As insulin resistance increases, LDL particle number rises disproportionately to LDL cholesterol, with VLDL contributing.

“the combined effect of HDL triglyceride enrichment and elevated hepatic light base activity so hyper triglyceridemia and low plasma concentrations of HDL and quantitative qualitative excuse me changes in lowdensity lipoproteins which are small dense LDL as opposed to um my large buoyant LDL with a typical size of 24.7 anomet comprise the typical dyslipidemia of insulin resistant States in type two diabetes”

“in the insulin resistant patient where we typically see the LDL particle number being disproportionately higher than the LDL cholesterol by percentiles of course in absolute numbers that's always the case”

“I do know though there seems to be a longer residence time with vldls and we see that because that's the fasted blood yeah no we know that that's explained very clearly by a possi three the residence time on the LDL for that matter as well in pathologic states”

“even though the relative change on the LDL P is smaller it's starting from such a high base that it might add 3 to 400 in animal per liter which might only be a 30 or 40 percent increase but that absolutely dominates the lion's share of the increase not the extra 30 250 an animal per liter you might get on the VLDL”

“big vldls occur only in triglyceride rich lipoprotein pathologies by far the most common of which is insulin resistance”

“if you're not insulin resistant and you don't have a however you define a triglyceride issue which I might define as a trig above 130 or so anyway 40% of the april-b particles coming out of your liver or they're not vldls they're LDLs”

“there is more conversion of that VLDL particle into LDL particles which would be triglyceride rich through some transformation they become the small LDLs which are even less rapidly cleared so you're a poby particle rule number your LDL particle number goes through the roof”

“the more insulin resistance you get the more discordant you get between your LDL P and your LDL C and all things equal the LDL P is just going up and up and up as you become more insulin resistant”

“when you are presuming we're both insulin sensitive our VLDL really don't pose much of an Astra genic risk because they stick around for such a short period of time so we don't have many of them they don't stick around long our a possi 3 is quite down regulated”

“there's another apil protein that is made in excess and it's called APO protein C3 so the vldls coming out of the liver are now carrying something they shouldn't carry very much of apoc3 make a long story short it retards the catabolism of these triglyceride Rich vldls so it blocks their attachment to lipoprotein lipase so the plasma residence time of a vldl or kyom Micron which should be extremely short is now prolonged”

“if you look at certain characteristics of the low density lipoprotein the very low density lipoprotein and the high density lipoprotein you will see distinct patterns that that appear in insulin resistant people you would have bigger vldls cuz they're triglyceride carriers you would have smaller ldls because the triglycerides convert big ldls into small likewise you would not have big hdls because triglycerides enhance HDL catabolism making the HDL small so if you look at all those distinct and they're easily measurable by NMR”