The Peter Attia Drive’s Post

In this episode (#302) of The Drive, I speak with Julia Wattacheril, M.D., M.P.H., a physician scientist and director of the Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD) program at Columbia University Irving Medical Center. We delve deep into the complex world of liver health, beginning with a foundational overview of liver physiology. Julia provides an in-depth look at how alcohol impacts liver function, breaking down the metabolism of ethanol and its detrimental effects. Julia then shifts the focus to understanding liver function tests and optimal enzyme levels, providing a detailed explanation of AST and ALT and elucidating why fluctuations in these levels may or may not be concerning. Here’s a glimpse of what we discuss: - The complex and crucial functionality of the liver, its four most essential functions, and more - Methods of diagnosing liver disease and how insights guide treatment and management strategies - Potential impact of recreational drugs, statins, and other medications on liver function test results - The impact of fructose consumption on liver health and the challenges of disentangling its effects from other factors like obesity and insulin resistance - Emerging drugs and therapies for addressing fat accumulation and fibrosis related to MAFLD - More https://bit.ly/3V6pnCU

Excited to share our latest editorial with Dr. Milena Gulinac, MD, PhD: "Novel insights into autophagy in gastrointestinal pathologies, mechanisms in metabolic dysfunction-associated fatty liver disease and acute liver failure. Dive into our comprehensive exploration of three papers on the topic. 📑✨ Discover how our findings could pave the way for new therapeutic strategies. Don't miss out on these groundbreaking insights! #MedicalResearch #Gastroenterology #LiverDisease #Autophagy #ScientificInnovation #GROWTHresearchgroup #SUMMITproject #velikovamd 🔗 [https://lnkd.in/dmzhvzWg]

Researchers at St. Joseph's Healthcare Hamilton recently published an article in the Journal of Biological Chemistry highlighting the importance of a liver protein known as TDAG51, which is naturally expressed in healthy liver. TDAG51 was shown to be severely reduced in Non-Alcoholic Steatohepatitis (NASH) patient liver biopsies. Tamana Yousof, a PhD candidate in Dr. Richard Austin's laboratory, demonstrates that mice on a high-fat diet – which causes obesity and fatty liver disease – also display similar reductions in TDAG51 protein examined in the liver. She further demonstrates that increasing the levels of TDAG51 in the livers of obese mice improved metabolic outcomes and insulin sensitivity. These studies suggest that the maintenance of this liver protein may represent a viable therapeutic strategy for the treatment of obesity associated with Non-Alcoholic Fatty Liver Disease (NAFLD). Tamana's research focuses on examining endoplasmic reticulum stress pathways to find novel treatment strategies aimed at reducing obesity, diabetes, and metabolic dysfunction-associated fatty liver disease. She will be defending her PhD thesis in July. #PhDcandidate #research #liverdisease #NAFLD #NASH #healthscience #TDAG51

A recent study conducted by Prof. Ana Domingos's team at University of Oxford identified a group of sympathetic peripheral cells (#SPCs) expressing IL-33, which are LepR+ cells. These cells can wrap around nerve bundles, promote adaptive thermogenesis by preventing #inflammation. This study demonstrated that LepR+IL-33+ SPCs provide a cellular link between leptin and immune regulation of body weight, unifying #neuroendocrinology and #immunometabolism as previously disconnected fields of #obesity research. Read on: https://lnkd.in/g8hN2KEF #research #biotech #innovation #immune #bodyweight #metabolic

Non-alcoholic fatty liver disease (NAFLD) is a progressive disease that can further evolve towards liver fibrosis and hepatocellular carcinoma in the end stage. Costunolide (Cos) is a natural sesquiterpene lactone that exhibits both anti-inflammatory and antioxidant properties. However, the therapeutic effect of Cos on NAFLD is not clear. In this study, we explored the potential protective effect and mechanism of Cos on NAFLD. C57BL/6 mice were fed with high-fat diet (HFD) to induce NAFLD. Cos was administered by gavage to observe the effect of Cos on NAFLD. We demonstrated that oral administration of Cos reduced HFD-induced hepatic fibrosis and the release of inflammatory cytokines, limiting the generation of reactive oxygen species. In vitro experiments revealed that pretreatment with Cos significantly decreased PA-induced production of inflammatory cytokines and fibrosis in AML-12 cells. Mechanism study showed that the effect of Cos was correlated to the induction of Nrf-2 and inhibition of NF-κB pathways. Collectively, these findings indicated that Cos exerts hepatoprotective effect against NAFLD through blocking inflammation and oxidative stress. Our study suggested that Cos might be an effective pharmacotherapy for the treatment of NAFLD Wang J, Jin B, Chen Y, Chen Y, Zuo W, Huang L, Lin J, Jiang Y, Xie L, Lian X, Wang Y. Costunolide attenuates high-fat diet-induced inflammation and oxidative stress in non-alcoholic fatty liver disease. Drug Dev Res. 2024 Feb;85(1):e22150. doi: 10.1002/ddr.22150. PMID: 38349256. #Gesundheit #Bildung #Fuehrung #Coaching #Mindset #Motivation #Gehirn #Neuroscience #Psychologie #Persoenlichkeitsentwicklung #Kindheit #KeyNoteSpeaker #Humangenetik #Biochemie #Neuroleadership #Ernaehrung #Transformation #Stress #Demografie #Gender #Age #interkulturelleKompetenz #Epigenetik #Veraenderung #EmotionaleIntelligenz #Change #Gesellschaft #Organisationsentwicklung #Philosophie #Beratung # Quantum

