title: Shift work or food intake during the rest phase promotes metabolic disruption and desynchrony of liver genes in male rats.
abstract: In the liver, clock genes are proposed to drive metabolic rhythms. These gene rhythms are driven by the suprachiasmatic nucleus (SCN) mainly by food intake and via autonomic and hormonal pathways. Forced activity during the normal rest phase, induces also food intake, thus neglecting the signals of the SCN, leading to conflicting time signals to target tissues of the SCN. The present study explored in a rodent model of night-work the influence of food during the normal sleep period on the synchrony of gene expression between clock genes and metabolic genes in the liver. Male Wistar rats were exposed to forced activity for 8 h either during the rest phase (day) or during the active phase (night) by using a slow rotating wheel. In this shift work model food intake shifts spontaneously to the forced activity period, therefore the influence of food alone without induced activity was tested in other groups of animals that were fed ad libitum, or fed during their rest or active phase. Rats forced to be active and/or eating during their rest phase, inverted their daily peak of Per1, Bmal1 and Clock and lost the rhythm of Per2 in the liver, moreover NAMPT and metabolic genes such as Pparα lost their rhythm and thus their synchrony with clock genes. We conclude that shift work or food intake in the rest phase leads to desynchronization within the liver, characterized by misaligned temporal patterns of clock genes and metabolic genes. This may be the cause of the development of the metabolic syndrome and obesity in individuals engaged in shift work.
authors.affiliation: Departamento de Biología Celular y Fisiología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Distrito Federal, México.
authors.forename: Roberto C
authors.initials: RC
authors.lastname: Salgado-Delgado
authors.forename: Nadia
authors.initials: N
authors.lastname: Saderi
authors.forename: María del Carmen
authors.initials: Mdel C
authors.lastname: Basualdo
authors.forename: Natali N
authors.initials: NN
authors.lastname: Guerrero-Vargas
authors.forename: Carolina
authors.initials: C
authors.lastname: Escobar
authors.forename: Ruud M
authors.initials: RM
authors.lastname: Buijs
mesh_terms: D000818:Animals; D001835:Body Weight; D002940:Circadian Rhythm / Q000235:genetics; D005247:Feeding Behavior; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D018149:Glucose Intolerance; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009243:NAD / Q000378:metabolism; D054409:Nicotinamide Phosphoribosyltransferase / Q000235:genetics / Q000378:metabolism; D056950:Period Circadian Proteins / Q000235:genetics*; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D047492:Peroxisome Proliferator-Activated Receptors / Q000235:genetics; D010805:Physical Conditioning, Animal; D051381:Rats; D013997:Time Factors; D014157:Transcription Factors / Q000235:genetics
chemical_list: D056950:Period Circadian Proteins; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D047492:Peroxisome Proliferator-Activated Receptors; C501429:Ppargc1a protein, rat; D014157:Transcription Factors; D009243:NAD; D054409:Nicotinamide Phosphoribosyltransferase
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