Step 1: Recall the substrate of lipoprotein lipase. This endothelial enzyme strips triacylglycerol out of the two largest, most TG-loaded particles: chylomicrons (dietary fat) and VLDL (hepatic fat). Apo CII switches the enzyme on.
Step 2: Knock out the enzyme and the particle that arrives first and is most TG-rich piles up the most. Dietary chylomicrons enter the blood after every meal, so with no LPL they are not degraded and their level rises sharply, producing milky plasma. This picture is Type I hyperlipoproteinemia.
Step 3: Map the distractors to their own disorders. $LDL$ rises in familial hypercholesterolemia (Type II, receptor problem). $VLDL$ predominates in Type IV. $HDL$ is the anti-atherogenic carrier and is not the accumulating fraction here.
Step 4: Clinically the patient shows eruptive xanthomas, an enlarged tender liver and bouts of abdominal pain or pancreatitis, treated by cutting fat intake and giving medium chain triglycerides that bypass the chylomicron route.
\[\boxed{\text{Chylomicrons}}\]