J. Jeppesen et al., RELATION BETWEEN INSULIN-RESISTANCE, HYPERINSULINEMIA, POSTHEPARIN PLASMA-LIPOPROTEIN LIPASE ACTIVITY, AND POSTPRANDIAL LIPEMIA, Arteriosclerosis, thrombosis, and vascular biology, 15(3), 1995, pp. 320-324
We examined the relation between insulin resistance, plasma glucose an
d insulin responses to meals, lipoprotein lipase (LPL) activity, and p
ostprandial lipemia in a population of 37 healthy nondiabetic individu
als. Plasma glucose and insulin concentrations were determined at freq
uent inter vals from 8 AM through midnight (breakfast at 8 AM and lunc
h at noon); resistance to insulin-mediated glucose disposal was determ
ined by measuring the steady-state plasma glucose (SSPG) concentration
at the end of a 180-minute infusion of glucose, insulin, and somatost
atin; LPL activity was quantified in postheparin plasma; and postprand
ial concentrations of triglyceride (TG)-rich lipoproteins were assesse
d by measuring the TG and retinyl palmitate content in plasma and the
Svedberg flotation index (S())f >400 and S-f 20 to 400 lipoprotein fra
ctions. Significant simple correlation coefficients were found between
various estimates of postprandial lipemia and SSPG (r=.38 to .68), da
ylong insulin response (r=.37 to .58), daylong glucose response (r=.10
to .39), and LPL activity (r=-.08 to -.58). However, when multiple re
gression analysis was performed, only SSPG remained independently asso
ciated with both postprandial TG and retinyl palmitate concentrations.
These data provide evidence that insulin resistance plays an importan
t role in regulating the postprandial concentration of TG-rich lipopro
teins, including those of intestinal origin.