Diverse development and higher sensitivity of the circadian clocks to changes in maternal-feeding regime in a rat model of cardio-metabolic disease

Apr 4, 2015Chronobiology international

Varied growth and increased sensitivity of body clocks to changes in mother’s feeding in a rat model of heart and metabolism disease

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Abstract

Significant differences in circadian clock gene expression rhythms were observed in spontaneously hypertensive rats compared to healthy Wistar rats during development.

The development of a high-amplitude expression rhythm for the Bmal1 gene was delayed in the suprachiasmatic nuclei and liver of spontaneously hypertensive rats.
Atypical circadian clock development in spontaneously hypertensive rats may be linked to differences in maternal behavior detected shortly after delivery.
Spontaneously hypertensive rats exhibited higher sensitivity of circadian clocks in the suprachiasmatic nuclei, liver, and colon to maternal feeding regime changes.
Maternal restricted feeding shifted the circadian clocks in spontaneously hypertensive rats, even while mothers were kept under a normal light/dark cycle.
The diverse development and heightened sensitivity of the SHR circadian system to maternal cues could be associated with their predisposition to cardiovascular and metabolic diseases.

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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.

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Diverse development and higher sensitivity of the circadian clocks to changes in maternal-feeding regime in a rat model of cardio-metabolic disease

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