Vern Dolinsky

Incretin hormones GLP-1 and GIP connect #metabolism and cardiovascular #health. Our new review highlights the latest about how endogenous incretins shape cardiometabolic disease @khushali_triv @cdnsciencepub @PhysiolPharma @UM_RadyFHS cdnsciencepub.com/doi/10.1139/cj…

REVIEW: #Heart Failure in Type 1 vs. Type 2 #diabetes Shared Pathways, Distinct Challenges onlinelibrary.wiley.com/doi/10.1155/jd…

REVIEW: #Proteomics of the #heart @physiolrev journals.physiology.org/doi/full/10.11…

Functional validation of a non-canonical HNF1B splice-site variant in MODY5 #diabetes @FrontEndocrinol frontiersin.org/journals/endoc…

Check out this interesting paper @DREAM_diabetes @DREAM_trainees #diabetes

Maternal #obesity alters adipogenic potential and #mitochondrial maximal respiration in infant mesenchymal stem cells #DOHaD @FrontEndocrinol frontiersin.org/journals/endoc…

🚨Excited to share our single-cell multi-omic atlas of #stemcell islet differentiation that predicts cell fate decisions and identifies causal regulators of lineage specification. You can start browsing the data now 👉 synbioelab.com/islettwin Preprint 👉 biorxiv.org/content/10.648…

1. Our main biomedical funding body is telling Canadian PIs its review system is collapsing. 50% increase in applications (attributed to AI but really due to PIs dealing w/ is essentially a lottery). PIs declining to review due to fatigue from turning down so much awesome science

@mrlakin13 @JCI_insight Nice paper congrats

What do aging, inflammation, and mechanical stretch have in common? They all set the stage for atrial fibrillation (AF). We've long studied AF risk in endurance athletes, who paradoxically develop the same atrial remodeling as elderly patients with heart disease. The culprit?

The fascinating biology of targeting nuclear receptor ligands to GLP-1 receptor + cells continues, with the latest chapter studying GLP-1 E2 in NOD mice, with or without low dose aCD3 @DiabetologiaJnl #Sec" target="_blank" rel="nofollow noopener">link.springer.com/article/10.100…

Blood NAD+ may not be the aging biomarker many hoped for. Across 7 human cohorts, whole-blood NAD+ levels stayed remarkably stable with age and lifestyle changes—shifting mainly with nicotinamide riboside supplementation. #Aging #NAD #Longevity nature.com/articles/s4225…

From earlier this week: A landmark in cardiac metabolism: doi.org/10.1172/JCI202… Jay D. Horton & team @UTSWMedCenter find unrestrained fat oxidation in heart cells deplete cardiolipins that are needed for mitochondrial energy, triggering heart failure in mice and revealing a potential metabolic target. The figure shows decreased heart function in cardiac-specific ACC1/ACC2 double KO (dHKO) mice. #CardiacMetabolism #HeartFailure

New advances in understanding the wide range in human islet cell heterogeneity and secretory phenotypes from the Integrated Islet Distribution Program (IIDP). The abundance of δ cells showed the strongest association with insulin secretion and #T2D nature.com/articles/s4146…

Timing matters 🕒 For type 2 diabetes, afternoon/evening exercise boosts insulin sensitivity & glycemic control, while morning workouts may raise blood sugar. Later workouts are also linked to lower cortisol, less inflammation & better oxidative capacity. #Diabetes #ExerciseScience @WuTsaiAlliance sciencedirect.com/science/articl…

After Hungary, Putin and Trump’s overlapping influence operations have a new target. And this time it’s Canada. My latest… olgalautman.substack.com/p/putin-and-tr…

Plasma proteomic signature of frailty in 50,506 adults dlvr.it/TSQbyw

U.S., Russia interfering in Alberta separatist debate, study says globalnews.ca/news/11831073/…

🇨🇦 "How to hand your province to a foreign power in 10 steps. Danielle Smith’s playbook (at least as I see it.)" - Arlene Dickinson

