Experimental data show that insulin administration in the postprandial state increases LPL activity in adipose tissue. What is the most plausible physiological interpretation of this observation?

Insulin stimulates adipose LPL activity to promote hydrolysis of chylomicron triglycerides and uptake of liberated fatty acids into adipocytes for re-esterification and storage, facilitating nutrient storage during the fed state.

Insulin acts primarily in the liver to suppress LPL gene expression, so adipose increases in LPL activity are an artifact resulting from redistribution of pre-existing enzyme rather than a true upregulation in adipocytes.

Insulin upregulates LPL systemically to prevent any fatty acid uptake by adipose tissue and instead forces all released fatty acids to be oxidized immediately in muscle, thereby decreasing adipose lipid storage.

Insulin binding to chylomicron apolipoproteins directly converts LPL into a non-specific protease that degrades lipoproteins to amino acids for gluconeogenesis, which accounts for observed increases in LPL activity measurements.