Commonly, the dietary sources of fat exceed the actual needs and the tissues are faced with dealing with the excess. Under these circumstances, the removal process of dietary triglycerides and fatty acids becomes overloaded, resulting in excessive postprandial lipemia and accumulation of chylomicrons, remnant particles and non-esterified fatty acids. These particles are associated with disruptions in lipoprotein metabolism and changes in inflammatory factors, thus their association with cardiovascular disease, metabolic syndrome and diabetes is not surprising. Dietary factors, not just fat, influence postprandial fluxes. This leads to the question: do we need a standardized fat tolerance test?
I've been reading a lot of studies lately dealing with postprandial clearance of fats from the blood and it certainly seems to me that these are coalescing to a hypothesis that the fat tissue fails first. Oh but CarbSane, you've been saying this for over a year now This is news? Well, yes, in a way. Gratuitous third person self referencing aside, it does still appear that a breakdown in fat tissue regulation is the precipitating factor in the metabolic dysfunction cascade in the majority of cases. However this initial breakdown appears to occur on the uptake side of the adipocyte. Impaired fatty acid uptake by adipose tissue leads to elevated postprandial circulating NEFA that are:
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- Excessive in the postprandial phase when they should be low, and/or
- Different in composition, reflecting dietary intake, from the types of fatty acids released from stored body fat.
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