Insulin suppression of VLDL apo B secretion is not mediated by the LDL receptor

DV Chirieac, J Cianci, HL Collins, JD Sparks… - Biochemical and …, 2002 - Elsevier
DV Chirieac, J Cianci, HL Collins, JD Sparks, CE Sparks
Biochemical and biophysical research communications, 2002Elsevier
Insulin inhibits hepatic very low density lipoprotein (VLDL) apo B secretion in rats. Current
studies test whether the insulin effect is LDL receptor-mediated by examining the effect of
insulin on VLDL apo B secretion in hepatocytes derived from Ldlr-/-and control mice.
Primary hepatocytes were incubated overnight with media containing 14C-leucine and
either 0.1 nM (basal) or 200nM insulin. Afterwards, secreted VLDL B100 and B48 were
quantitated. Insulin reduced 14C-labeled B100 and B48 comparably in control and Ldlr …
Insulin inhibits hepatic very low density lipoprotein (VLDL) apo B secretion in rats. Current studies test whether the insulin effect is LDL receptor-mediated by examining the effect of insulin on VLDL apo B secretion in hepatocytes derived from Ldlr-/- and control mice. Primary hepatocytes were incubated overnight with media containing 14C-leucine and either 0.1nM (basal) or 200nM insulin. Afterwards, secreted VLDL B100 and B48 were quantitated. Insulin reduced 14C-labeled B100 and B48 comparably in control and Ldlr-/- hepatocytes with a 62±12% vs. 59±12% decrease in B100, and a 56±11% vs. 61±9% decrease in B48. Results indicate: (1) mouse hepatocytes respond to insulin by reducing VLDL apo B output; (2) both VLDL B100 and B48 secretion are suppressed; and (3) insulin inhibition of VLDL apo B secretion is retained in Ldlr-/- hepatocytes.
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