Insulin receptor differential splicing
Hi, I was just reading a bit on the differential splicing of the insulin receptor. In one form it binds well to IGFII, but in another form it does not. It is thought the upregulation of one form might be important to the development of insulin resistance. Anyone here have some thoughts on this?
This is true of a lot of genes. For example, it also happens with the thyroid hormone nuclear receptor. As a general mechanism, it greatly adds to the complexity of molecular biology and physiology. It's a prime example of why I try not to be too black-and-white about nutrition and physiology. There's just so much that don't understand fully yet.
Every time I hear black-and-white pronouncements (whether it's cholesterol causes atherosclerosis; or LDL is bad and HDL is good; or the absolute lowest carb intake is the healthiest; or PUFAs are good, or PUFAs are bad), I figure it's only a matter of time before science figures out that there are variant types (of substances in the diet, or of proteins in the body, like enzymes, receptors, etc.) involved that weren't taken into account. It's fascinating but frustrating too!