At #DDW2024, Fractyl Health, Inc. (Nasdaq: GUTS) shared our latest developments with the scientific and medical community. We presented new preclinical data on liver metabolism in a diet induced obesity model and the potential of Rejuva® to durably impact obesity
The plenary presentation was delivered by Harith Rajagopalan, CEO of Fractyl Health. https://lnkd.in/edBc3dqY#type2diabetes#health#obesity#genetherapy#biotech
*The Rejuva platform is in preclinical development and has not yet been evaluated by regulatory agencies for investigational or commercial use.
Source: International journal of biological sciences
IL-33 is a key inflammatory factor in chronic atrophic gastritis (CAG) and is induced by H. pylori and MNNG through the ROS-STAT3 signaling pathway. IL-33 enhances autophagy in gastric epithelial cells through the AMPK-ULK1 axis, and inhibiting autophagy alleviates CAG severity. IL-33 also promotes GKN1 degradation through the autolysosomal pathway. IL-33 and GKN1 in serum show potential as diagnostic markers, and targeting the IL-33-AMPK-ULK1 pathway could be a therapeutic strategy for CAG.
Congratulation to Dr. Priyankar Dey’s team on their recent research investigating the cellular mechanisms underlying the hepatoprotective effects of Nerium oleander.
Their study revealed how oleander mitigates endotoxin-induced damage to hepatocytes. By using an in vivo model to test anti-inflammatory and metabolic health benefits, followed by evaluating oleander's impact on LPS-treated HepG2 cells, they provided strong evidence of oleander's hepatoprotective effects.
In this study, HepG2 cell counting was performed using our automated cell counter, FACSCOPE® B.
We are grateful for FACSCOPE® B being part of the research.
To read the full article:
https://lnkd.in/gMf3JAu9
More information about FACSCOPE® B:
https://lnkd.in/gQ6SBw-H#cellcounting#FACSCOPE#Curiosis#HepG2#LPM#oxidative#Nrf2
Accomplished drug discovery professional with a strong track record of pre-clinical development & strategic leadership from target inception to IND approvals.
Increased catalytic activity of the enzyme alcohol dehydrogenase (adh-1) is linked to extended lifespan & longevity of C. elegans through the degradation of glycerol, and glyceraldehyde, 2 major byproducts of lipid metabolism.
Another enzyme with promising translational and therapeutic implications.
https://lnkd.in/eMmyy4_k
I see metformin is getting quite some of attention in the media, so I will share again this study in which we very clearly showed that positive effects of metformin on glycans can be seen only in a very small subset of individuals. Glycans integrate genetic, epigenetic and metabolic factors and are therefore excellent tool to monitor effects of any kind of intervention. There are some individuals who benefit from metformin, but in a non-diabetic population this is surely less than 10%, and probably even less than 5% of population. Only when we looked in people with type 2 diabetes we see that 50% of more benefit from metformin (this study is still not published). Metformin has some serious side effects and taking it is an anti-ageing supplement without close supervision of a medical professional is probably not the best idea...
The link I am providing here is for a preprint, but with minor changes this is now accepted in Geroscience and will be published soon.
https://lnkd.in/ep_xeXa4
Over 1 billion people worldwide suffer from migraine. Recent breakthroughs in understanding its molecular basis have led to innovative treatments targeting the calcitonin gene-related peptide (CGRP). These developments are revolutionizing migraine management and paving the way for future and novel therapies. #migraine#HealthInnovation#painreliefhttps://shorturl.at/elMQS
Exciting breakthrough in diabetes research! 🌟 Just came across a compelling paper by Cell that unveils a novel mechanism potentially shaping the landscape of diabetes mellitus development. Could this be a groundbreaking subtype of diabetes? 🤔 The findings open up fresh avenues for exploring physiology and identifying promising therapeutic targets. Kudos to the researchers for pushing the boundaries! 🚀 #DiabetesResearch#Innovation#MedicalAdvancementshttps://lnkd.in/d6ThHYkR
Check out our new article where we explored how ( +)-Lipoic acid (ALA) affects inflammation and oxidative stress within an in vitro model. This model utilized HepG2 cells treated with palmitic acid and oleic acid to induce steatosis.
https://lnkd.in/d7-_CjH7
One of the challenge for such treatments is lack of clear understanding about how metabolism functions. Not everyone should receive same dosage, it must be adjusted according to each individual metabolic activity. Something that clinicians often fail to recognize. The metabolic capacity of each and every person is not the same, and how they would respond to metabolic inhibitors also vary. The dosages of metabolic inhibitory drugs must be titrated to keep the intended metabolite just below the threshold of where it should be. Most often in clinical practice, I see that they let cholesterol to dip below sub-physiological levels and say it's OK. I disagree, our body requires maintaining physiologically optimal levels of many metabolites, including cholesterol. So attempting to reducing cholesterol below certain levels will have rippling impacts on the entire bodily metabolic functions and could lead to serious damages. Knowing this biochemistry, and understanding the mechanistic basis of the side effects, I argued to adjust my dosage, which resulted in reversing the side-effects while maintaining the metabolism at clinically appropriate levels. When the clinician realized that I am biochemist, he appreciated my explanations.
Creating Scientific Success Stories with Metabolomics and Multiomics
𝗠𝗼𝗹𝗲𝗰𝘂𝗹𝗮𝗿 𝗺𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺𝘀 𝗼𝗳 𝘀𝘁𝗮𝘁𝗶𝗻-𝗿𝗲𝗹𝗮𝘁𝗲𝗱 𝗮𝗱𝘃𝗲𝗿𝘀𝗲 𝗲𝗳𝗳𝗲𝗰𝘁𝘀
Statins are generally very safe, but a small minority of patients face side effects that can lead to discontinuation of therapy. Muscle-related side affects (Statin Associated Muscle Symptoms, SAMS) are relatively common but poorly understood on a mechanistic basis. This metabolomics changes adds to our knowledge.
The authors conclude that changes in pro-inflammatory lipids and mitochondrial metabolism are key contributors to SAMS. This understanding may pave the way to better management of this side effect to this staple class of therapeutics that has attracted interest for its potential well beyond cardiometabolic diseases. https://lnkd.in/dYDRfaE3
Full citation: Garrett TJ, Puchowicz MA, Park EA, Dong Q, Farage G, Childress R, et al. (2023) Effect of statin treatment on metabolites, lipids and prostanoids in patients with Statin Associated Muscle Symptoms (SAMS). PLoS ONE 18(12): e0294498. https://lnkd.in/dX7cAY_y. Freely available under a Creative Commons license: https://lnkd.in/dATi2mun#science#metabolism#precisionmedicine#phermacology
Source: Phytomedicine : international journal of phytotherapy and phytopharmacology
Co-catalpol can alleviate fluoxetine-induced liver injury by inhibiting ferroptosis through ATF3/FSP1 signaling. This study provides insights into the detoxification mechanism and efficacy of co-catalpol in combination with fluoxetine for depression therapy. PMID: 38401490 | DOI: 10.1016/j.phymed.2024.155340
Global Strategic Partnerships Manager - driving medical education growth
4moHave a fantastic congress Fractyl team, unfortunately due to cancelled flights, I am now not able to attend and catch up 😕