long-term effects on the offspring circadian system, wherein a normal SCN coexists with altered endocrine, cardiovascular, and metabolic function.

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Gestational Chronodisruption Impairs Circadian Physiology in Rat Male Offspring, Increasing the Risk of Chronic Disease

Abstract

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