The medical research you trust to keep you healthy is being manufactured by machines. Not peer reviewed. Not replicated. Not even based on real analysis. Just AI-assisted paper mills churning out thousands of studies that look legitimate, pass basic editorial checks, and enter the scientific record — where they will be cited, built upon, and eventually inform the treatment recommendations your doctor reads. A study published in PLOS Biology on May 8, 2025 — by researchers from the University of Surrey, Aberystwyth University, and the University of Bristol — documented what is happening to one of the most widely used health databases in the world. The US National Health and Nutrition Examination Survey. NHANES. A massive, freely available, AI-ready dataset containing health records from tens of thousands of Americans. The source data behind thousands of nutrition studies, disease risk analyses, and clinical recommendations. The systematic search strategy used here identified an average of 4 papers per annum from 2014 to 2021, but 190 in 2024 — up to October 9 alone. Four papers a year to 190 in ten months. Many post-2021 papers used a superficial and oversimplified approach to analysis, focusing on a single variable while ignoring more realistic multi-factor explanations. Here is the technique one researcher described with brutal clarity: "Imagine you're trying to pass an exam that has a particular pass rate, and you add as many questions as you want. You see which ones you got right, and you remove the ones that you got wrong. That's basically what they're doing." You run AI through every possible combination of variables in the dataset. Thousands of combinations. Some will produce a statistically significant result by pure chance. You publish those. You hide the rest. It looks like a finding. It gets past peer review. It enters the scientific record. This is called p-hacking. AI has industrialized it. The rise is entirely driven by papers from China, and there is evidence that some are being produced by paper-mill-like factories using AI. Paper mills are companies that produce fake scientific papers to order. A researcher — or a student, or a hospital administrator trying to meet publication quotas — pays for a paper. The mill produces it. AI has made the mill faster, cheaper, and harder to detect. The implications for public health are not hypothetical. Every systematic review — the gold standard of medical evidence used to produce clinical guidelines — draws from the published literature. If that literature contains thousands of AI-generated, statistically manipulated studies that claim associations between health conditions and dietary factors, environmental exposures, or medications — those false associations get pooled into the review. The review shapes the guideline. The guideline shapes what your doctor recommends. The scientific literature is at risk of becoming flooded with papers that make misleading health claims based on openly available data that are easy to process using artificial intelligence tools. (Leanware) That warning was published in May 2025. The flood has not slowed. Source: Suchak, Aliu, Harrison, Zwiggelaar, Geifman, Spick · University of Surrey + Aberystwyth University · PLOS Biology · May 8, 2025 · doi.org/10.1371/journa…

Why does cardiovascular risk of obesity persist for years despite weight loss? Why is it obesity so difficult to treat? We know the brain "defends" against weight loss via neuro-hormonal mechanisms back toward a previous state. --Adipocytes also carry memory of obesity (Hinte 2024). --So do adipose macrophages (Miranda 2025). 🆕 paper in EMBO Reports identifies long lasting memory in CD4 T cells. Researchers sequenced DNA methylation in CD4 memory T cells from mice on chow, mice on a high-fat diet, and mice that lost the weight on chow recovery. The recovery group's T cells retained characteristics of the obese phenotype: 104 genes methylated like the high-fat group, not the lean controls. Inflammatory effector memory cells stayed high through 5 weeks of weight loss. Six months of semaglutide in patients didn't shift them either. Some of the mechanisms identified: autophagy through STK26, immune senescence through CDKN1C. Palmitate stiffened the T cell membrane enough to alter receptor signalling and change DNA methylation downstream. The authors think it takes 5 to 10 years of sustained weight loss before the "methylome" resets. The inflammatory pathway is laid down long before obesity is treated and it lingers long after the scale moves. Obesity needs to be treated chronically, and we need to keep thinking of the disease in a deeper way that extends beyond weight loss itself. 🏁 doi.org/10.1038/s44319…

The Crewe lab is looking for a postdoc to study adipose extracellular vesicle signaling in cardiovascular disease. Send me an email if you are interested!