Summary It has been reported that the enzymic activity of fatty acid synthase (Fas) in rat liver increases during suckling-weaning transition. In this study, we investigated whether induction of the gene (Fasn) in the rat liver during the suckling-weaning transition is regulated by histone acetylation, and the nuclear transcription factors carbohydrate response element-binding protein (ChREBP) and sterol regulatory element-binding protein 1 (SREBP1). We observed that levels of Fas and Fasn increased during suckling-weaning transition. Binding levels of ChREBP and SREBP1 to upstream regions of Fasn increased during the suckling-weaning transition. Acetylation of histones H3 and H4 around Fasn increased during the transient period. Our results suggest that induction of liver Fasn during the suckling-weaning transition is closely associated with increased levels of ChREBP and SREBP1 binding, and acetylation of histones H3 and H4 around the gene.

Introduction Exercise therapies during rehabilitation significantly promote recovery from various deficits after cerebral infarction, which is mediated by neuronal plasticity with distinct inputs. Although adult neurogenesis can also be modulated by neuronal activity before synaptogenesis, how distinct exercises contribute to the neurological reorganization of the injured cerebral cortex remains unclear. In the present study, we aimed to elucidate the effects of different exercise therapies on motor recovery and neuronal reorganization after photochemically induced focal cerebral infarction. Methods Here, we examined the effects of three different exercises—(a) forced lower‐intensity and (b) higher‐intensity treadmill exercises, and (c) voluntary exercise with wheel running—on motor recovery and adult neurogenesis in a rat model of focal cerebral infarction. Photochemically induced thrombosis (PIT) was used to generate focal infarction in rats that was mostly confined to their motor cortices. Results Beam walking tests showed that recovery after PIT‐induced cortical infarction differed in acute and chronic stages and was influenced by the type of exercise. Furthermore, forced low‐intensity training had more positive effects on functional recovery than other exercises or control. To evaluate the production of newly generated cells including de novo neurogenesis, we performed lineage analysis with BrdU labeling and immunofluorescence experiments. Lower‐intensity treadmill exercise increased the number of BrdU/NeuN colabeled cells, but not total BrdU‐retaining or BrdU/Sox2‐colabeled cells, in the peri‐infarct region of the ipsilateral cortex. In contrast, high‐intensity treadmill or voluntary exercises had the opposite effects. Conclusions These results suggest that neuronal maturation can be differently modulated by distinct exercises and that low‐intensity treadmill exercise could result in more potent generation of mature neurons. This also suggests the possibility that the generation of neural stem/progenitor cells and differentiation might be modulated by rehabilitation‐mediated neural plasticity.

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