🚨New @LyssiotisLab paper led by Dr. Megan Radyk in @NatureMetabolism "NADPH-producing enzymes restrict the formation of pancreatic precancerous lesions" 🧵Follow for a tweetorial... and bonus highlight of @LabVousden co-published study and News & Views link from @WellenLab!

Hail to the Victors! 〽️

I'm very happy to share the final version of our paper, “MCT1-dependent mitochondrial lactate import sustains cardiac metabolism,” out in Nature! We show how lactate fuels heart mitochondria and helps protect the heart during stress. nature.com/articles/s41586-0… @UofUBiochem 1/10

Thank you @AACR and Silvia Licciulli for highlighting Eileen Carpenter, MD, PhD. Last month, Dr. Carpenter delivered the Rising Star Keynote at the 2026 AACR Conference on Pancreatic Cancer. Check out their blog shining a light on Dr. Carpenter's research and the role of fibroblasts in the interaction between tumor cells and nerves in the pancreas: aacr.org/blog/2026/10/23/str…

Was wild to see us on the BIG screen at the BIG HOUSE 〽️

Grateful for the opportunity to stand in solidarity with those battling a cancer diagnosis #BlockCancer @UMRogelCancer, @UMPhysiology, @UMICHpancreas piped.video/watch?v=fujsoQ…

Reminder that xCT-driven cell death (for instance induced by glucose deprivation) does not mean disulfidptosis, That iron-dependent cell death does not equal ferroptosis, That cysteine toxicity does not mean ferroptosis even if it's iron-dependent, etc nature.com/articles/s42255-0…

Two proteins that permeabilize mitochondria promote cell death through distinct mechanisms @ScienceMagazine @MSKCancerCenter science.org/doi/10.1126/scie… science.org/doi/10.1126/scie…

Today I am sharing a new preprint and accompanying blog post. Hundreds of published papers include impossible western blots showing protein expression in cell lines that have deleted or mutated genes. These clumsy mistakes are widespread and repeated by LLMs.

Our new work by @YuyangLiu1996! Short-lived proteins are key regulators of metabolic homeostasis. By investigating their degradation, we identified TXNDC15 as a regulator of ER protein degradation and lipid homeostasis via a catalysis-independent mech. cell.com/cell-chemical-biolo…

Our work deorphanizing MCT6 as the missing gut Lac-Phe transporter is out today @CellCellPress: local gut lactate metabolism influences gut-brain crosstalk, and also explains metformin’s effects on body weight. Congratulations to @Shuke_Xiao @alanshtung! cell.com/cell/fulltext/S0092…

Glutamine + chemo in pancreatic cancer: Phase 1 GlutaPanc, n=16, 81% cachectic at baseline. 30g/day oral glutamine + full-dose gem/nab-paclitaxel, no glutamine DLTs. ORR 44%. nature.com/articles/s43018-0…

Hail to the Victors! 〽️

Keto suppressed colon tumors but promoted small-intestine adenomas in mice, via dietary fat → FAO → PPAR, not ketones. Same diet, opposite effects by site. Diet-as-therapy must be tumor- and site-specific. @ohyilmaz nature.com/articles/s41586-0…

Same calories, same macros — different metabolism. In a crossover trial (n=32 metabolic), an ultraprocessed meal drove higher insulin AUC than a matched minimally processed meal, with glucose AUC unchanged. nature.com/articles/s42255-0…

Excited to share our new publication in Nature Metabolism @NatMetabolism led by the fantastic @XingxiuPan, where we uncover an unexpected connection between reductive and oxidative stress. This study contains many exciting findings, and I will be highlighting different aspects of this work in a series of posts. One of the central conclusions is that the NADPH/NADP+ ratio is a critically underappreciated parameter in mitochondrial dysfunction. In this study we present SaNADK, a new xenotopic tool based on the S. aureus NAD kinase, which expands the cellular NADP(H) pool nearly six-fold! Most remarkably, together with the Peter Adams lab @AdamsBioAging, we found that increasing NADP(H) levels with SaNADK alone was sufficient to reverse age-associated hepatic transcriptomic signatures linked to metabolic dysfunction and inflammation as well as liver fibrosis highlighting the profound influence of NADP(H) metabolism on cellular aging. We also uncovered an important aspect of mitochondrial bioenergetics. We found that NADH-driven reductive stress can cause excessive reduction of the coenzyme Q pool, creating a bottleneck for multiple coenzyme Q-dependent reactions. As a consequence, electron flow through CoQ-linked systems is impaired, including DHODH activity and de novo pyrimidine biosynthesis. These findings may help explain numerous observations in the literature that have long appeared counterintuitive, namely that mild mitochondrial complex I inhibition can sometimes be beneficial. Here is the link to the study: nature.com/articles/s42255-0…

Introducing our next-gen “hypoxia in a pill” - we upgrade the combo by replacing GBT440 w/ 2nd-gen Hb affinity enhancer GBT601, and continue to pair with HIF-2α inhibitor PT2399. Highly effective in advanced Parkinson’s dz and Leigh syndrome mouse models tinyurl.com/35x36ayx

After many years of effort, deliberation, excitement, angst, joy, and Wednesday afternoon lab lunches, our group's first manuscript on cachexia, led by Venise Jan Castillon, Amy Xie, and really our whole lab nature.com/articles/s41591-0… @NatureMedicine

Shining the spotlight on our 🌟, Eileen Carpenter, MD, PhD. Dr. Carpenter recently gave the Rising Star Keynote address at the AACR Conference on Pancreatic Cancer @AACR @UMRogelCancer

Cool video about the discovery research on healthy aging and lifespan happening in @UMPhysiology in the @LeiserLab and by PhD student Sarah Easow. If you are interested in supporting discovery research like this go here: michiganmedicine.org/giving/…