021: When Fat People Can’t Get Fat Enough and Lean People Get Fat in All the Wrong Places
Mastering Nutrition Episode 21
Introduction
In episode 20, 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 21, 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.
Show Notes
In this episode, you will find all of the following and more:
0:02:58 Cliff Notes
0:06:27 Mechanics of adipose tissue expansion
0:08:57 Consequences of poor adipose tissue expansion
0:10:32 Internal Stress as a consequence
0:12:55 Animal models of limitations to adipose expansion
0:17:29 Glycerol availability manipulated by PEPCK expression
0:20:38 Carbohydrate could play a role in preventing metabolic dysfunction by providing glycerol if glyceroneogenesis is limiting
0:21:23 Deletion of genes involved in lipid droplet formation
0:22:01 Septa organization
0:22:14 Deletion of collagen genes
0:23:11 Matrix metalloproteinases (MMPs)
0:24:21 Hypoxia and HIF1 – alpha
0:25:37 Inflammation (tumor necrosis factor alpha or TNF -alpha, interleukins or ILs toll-like receptors or TLRs) is necessary to allow proper extracellular matrix (ECM) reorganization and capillary bed reorganization
0:30:17 Visceral abdominal fat expansion is most protective because visceral fat drains directly into the liver via the portal vein, and releases more fat into the liver when it cannot expand further
0:35:10 Liver as the metabolic hub of fat and carbohydrate metabolism
0:37:02 Fat accumulation in liver likely directly compromises glycogen storage
0:42:05 Factors in fatty liver disease
0:44:04 Sources of liver fat: adipose, dietary fat, de novo lipogenesis (DNL) from carbohydrate is minor
0:50:34 Factors in triglyceride export: oxidative stress and choline
0:52:25 The choline requirement is increased more by fat than other macronutrients and more by long-chain saturated fats than other fats
0:58:11 Practical strategies: body composition is king and queen, but it might not be the right time to lose fat
0:59:38 A well rounded nutrient-dense diet is low-hanging fruit at any time
1:04:09 Additional strategies require nutritional analysis with the help of a health care professional and data generation
Related Links and Research
Episode 25 on what causes insulin resistance in an individual cell.
The Cell Biology of Fat Expansion
Adipocyte Inflammation Is Essential for Healthy Adipose Tissue Expansion and Remodeling
Mesenteric Fat Lipolysis Mediates Obesity-Associated Hepatic Steatosis and Insulin Resistance
Start Here for Fatty Liver Disease (and index of my related posts)
Episode 3 on The Sugar Conspiracy
AJCN Publishes a New PUFA Study That Should Make Us Long for the Old Days
Episode 23 on how I lost 30 pounds in four months, how I knew it was time, why it sometimes isn’t the right time to lose weight, and how to make it time.
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