title: Internal desynchronization in a model of night-work by forced activity in rats.
abstract: Individuals engaged in shift- or night-work show disturbed diurnal rhythms, out of phase with temporal signals associated to the light/dark (LD) cycle, resulting in internal desynchronization. The mechanisms underlying internal desynchrony have been mainly investigated in experimental animals with protocols that induce phase shifts of the LD cycle and thus modify the activity of the suprachiasmatic nucleus (SCN). In this study we developed an animal model of night-work in which the light-day cycle remained stable and rats were required to be active in a rotating wheel for 8 h daily during their sleeping phase (W-SP). This group was compared with rats that were working in the wheel during their activity phase (W-AP) and with undisturbed rats (C). We provide evidence that forced activity during the sleeping phase (W-SP group) alters not only activity, but also the temporal pattern of food intake. In consequence W-SP rats showed a loss of glucose rhythmicity and a reversed rhythm of triacylglycerols. In contrast W-AP rats did not show such changes and exhibited metabolic rhythms similar to those of the controls. The three groups exhibited the nocturnal corticosterone increase, in addition the W-SP and W-AP groups showed increase of plasma corticosterone associated with the start of the working session. Forced activity during the sleep phase did not modify SCN activity characterized by the temporal patterns of PER1 and PER2 proteins, which remained in phase with the LD cycle. These observations indicate that a working regimen during the sleeping period elicits internal desynchronization in which activity combined with feeding uncouples metabolic functions from the biological clock which remains fixed to the LD cycle. The present data suggest that in the night worker the combination of work and eating during working hours may be the cause of internal desynchronization.
authors.affiliation: Departamento de Anatomía, Facultad de Medicina, Edificio "B" 4 Piso, Universidad Nacional Autónoma de México, México DF 04510, Mexico.
authors.forename: R
authors.initials: R
authors.lastname: Salgado-Delgado
authors.forename: M
authors.initials: M
authors.lastname: Angeles-Castellanos
authors.forename: M R
authors.initials: MR
authors.lastname: Buijs
authors.forename: C
authors.initials: C
authors.lastname: Escobar
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000502:physiology; D002452:Cell Count; D018797:Cell Cycle Proteins / Q000378:metabolism; D002940:Circadian Rhythm / Q000502:physiology*; D003345:Corticosterone / Q000097:blood; D004435:Eating / Q000502:physiology; D006728:Hormones / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D008660:Metabolism / Q000502:physiology; D009043:Motor Activity / Q000502:physiology*; D009687:Nuclear Proteins / Q000378:metabolism; D056950:Period Circadian Proteins; D051381:Rats; D017208:Rats, Wistar; D020178:Sleep Disorders, Circadian Rhythm / Q000503:physiopathology* / Q000523:psychology; D013493:Suprachiasmatic Nucleus / Q000166:cytology / Q000378:metabolism / Q000502:physiology
chemical_list: D001786:Blood Glucose; D018797:Cell Cycle Proteins; D006728:Hormones; D009687:Nuclear Proteins; C539024:Per1 protein, rat; C513311:Per2 protein, rat; D056950:Period Circadian Proteins; D003345:Corticosterone