PMID- 25839096 OWN - NLM STAT- MEDLINE DCOM- 20160216 LR - 20150505 IS - 1525-6073 (Electronic) IS - 0742-0528 (Linking) VI - 32 IP - 4 DP - 2015 May TI - Diverse development and higher sensitivity of the circadian clocks to changes in maternal-feeding regime in a rat model of cardio-metabolic disease. PG - 531-47 LID - 10.3109/07420528.2015.1014095 [doi] AB - Spontaneously hypertensive rats (SHR) develop cardiovascular and metabolic pathology in adulthood when their circadian system exhibits significant aberrances compared with healthy control rats. This study was aimed to elucidate how the SHR circadian system develops during ontogenesis and to assess its sensitivity to changes in maternal-feeding regime. Analysis of ontogenesis of clock gene expression rhythms in the suprachiasmatic nuclei, liver and colon revealed significant differences in SHR compared with Wistar rats. In the suprachiasmatic nuclei of the hypothalamus (SCN) and liver, the development of a high-amplitude expression rhythm selectively for Bmal1 was delayed compared with Wistar rat. The atypical development of the SHR circadian clocks during postnatal ontogenesis might arise from differences in maternal behavior between SHR and Wistar rats that were detected soon after delivery. It may also arise from higher sensitivity of the circadian clocks in the SHR SCN, liver and colon to maternal behavior related to changes in the feeding regime because in contrast to Wistar rat, the SHR SCN and peripheral clocks during the prenatal period and the hepatic clock during the early postnatal period were phase shifted due to exposure of mothers to a restricted feeding regime. The maternal restricted feeding regime shifted the clocks despite the fact that the mothers were maintained under the light/dark cycle. Our findings of the diverse development and higher sensitivity of the developing circadian system of SHR to maternal cues might result from previously demonstrated differences in the SHR circadian genotype and may potentially contribute to cardiovascular and metabolic diseases, which the animal model spontaneously develops. FAU - Olejnikova, Lucie AU - Olejnikova L AD - Department of Neurohumoral Regulations, Institute of Physiology, v.v.i., Academy of Science of the Czech Republic , Prague , Czech Republic. FAU - Polidarova, Lenka AU - Polidarova L FAU - Pauslyova, Lucia AU - Pauslyova L FAU - Sladek, Martin AU - Sladek M FAU - Sumova, Alena AU - Sumova A LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20150403 PL - England TA - Chronobiol Int JT - Chronobiology international JID - 8501362 SB - IM MH - Animals MH - Animals, Newborn MH - Circadian Clocks/*genetics MH - Circadian Rhythm/genetics/physiology MH - Feeding Behavior/*physiology MH - Female MH - Gene Expression/physiology MH - Gene Expression Regulation, Developmental/*physiology MH - Heart Diseases/*genetics/physiopathology MH - Liver/*metabolism MH - Male MH - Maternal Behavior/*physiology MH - Metabolic Diseases/*genetics/metabolism MH - Motor Activity/physiology MH - Photoperiod MH - Rats MH - Suprachiasmatic Nucleus/metabolism OTO - NOTNLM OT - Circadian clock OT - clock gene OT - colon OT - liver OT - ontogenesis OT - spontaneously hypertensive rat OT - suprachiasmatic nucleus EDAT- 2015/04/04 06:00 MHDA- 2016/02/18 06:00 CRDT- 2015/04/04 06:00 PHST- 2015/04/04 06:00 [entrez] PHST- 2015/04/04 06:00 [pubmed] PHST- 2016/02/18 06:00 [medline] AID - 10.3109/07420528.2015.1014095 [doi] PST - ppublish SO - Chronobiol Int. 2015 May;32(4):531-47. doi: 10.3109/07420528.2015.1014095. Epub 2015 Apr 3.