One ABS patient received a faecal microbiota transplant and remained symptom-free for over 16 months. Gut microbiome composition and fermentation genes correlated with ABS symptoms. UC San Diego Nature Microbiology
doi.org/10.1038/s415... 🧪

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Metagenomic sequencing identified Proteobacteria overgrowth, particularly E. coli and K. pneumoniae, with enriched mixed-acid and heterolactic fermentation pathways. Faecal acetate levels correlated with blood alcohol concentration. Are there treatment options? ⤵️
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Link to original paper in Nature Medicine

doi.org/10.1038/s415... 🧪

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I only learnt this now because Hinney, Peters & Rajcsanyi @unidue.bsky.social now note that this is a remarkably benign form of monogenic obesity. Central MC4R signaling may be a new therapeutic target. Spotlight in Cell Metabolism

doi.org/10.1016/j.cm... 🧪

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After a high fat meal, MC4R deficient individuals showed faster clearance of lipids and reduced fatty acid oxidation, favoring fat storage in adipose tissue rather than circulation. This metabolic profile resembles prolonged fasting.

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Despite higher BMI, people with loss of function MC4R mutations had lower LDL cholesterol, lower triglycerides, and reduced blood pressure compared to controls. These benefits appeared already in adolescents and persisted into adulthood ("healthy obese")...

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From what we understand today about microbial complexity, I guess the vending machine would only have three to four different offers, like ice cream or sushi (: So not quite there, yet.

Thanks, yes, companies do that already. I think there will be personalised drug prescriptions based on microbiome.

FMT, probiotics, and prebiotics show modest, inconsistent effects in humans. The field must shift from taxonomy to function, embrace machine-learning and multi-omics, and stratify patients by microbiome features. Cell Metabolism
doi.org/10.1016/j.cm... 🧪

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The M66I mutation leads to high resistance but reduces viral fitness to below 20% of wild type. Over time, viruses accumulate compensatory mutations restoring both resistance and fitness. Very interesting! Harvard Medical School @science.org
doi.org/10.1126/scit... 🧪

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Mice lacking OCR369 lose ILC3s and (DC-like) Thetis cells, fail to establish oral tolerance, and develop spontaneous intestinal inflammation. Cool mechanism summed up by Arthur Mortha @preprintclub.bsky.social in Nature Reviews Immunology doi.org/10.1038/s415... 🧪
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The miRNA cargo in healthy Ad-EVs targets inhibitors of leptin receptor signaling like SOCS3 and PIAS3. Engineered EVs delivering these miRNAs to the brain reversed leptin resistance and induced weight loss in obese mice. Cell Metabolism
doi.org/10.1016/j.cm... 🧪

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SCoR2 removes nitric oxide from proteins to unlock lipid synthesis. In (pre)adipocytes, it targets Myh9 to activate PPARγ and SREBP1. In liver, it directly activates lipogenic enzymes ACLY and FASN. A potential new drug target for obesity. @science.org
doi.org/10.1126/scis... 🧪

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In vivo: Fasting combined with intratumoral LPS regresses tumors via mTORC2 dependent mitoxyperilysis. mTOR inhibitors block the effect. Kanneganti lab at St. Jude. @cp-cell.bsky.social
doi.org/10.1016/j.ce... 🧪
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mTORC2 (not mTORC1) suppresses cytoskeletal activity, trapping oxidatively damaged mitochondria at the plasma membrane for over 20 minutes. Local ROS accumulation causes membrane bursting. Can this be exploited therapeutically? ⤵️
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