Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12774044_1.fastq.gz | Fastqsanger.gz | |||
| SRR12774044_2.fastq.gz | Fastqsanger.gz | |||
| SRR12774045_1.fastq.gz | Fastqsanger.gz | |||
| SRR12774045_2.fastq.gz | Fastqsanger.gz | |||
| SRR12774046_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:<p>Blood metabolomics of 12-week-old female and male C57BL/6J mice that were exposed to either a control or an unhealthy high-fat/high-sugar (HFHS) diet during early-life, or early-life HFHS diet supplemented with a microbiota-targeted intervention (either a prebiotic combination (fructo-oligosaccharides and galacto-oligosaccharides), FOS+GOS) or a putative probiotic (<em>B. longum</em> APC1472)). The overall aim of the project is to investigate the potential of microbiota-targeted approaches, via prebiotic combination FOS+GOS or the putative probiotic <em>B. longum</em> APC147, to attenuate detrimental enduring effects of an early-life HFHS diet, as a model of western diet, on offspring’s feeding behavior in adulthood.</p>
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Project description:Given the salient role of early-life adversity and the resulting biological embedding in disease risk, there is a critical need to understand the mechanisms operating at multiple levels of analysis in order to promote effective clinical treatments and intervention efforts for survivors. An example for such an effort could be to utilize models of dynamic cellular markers as individual-level factors to account for variation in intervention response and clinical outcomes. Results of this study will lead to new knowledge about specific gene expression pathways in response to stress, and whether the response is moderated by previous exposure to early adversity, shorter telomere length (a marker of cellular aging) and self-report mental-health measures. Thus, the long-term effects of this study will advance our understanding on stress-related transcriptomic changes that play a downstream role in disease susceptibility and accelerated aging, with the goal of targeting specific pathways and genes for potential intervention studies and pharmacological treatments to reverse the effects of exposure to early adversity. For example, considering high failure rates for depression treatments, and in order to tailor individual interventions, identifying objective changes in stress-induced gene expression may help to predict intervention efficacy in clinical and non-clinical settings, as seen, for example, in breast and leukemia cancers. Thus, findings will have a range of impacts for basic science, intervention studies and clinical practice that will influence treatments to match the specific cellular processes operating within an individual.
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Project description:Given the salient role of early-life adversity (ELA) and the resulting biological embedding in disease risk, there is a critical need to understand the mechanisms operating at multiple levels of analysis in order to promote effective clinical treatments and intervention efforts for survivors. An example for such an effort could be to utilize models of dynamic cellular markers as individual-level factors to account for variation in intervention response and clinical outcomes. Results of this study will lead to new knowledge about specific gene expression pathways in response to stress, and whether the response is moderated by previous exposure to early adversity, shorter telomere length (a marker of cellular aging) and self-report mental-health measures. Thus, the long-term effects of this study will advance our understanding on stress-related transcriptomic changes that play a downstream role in disease susceptibility and accelerated aging, with the goal of targeting specific pathways and genes for potential intervention studies and pharmacological treatments to reverse the effects of exposure to early adversity. For example, considering high failure rates for depression treatments, and in order to tailor individual interventions, identifying objective changes in stress-induced gene expression may help to predict intervention efficacy in clinical and non-clinical settings, as seen, for example, in breast and leukemia cancers. Thus, findings will have a range of impacts for basic science, intervention studies and clinical practice that will influence treatments to match the specific cellular processes operating within an individual.
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