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Showing posts from June, 2023

Parabacteroides distasonis uses dietary inulin to suppress NASH via its metabolite pentadecanoic acid

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Study shows that gut microbiota members can use dietary fibre to generate beneficial metabolites to suppress metabolic disease.  

Pacific has one of most successful years for grants in school history

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University of the Pacific secured 62 grants from federal, state and county agencies totaling more than $36 million—one of the best years for government grants in school history.

Hunter-gatherer lifestyle fosters thriving gut microbiome

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Sequencing the microbiome of hunter-gatherers & city-dwellers shows that Western lifestyle decreases diversity of gut-bacteria populations. The microbiome of a hunter-gatherer society in northern Tanzania has more than twice as many species as Californians.

Researchers uncover a cellular process that leads to inflammation

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Cedars-Sinai investigators have identified several steps in a cellular process responsible for triggering one of the body's important inflammatory responses. Their findings, published in the journal  Science Immunology , open up possibilities for modulating the type of inflammation associated with several infections and inflammatory diseases.  Specifically, the investigators have improved understanding of the steps that lead to the production of IL-1 beta, a potent inflammatory protein signal released during many inflammatory responses.

Negative Regulatory NLRs Mitigate Inflammation via NF-κB Pathway Signaling in Inflammatory Bowel Disease

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A subset of NLRs function to mitigate overzealous pro-inflammatory signaling produced by NF-κB activation. Under normal pathophysiologic conditions, proper signaling by these NLRs protect against potential autoimmune responses. These NLRs associate with several different proteins within both the canonical and noncanonical NF-κB signaling pathways to either prevent activation of the pathway or inhibit signal transduction. Inhibition of the NF-κB pathways ultimately dampens the production of pro-inflammatory cytokines and activation of other downstream pro-inflammatory signaling mechanisms. Dysregulation of these NLRs, including NLRC3, NLRX1, and NLRP12, have been reported in human inflammatory bowel disease (IBD) and colorectal cancer patients, suggesting the potential of these NLRs as biomarkers for disease detection. Mouse models deficient in these NLRs also have increased susceptibility to colitis and colitis-associated colorectal cancer. While current standard of care for IBD patien...

Taurine deficiency as a driver of aging

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  Studying various animals, a study  found that the amount of the semi-essential amino acid taurine in circulation decreased with age. Supplementation with taurine slowed key markers of aging such as increased DNA damage, telomerase deficiency, impaired mitochondrial function, and cellular senescence. Loss of taurine in humans was associated with aging-related diseases, and concentrations of taurine and its metabolites increased in response to exercise. Taurine supplementation improved life span in mice and health span in monkeys.

Microbiota and Nod-like receptors balance inflammation and metabolism during obesity and diabetes

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Gut microbiota influence host immunity and metabolism during obesity. Bacterial sensors of the innate immune system relay signals from specific bacterial components (i.e., postbiotics) that can have opposing outcomes on host metabolic inflammation. NOD-like receptors (NLRs) such as Nod1 and Nod2 both recruit receptor-interacting protein kinase 2 (RIPK2) but have opposite effects on blood glucose control. Nod1 connects bacterial cell wall-derived signals to metabolic inflammation and insulin resistance, whereas Nod2 can promote immune tolerance, insulin sensitivity, and better blood glucose control during obesity. NLR family pyrin domain containing (NLRP) inflammasomes can also generate divergent metabolic outcomes. NLRP1 protects against obesity and metabolic inflammation potentially because of a bias toward IL-18 regulation, whereas NLRP3 appears to have a bias toward IL-1β-mediated metabolic inflammation and insulin resistance. Targeting specific postbiotics that improve immunometabo...