Just to finish on glycation before moving on to signaling molecules, I'd like to add to Dave Dixon's comments about meal timing and chylomicron peaks after the segragation post. Let's just have a quick think about a serious low fat diet, using real food, say as eaten on Kitava or by the non vegetarian Bantu. These people are up at 70% of calories from carbohydrate. They tend to have the typical elevated fasting triglycerides of carbohydrate based diets, but not the heart disease associated with similarly elevated triglycerides in Western populations. Fasting triglycerides are VLDL particles released from the liver to move carbohydrate derived lipid to adipose tissue or muscle. They may have some PUFA from chylomicrons which have been taken up by the liver. They're certainly not chylomicrons in healthy people.
What's happening on the glycation front here? Post prandially there will be a marked glycation hot spot in the portal vein. This is unavoidable on a high carbohydrate diet. Insulin will rise and insulin promptly inhibits the release of VLDL particles from the liver. Same principle as we went through in this post, using all night glucose bingeing to "treat" hypertiglyceridaemia.
So, post prandially there are minimal chylomicrons due to the low fat content of the diet and VLDL secretion is inhibited. This is a neat way of separating glycation after a carb load from contact with any apoB containing lipids. As glucose uptake tails off, insulin falls and the processed glucose beyond acute needs can be shipped out as VLDLs, primarily as saturated fat which won't generate lipid peroxides anyway.
So there is some scope for genuine low fat diets to avoid glycation problems. You can have your fasting VLDLs up at 3.0mmol/l, just so long as they are full of palmitic acid and don't have sugar all over their apoB100 tags. You'll barely have a chylomicron anywhere to be seen at any stage, so who cares about that apoB48 tag?
It's the three times daily mix of sugar and soy oil (with fridge raid at 3am) which sets the scene for vascular catastrophe. The apoB counts might be the same in Kitava as in the USA, but the sugar coating and rancid fatty acid contents on and in those apoB tagged particles may be very different.