The triacylglycerol hypothesis
Dietary effects on serum cholesterol or LDLs alone provide an
inadequate basis on which to explain the relationship between diet and CHD
within populations. The ability of humans to protect themselves against an
overaccumulation of cholesterol in their vascular system through nutritional
changes depends to a much greater extent on increasing the efficiency of the
HDL pathway and utilization of TAG-rich lipoproteins. The latter represent the
precursors of potentially harmful cholesterol-rich remnants and LDLs that contribute
to coronary atherosclerosis. The effects of diet, and in particular dietary
fats, in modu-lating the clearance of TAG-rich lipoproteins in the postprandial
period is of paramount importance in preventing the accumulation of atherogenic
remnants and development of proatherogenic abnormalities in LDL and HDL. The
actions of insulin coordinate the metabolism of TAG-rich lipoproteins but can
become defective through energy imbalance, weight gain, and ultimately obesity.
As a consequence, the most common abnormalities in lipoproteins to increase
risk in populations arise from a primary defect in the metabolism of TAG,
induced through insulin resis-tance and not cholesterol per se. Equally
important is the fact that these metabolic defects originate, in part, through
nutrient–gene interactions and are thus highly amenable to dietary
modification.
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