The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
when you get this imbalance between fatty acid uptake versus oxidation in the mido versus storage is neutral lipid you get activation of these two novel pkcs in muscle theta and epsilon theta blocks insulin action at the level somewhere between the receptor and irs-1 tyrosine phosphorylation and epsilon and we'll get into this for the liver directly binds to the insulin receptor and then hits the receptor kinase
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basically it's a hydroxyl group a simple hydroxyl group it's the two fatty acids of the dag that sit into the bilayer membrane bilayer and then the hydrophilic hydroxyl group sits in the cytoplasm and that's what then will pull the novel pkcs to the plasma membrane
Lipid accumulation in the liver, specifically diacylglycerols, activates novel protein kinase C epsilon (PKCε), which directly inhibits the insulin receptor kinase.
um that uh diog glycerol or ceramides will feed back to the insulin receptor the glute four transport and the insulin receptor and cause insulin resistance
so what Jerry has shown very elegantly okay is that there are certain lipids uh deat is uh that's right is uh and it's a specific Decat they're like several types of Decat molecules which has confused things so he's shown this is specific one of the dgats that uh activates these eight atypical pkc uh uh uh molecules and that sering phosphates the insulin receptor when you serin phosphorate the molecules in that pathway it inactivates them okay and so he's done these very nice elegant studies both in peripheral muscle and in the liver showing that this plays a very very important role in the insulin resistance
what Jerry has shown very elegantly okay is that there are certain lipids uh deat is uh that's right is uh and it's a specific Decat they're like several types of Decat molecules which has confused things so he's shown this is specific one of the dgats that uh activates these eight atypical pkc uh uh uh molecules and that sering phosphates the insulin receptor when you serin phosphorate the molecules in that pathway it inactivates them