Abstract:Taken together, we suggest that physical activity in water acts as a beneficial factor in LE diets of dams during the perinatal period. Further study is necessary to investigate the role of physical activity for adaptation against adverse nutritional stimuli.
“…P8 in rats corresponds to approximately 1-year-old children. 37 This research study adopted the 8-day-old SD pups’ early swimming training program established by Muniz et al 38 To confirm whether the rat model of ASD could complete the swimming training program, the early swimming intervention program was validated and refined. We extended the period of the training program from P52 to 60, and according to the record of rats’ swimming status, the duration of each training session was increased from 30 min to 40 min at P27-60, as shown in Figure 1 .…”
Background
Autism spectrum disorder (ASD) is a developmental disorder characterized by social behavior deficits and stereotyped behaviors in childhood that lacks satisfactory medical intervention. Early swimming intervention is a noninvasive method combining enriched environment and exercise, which has been proven to improve brain development in young children and to treat neurodevelopmental diseases.
Methods
In this study, we tested the autism-like behavior of rats with deletions in exons 11–21 of the
Shank3
gene and evaluated the effect of early swimming intervention (from postnatal day 8 to 60) on the behavior of this animal model of autism. In addition, the transcriptomes of the striatal tissues of wild-type,
Shank3
knockout and
Shank3
knockout swimming groups rats were analyzed.
Results
Shank3
knockout rats exhibit core symptoms of autism, and early swimming improved the social and stereotyped behaviors in this autism rat model. Transcriptomics results revealed that compared to the wild-type group, 291 differentially expressed genes (DEGs) were identified in the striatum of the
Shank3
knockout group. Compared to
Shank3
knockout group, 534 DEGs were identified in the striatum of
Shank3
knockout swimming group. The DEGs annotated by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway shows that the impacts of
Shank3
deletion were primarily reflected in synaptic structure, development, morphology, receptor function and signaling, and swimming primarily changed the terms related to the synapses in the striatum of
Shank3
knockout rats, including the morphology, structure, composition, development and regulation of synapses.
Conclusion
Early swimming intervention can ameliorate behavioral abnormalities caused by
Shank3
knockout, by a mechanism that may involve the process of striatal synaptic development and should be further investigated.
“…P8 in rats corresponds to approximately 1-year-old children. 37 This research study adopted the 8-day-old SD pups’ early swimming training program established by Muniz et al 38 To confirm whether the rat model of ASD could complete the swimming training program, the early swimming intervention program was validated and refined. We extended the period of the training program from P52 to 60, and according to the record of rats’ swimming status, the duration of each training session was increased from 30 min to 40 min at P27-60, as shown in Figure 1 .…”
Background
Autism spectrum disorder (ASD) is a developmental disorder characterized by social behavior deficits and stereotyped behaviors in childhood that lacks satisfactory medical intervention. Early swimming intervention is a noninvasive method combining enriched environment and exercise, which has been proven to improve brain development in young children and to treat neurodevelopmental diseases.
Methods
In this study, we tested the autism-like behavior of rats with deletions in exons 11–21 of the
Shank3
gene and evaluated the effect of early swimming intervention (from postnatal day 8 to 60) on the behavior of this animal model of autism. In addition, the transcriptomes of the striatal tissues of wild-type,
Shank3
knockout and
Shank3
knockout swimming groups rats were analyzed.
Results
Shank3
knockout rats exhibit core symptoms of autism, and early swimming improved the social and stereotyped behaviors in this autism rat model. Transcriptomics results revealed that compared to the wild-type group, 291 differentially expressed genes (DEGs) were identified in the striatum of the
Shank3
knockout group. Compared to
Shank3
knockout group, 534 DEGs were identified in the striatum of
Shank3
knockout swimming group. The DEGs annotated by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway shows that the impacts of
Shank3
deletion were primarily reflected in synaptic structure, development, morphology, receptor function and signaling, and swimming primarily changed the terms related to the synapses in the striatum of
Shank3
knockout rats, including the morphology, structure, composition, development and regulation of synapses.
Conclusion
Early swimming intervention can ameliorate behavioral abnormalities caused by
Shank3
knockout, by a mechanism that may involve the process of striatal synaptic development and should be further investigated.
“…The length longitudinal (LL, distance for nose to anus) was measured weekly from birth to the end of the experiment, containing the animal gently (Santana Muniz et al, 2013) was Brazilian Journal of Health Review, Curitiba, v. 5, n. 4, p. 13111-13129, jul./aug., 2022 measured with digital caliper (Starret ®, series 799, São Paulo, Brazil) with a 0.01mm precision.…”
Section: Somatic Growthmentioning
confidence: 99%
“…Offspring were housed in pairs (constituting a sample unit) and animal´s daily food consumption was determined by the difference between the amount of provide (50 to 60g) at the onset of the light phase and the amount of food remaining 24h later. Body and food weight was measured with a digital electronic scale was used, Marte XL 500, class II, maximum capacity 500g (smaller division 0.001g) (Santana Muniz et al, 2013)…”
The pre and early post natal is a period high susceptible to environmental insults for instance nutrition. There is a high metabolic demand necessary for the multiplication and differentiation of cells for the formation of tissues and organs and unbalanced diets affect metabolism at long term. The present study aimed to analyze physiological and metabolic parameters in male offspring submitted to the low protein diet in the perinatal life followed by a normoprotein diet or kept on the same maternal low protein diet after weaning. 12 female Wistar rats were matched with male of same strainand according maternal diet forming normoproteic and low-protein groups during gestation and lactation. At weaning three groups were randomly formed: CC (control-control), LP (low-protein-low protein) and LPC (low-protein-control). Somatic growth, feed intake, organ weight, biochemical parameters, liver fat, blood cell count and glucose tolerance test were analysed. The post-weaning "nutritional recovery" diet improved body mass and longitudinal length. But, the maintenance with low protein diet post weaning caused weight and length deficiency (P<0.001). Other parameters such as food intake, murinometric measurements, fasting gliscemia, visceral fat, organ weight, OGTT and biochemical parameters observed in the LPC were similar to CC. The LP groups caused lower area under the glycemic curve, lower visceral fat, but similar blood count, tibial growth and liver fat compared to control. The parameters evaluated in offspring submitted to nutritional recovery corroborate previous study, but the maintenance of offspring with low protein diet minimizes catch-up growth, but alters metabolic response to glucose.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.