We have reported previously that a cinnamon extract (CE), high in type A
polyphenols, prevents
fructose feeding-induced decreases in
insulin sensitivity and suggested that improvements of
insulin sensitivity by CE were attributable, in part, to enhanced
insulin signaling. In this study, we examined the effects of CE on postprandial
apolipoprotein (
apo) B-48 increase in
fructose-fed rats, and the secretion of
apoB48 in freshly isolated intestinal enterocytes of
fructose-fed hamsters. In an
olive oil loading study, a water-soluble CE (
Cinnulin PF, 50 mg/kg
body weight, orally) decreased serum
triglyceride (TG) levels and the over production of total- and TG-rich lipoprotein-apoB48. In ex vivo (35)S labeling study, significant decreases were also observed in
apoB48 secretion into the media in enterocytes isolated from
fructose-fed hamsters. We also investigated the molecular mechanisms of the effects of CE on the expression of genes of the
insulin signaling pathway [
insulin receptor (IR), IR substrate (IRS)1, IRS2 and Akt1], and
lipoprotein metabolism [
microsomal TG transfer protein (MTP),
sterol regulatory element-binding protein (SREBP1c) in isolated primary enterocytes of
fructose-fed hamsters, using quantitative real-time polymerase chain reaction. The CE reversed the expression of the impaired IR, IRS1, IRS2 and Akt1
mRNA levels and inhibited the overexpression of MTP and SREBP1c
mRNA levels of enterocytes. Taken together, our data suggest that the postprandial hypertriglycerides and the overproduction of
apoB48 can be acutely inhibited by a CE by a mechanism involving improvements of
insulin sensitivity of intestinal enterocytes and regulation of MTP and SREBP1c levels. We present both in vivo and ex vivo evidence that a CE improves the postprandial overproduction of intestinal apoB48-containing
lipoproteins by ameliorating intestinal
insulin resistance and may be beneficial in the control of lipid metabolism.