Congrats, Ivy!

Congratulations, Ivy!!

Thank you @ivyxiong.bsky.social for being part of the team!

Thank you, Jonny!

Thank you!

Fits nicely with what you showed in brown adipose.

Thank you, Marc!

Thank you, Doug!

Thank you, Sarah! Your insights into PLIN5 functions were invaluable!

Fantastic teamwork in the Porat-Shliom lab AND the amazing resources at the IRP at NCI!

10. In WD conditions, increasing PLIN5 levels enables hepatocytes to regulate the proportion of mitochondria bound to LDs versus those free in the cytosol, facilitating more efficient management of lipid overload.

9. This could explain how, under nutritional deficits, mito simultaneously supports lipid oxidation for ketogenesis while promoting TG synthesis and storage to mitigate lipotoxicity. READ ON...

8. During nutritional stress like fasting, the spatial division is lost, in part due to the upregulation of PLIN5 and its phosphorylation status, leading to the emergence of both types of mitochondria in most hepatocytes. READ ON...

7. Our model: in homeostasis, two types of mitochondria operate simultaneously: periportal mitochondria with a round morphology and a preference for fatty acid oxidation and pericentral mitochondria that synthesize TGs and store them through contact with LDs. more coming...

6. Can introducing mito-LD contacts in WD reduce toxicity? YES! OE of PLIN5 increased mito-LD interactions, improved redox status, and reduced steatosis—highlighting the physiological significance of organelle interactions in lipid homeostasis and tissue health.