I would like to inform you about the newly launched Research Topic “The Role of the Human Virome in Gastrointestinal, Liver, and Metabolic Disorders” in “Frontiers in Medicine" journal as the Topic Editors. The deadline for submitting the manuscript is 25 May 2024.  This research topic is to provide an up-to-date summary of recent findings on the role and the relationship of the human virome with gastrointestinal, liver, and metabolic disorders. #Frontiers

Welcome to this week's curated selection of cutting-edge research papers focusing on cardiometabolic diseases and mitochondrial function. My highlights: -> While German researchers found a new adrenergic agonist with potentially no complications for the cardiovascular system, a Danish group showed in humans activation of beta-2 adrenergic agonist leads to insulin resistance. -> The never-ending mission of understanding the interaction between carbohydrates and lipid metabolism was addressed in JBC. Good tools, and interesting findings. -> Adipose tissue inflammation gains another piece of the puzzle. IRF3 is a transcription factor activated in obesity and its inactivation protects mice from diet-induced obesity. The complete list can be found here 👇👇 👇 https://lnkd.in/gqa9vWSh Shout out to Biomed News for pre-sorting. #science #technology #machinelearning #mitochondria #diabetes

During oxidative stress, excess production of reactive oxygen species causes cell and tissue damage. Reductive stress is the counterpart of oxidative stress and occurs when cells build up too much of a molecule called NADH (nicotinamide adenine dinucleotide + hydrogen), which plays a role in energy production. New research led by scientists Russell Goodman, MD, DPhil, Charandeep Singh, PhD, and Vamsi Mootha, MD, at Massachusetts General Hospital (MGH), a founding member of the Mass General Brigham healthcare system, indicates that reductive stress causes changes in the liver and circulation, resulting in poor metabolic traits that can contribute to obesity and fatty liver disease. Learn more about the work published in Cell Metabolism: https://lnkd.in/g4j3nFzX

Astrocytes are more vulnerable to damage and can even become dysfunctional when the ɛ4 variant of apolipoprotein E (APOE ɛ4) surrounds their lipid storage centers. I.- Introduction. 1. Apolipoprotein E (APOE), a protein made up of 299 amino acids, is an amphipathic molecule that interacts both with the lipids of the core of a lipoprotein particle and with the aqueous environment. 2. In the brain, lipids perform essential functions such as storing energy and forming myelin. 3. When neurons are excited or stressed, they release toxic lipids into the environment and astrocytes (which produce APOE) are tasked with cleaning up those free-floating lipids and preventing them from accumulating in the brain by secreting APOE. 3.1. The task of APOE is to monitor the release and transport of lipids between cell types in the brain. 4. In astrocytes, lipids are stored in specialized compartments known as lipid droplets (LD). 4.1. If astrocytes do not do their cleaning task, microglia will not be able to clean amyloid beta plaques in the brain, a determining factor in Alzheimer's disease (AD). II.- Summary of the findings 5. The study suggests that the APOE ɛ4 variant can escape from secretion, become enclosed within astrocytes and migrate to LD within astrocytes, changing its shape and size. 5.1. Specifically, APOE ɛ4 in astrocytes can prevent translocation to the lumen of the endoplasmic reticulum (ER) and trafficking of LDs across membrane bridges at ER-LD contacts. 5.2. In this way, this APOE variant promotes fewer but larger LDs that contain more unsaturated triglycerides.

Part 1: The entry of micro- and nanoplastics (MNPs) into the human body is inevitable. They enter blood circulation through ingestion, inhalation, and dermal contact by crossing the gut-lung-skin barrier (the epithelium of the digestive tract, the respiratory tract, and the cutaneous layer). There are many reports on their toxicities to organs and tissues. This paper presents the first thorough assessment of MNP-driven bloodstream toxicity and the mechanism of toxicity from the viewpoint of both MNP and environmental co-pollutant complexes. Toxic impacts include plasma protein denaturation, hemolysis, reduced immunity, thrombosis, blood coagulation, and vascular endothelial damage, among others, which can lead to life-threatening diseases. Protein corona formation, oxidative stress, cytokine alterations, inflammation, and cyto- and genotoxicity are the key mechanisms involved in toxicity. MNPs change the secondary structure of plasma proteins, thereby preventing their transport functions (for nutrients, drugs, oxygen, etc.). MNPs inhibit erythropoiesis by influencing hematopoietic stem cell proliferation and differentiation. They cause red blood cell and platelet aggregation, as well as increased adherence to endothelial cells, which can lead to thrombosis and cardiovascular disease. Rajendran D, Chandrasekaran N. Journey of micronanoplastics with blood components. RSC Adv. 2023 Oct 27;13(45):31435-31459. doi: 10.1039/d3ra05620a. PMID: 37901269; PMCID: PMC10603568. #Gesundheit #Bildung #Fuehrung #Coaching #Mindset #Motivation #Gehirn #Neuroscience #Psychologie #Persoenlichkeitsentwicklung #Kindheit #KeyNoteSpeaker #Humangenetik #Biochemie #Neuroleadership #Ernaehrung #Transformation #Stress #Demografie #Gender #Age #ArtificialIntelligence #Epigenetik #Veraenderung #Organoidintelligence #Change #Gesellschaft #Organisationsentwicklung