The College of Glycation is an educational video series dedicated to helping viewers understand one of the most critical and often overlooked processes in human biology: glycation. Led by Dr. Paul Reynolds, Professor of Cell Biology and Physiology at Brigham Young University, this series explores how sugar interacts with proteins and fats in the body, forming harmful compounds called Advanced Glycation End-products (AGEs). These compounds accelerate aging, contribute to chronic diseases, and play a key role in metabolic dysfunction. Each video is designed to break down complex topics into clear, practical insights. Whether you’re a healthcare professional, student, or simply someone seeking to improve your health, this series will give you a deeper understanding of the biological roots of inflammation, insulin resistance, and cellular damage—and what you can do to address them.
Curated by: PaulReynoldsPhD (74 videos)
Topic Adipose glycation and fat cell hypertrophy: big fat cells aren’t just “full” — they’re chemically modified, inflamed, and driving their own enlargement. Paul Reynolds reveals how glycation inside adipocytes creates a vicious, self-sustaining loop of methylglyoxal production, AGE-RAGE signaling, hypoxia, and insulin resistance — turning fat storage into a primary engine of metabolic disease, independent of total body weight. Summary Paul Reynolds, biomedical scientist and Professor of Cell Biology, dives deep into the hidden chemistry of adipose tissue in this eye-opening episode of the College of Glycation. He explains how glycation — the non-enzymatic attachment of sugars to proteins and lipids — doesn’t just happen to fat cells; it happens inside them, especially when adipocytes become hypertrophic. Far from being passive storage tanks, fat cells actively sense, secrete, and signal. When they exceed their healthy expansion limit (the “fat expandability hypothesis” of Antonio Vidal-Puig and others), they generate methylglyoxal (MGO), upregulate RAGE (receptor for advanced glycation end-products), and trigger NF-κB-driven inflammation. Landmark studies show this process actively drives hypertrophy rather than merely resulting from it: RAGE activation enlarges adipocytes, suppresses adiponectin and GLUT4, recruits macrophages into crown-like structures, and impairs insulin signaling at the receptor and PI3K level. Reynolds connects the dots between glycation, hypoxia (large adipocytes outgrow their blood supply, activating HIF-1α and fibrosis via lysyl oxidase), and microvascular damage caused directly by MGO. The result is a closed loop: more glycation → worse hypoxia → more inflammation → further hypertrophy. This explains why visceral fat is metabolically more dangerous, why some ethnic groups develop full metabolic syndrome at lower BMIs, and why two people with identical BMI can have dramatically different health outcomes. Practical takeaways are empowering: lower chronic insulin (the upstream driver of both hyperplasia and hypertrophy), reduce fructose and excess glucose to limit MGO formation, support the glyoxalase detoxification system with sulforaphane, polyphenols, magnesium, and glutathione precursors, and stay physically active to improve adipose perfusion and raise soluble RAGE. Glycation in fat cells is not destiny — it is a controllable metabolic input. References and more For complete show notes and references, we invite you to become an Insider subscriber. You'll enjoy a weekly newsletter, premier early access to College of Glycation episodes with full reprints of cited publications, a dedicated College of Glycation question portal with live recorded answers, Paul's Weekly Research Review Podcasts, and more. Learn more: paulreynoldsphd.com Translation Notes You can click the gear icon at the bottom of this video to auto-translate captions. For example, to translate into French, select Subtitles, choose Auto-Translate, then first choose English, then choose Auto-Translate again, then choose French. Timestamps 0:01 Adipose glycation intro 0:34 Glycation basics 2:43 Hyperplasia vs hypertrophy 3:29 Small vs hypertrophic fat cells 4:16 Fat expandability hypothesis 5:42 Hypertrophy glycation drivers (insulin/fructose/MGO) 7:57 MGO alters fat & insulin signaling 9:30 RAGE drives inflammation & hypertrophy 14:08 Hypoxia & fibrosis 15:49 MGO impairs blood supply 17:28 Visceral fat & ethnicity risks 19:02 Takeaways: lower insulin, cut fructose, exercise 22:05 Conclusion NOTE The information presented is for educational purposes only and is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Paul Reynolds is a biomedical scientist and professor of cell biology, not a licensed clinician. Always seek the advice of your own qualified health providers with questions you may have regarding medical conditions. #AdiposeGlycation #FatCellBiology #AdipocyteHypertrophy #Methylglyoxal #MGO #RAGE #Glycation #Inflammation #AGERAGE #AdiposeInflammation #FatExpandability #VisceralFat #BodyComposition Paul’s favorite yerba mate: https://unicity.link/121f260bfe Yerbe mate with a special formulated Balance fiber: https://ufeelgreat.com/c/PaulReynolds Full Metabolic System storefront: https://shop.unicity.com/paulreynolds Paul’s favorite source for clean, earth-sourced essentials such as salt, electrolytes, hydration, pre-workout and more. Go to https://redmond.life and use PAULSALT for 15% discount. Paul’s favorite exogenous ketones: A high-quality option is the NSF-certified goBHB from Clean Form Nutrition, where you can use the code Paul10 for a 10% discount: https://cleanformnutrition.com/products/go-bhb Paul’s favorite allulose source: https://rxsugar.com (discount: PAUL20) Paul’s favorite health check-up for men or women: https://blokes.co/DRPAUL (discount: DRPAUL for 50% off of labs and smart supplements and 15% off all other products)