FAT MAKES AN ASP OF ITSELF

Izvor: KiWi

Until quite recently, it was thought in the scientific community that fat was metabolically inert and insulin was the only mechanism in the human body to store fat. New evidence completely refutes this on both accounts.
Here is some information to validate this:
There has been a paradigm shift from the notion of adipose tissue merely as a storage site for energy to one in which adipose tissue plays an active role in energy homeostasis and various processes.1
Adipose tissue (fat) is a complex, essential, and highly active metabolic and endocrine organ. Besides adipocytes (fat cells), adipose tissue contains connective tissue matrix nerve tissue, stromovascular cells, and immune cells. Together these components function as an integrated unit.2
Why is this important? Because we have discovered that fat (adipose tissue) is an endocrine organ. Other endocrine organs include, for example, the kidney and pancreas. An endocrine organ is a gland that produces and secretes hormones (chemical messengers) that travel through the bloodstream to other parts of the body. A hormone will attach itself to a cell that has a receptor for it.
In other words, the hormone is the key, and the cell is the lock. So for a hormone to bind to a particular cell, it must have the right key to fit into the right lock. This tells us that when a hormone binds to a cell, it has a very specific purpose, and that is to initiate some type of action. For example, a hormone secreted by adipose tissue might signal the body to up-regulate triglyceride (fat) storage.
We now know that fat is the largest endocrine organ and that it performs complex, physiological functions-it’s not just an inactive blob of cells. Some of the more prominent hormones secreted by adipose tissue are acylation stimulating protein (ASP), leptin, and adiponectin. For the purpose of this article, I will discuss only ASP.
I think researchers know more about leptin and adiponectin than they do ASP. This is one of the reasons ASP grabs my attention.
Digested fat from an oral load-whether it’s just fat or part of a meal-is converted in the small intestine into a lipoprotein called chylomicron. Chylomicrons are microscopic particles made up primarily of fat and a small amount of protein.3 “Lipo” means fat, thus the name lipoprotein.
Cells in the small intestine cover the fat with a protein coat, which makes it water soluble and renders it travel worthy. From here, the chylomicrons are released into the bloodstream (50% water), where they travel to the liver and other tissues of the body such as fat tissue. When the chylomicrons reach the adipose tissue, they bind to enzymes called lipoprotein lipases (LPL), which are located in the walls of blood vessels in fat tissue, and initiate the ASP pathway. Once activated, ASP signals fat cells to increase fat storage and glucose transport. Research has also shown that it augments the effects of insulin.4
Chylomicrons survive for only about eight minutes in the bloodstream, as they are broken into fatty acids by the action of LPLs.5 Although they have a short lifespan, they set into motion the action of ASP, which some scientists think is an even more potent stimulator of fat storage than insulin. The keywords here are “some scientists think.” This leaves some room open for debate over which is a more potent stimulator of fat storage, insulin or ASP.
This is a chapter from my book BEST DIET BOOKS EVER, For Weight Watchers Who Want Diets That Work.