Obesity2
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB22917 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2163348_1.fastq.gz | Fastqsanger.gz | |||
| ERR2163348_2.fastq.gz | Fastqsanger.gz |
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Project description:Colorectal cancer (CRC) continues to increase globally, thus identification of mechanisms that prevent cancer are sorely needed. The microbiota has emerged as a key driver of CRC pathogenesis; however, little is known regarding how specific microbes might prevent CRC. Using transplantation of the microbiota from individuals with or without CRC into germfree mice, we identified that the microbiota harbored by non-diseased individuals can reduce tumor formation and Bacteroides uniformis was a potentially protective member of the microbiota. Single cell sequencing of CD45+ immune cells within the MC38 tumor shows a change in T and NK cell populations with B. uniformis treatment. T cell deficient mice were still protected from CRC in response to B. uniformis treatment, while NK cell depletion eradicated microbe-mediated protection. B. uniformis is reduced in individuals with CRC and thus our data identify B. uniformis as a microbe enriched in healthy individuals that can reduce tumor formation through enhanced NK cell activity.
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Project description:The crucial role of nutrition for cerebral health and the impact of dietary habits on brain structure and function have been long far recognized. To date a major health concern is associated with the increased consumption of fructose as added sugar in many types of drinks and processed foods, especially among young people. High-fructose intake has been pointed out as the possible culprit for the raised incidence of chronic diseases, such as obesity, cardiovascular disease, nonalcoholic fatty liver disease, and type 2 diabete. Further, it has been reported that high-fructose intake is associated with the over-activation of its cerebral metabolism, which was proposed to negatively impact on whole brain physiology and cognitive function. Notably, we previously reported that short-term fructose-rich diet induces mitochondrial dysfunction, oxidative stress, and neuroinflammation in hippocampus of young rats, as well as the imbalance of redox homeostasis, autophagic mechanisms and representation of synaptic markers in frontal cortex of both adult and young rats. Animal studies have also revealed the damaging effect of high-fructose diets on hippocampal functions during periods of neurocognitive development, such as childhood and adolescence. Hypothalamus plays a crucial role in maintaining whole body homeostasis. Long-term fructose overfeeding was reported to alter hypothalamic-pituitary-adrenal axis, leading to elevations in glucocorticoids in peri-adolescent rats [22]. Further, fructose overconsumption was associated with impairment of hypothalamic insulin signalling, oxidative stress and inflammation , and it was proposed that fructose-driven perturbations of hypothalamic function may compromise the potential for satiety, thereby increasing the prospect of developing obesity. Data currently available on hypothalamic dysfunctions related to a high-fructose diet essentially refer to the effects of long-term sugar feeding, while information on corresponding alterations associated with a short-term dietary treatment, particularly in the critical period of adolescence, is still lacking. Due to complexity and multiplicity of hypothalamic functions, there is also the need for a holistic characterization aimed at unveiling the general picture of hypothalamic dysfunctions associated with a high-fructose diet. To fill this gap, we investigated adolescent rats fed a fructose-rich or control diet, for 3 weeks. To verify whether the fructose-driven changes are rescued after the switch to a control diet, half of the rats from both animal groups were then fed a control diet for additional 3 weeks until young adulthood phase. Quantitative proteomics on hypothalamic extracts of all animal groups was used to identify molecular alterations triggered by fructose-rich diet and to obtain insights into the relationship between sugar feeding and possible dysfunctions of hypothalamus.
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