The Daily Lipid
About This Show
Chris Masterjohn has a PhD in Nutritional Sciences and is Assistant Professor of Health and Nutrition Sciences at Brooklyn College in Brooklyn, NY. In this show, he cuts through the noise of sloppy science and brings you solid health and nutrition information that you can use to feel your best and get the most out of life.
Most Recent Episode
026: When Fat People Can't Get Fat Enough and Lean People Get Fat in All the Wrong Places
In episode 25, Insulin Resistance Isn't All About Carbs and Insulin, I explained why an individual cell would "decide" to stop taking up energy. Here in episode 26, I explain tissue-level energy overload, focusing on adipose tissue and liver. At adipose tissue, the problem with fatness isn't the amount of fat. It's that we've reached the point where we can't get any fatter. Well, we can, but we can no longer do so while maintaining a healthy organizational structure within adipose tissue that allows blood, oxygen, and nutrients to get to where they need to go. Surprisingly, some of the things that enable proper expansion, and thus protect our metabolic health, are things that we usually think of as "bad," such as inflammation. In fact, the pro-inflammatory changes in the gut microbiome in response to an obesogenic diet provide information to adipose tissue that it needs to prepare for healthy expansion. And adipose expansion is most protective at the site of the "bad" body fat: visceral fat in the abdomen. At liver, the problem is fat gets trapped in the liver, flattening out everything in the cell and hogging the space needed for glycogen storage, and this can happen even in a lean person. I conclude with some practical recommendations about body composition and nutrient density. In this episode, you will find all of the following and more: How adipose tissue expands (triglyceride and lipid droplet formation, extracellular matrix reorganization, capillary bed growth and reorganization); consequences of poor adipose tissue expansion (liver spillover into ectopic deposition in tissues like liver, skeletal muscle, and pancreas, internal oxidative and endoplasmic reticulum stress, hypoxia); providing more glycerol for greater triglyceride formation (via genetic manipulation of PEPCK to allow greater glyceroneogenesis) protects against metabolic dysfunction (which may indicate a protective role of carbohydrate, which provides the glycerol on a mixed diet); deletion of genes involved in lipid droplet formation exacerbates metabolic dysfunction; allowing matrix metallopproteinases (MMPs) to reorganize the collagen-based extracellular matrix known as septa protects against metabolic dysfunction; expression of hypoxia-inducible factor 1-alph (HIF1alpha) contributes to metabolic dysfunction; inflammation (tumor necrosis factor alpha or TNF-alpha, interleukins or ILs, toll-like receptors or TLRs) is necess