We have previously reported that the
obesity-associated proinflammatory
cytokine,
TNF-alpha, stimulates the overproduction of intestinal
apolipoprotein (apo) B48 containing
lipoproteins. In the current study, we have evaluated whether a water-soluble cinnamon extract [CE (
Cinnulin PF)] attenuates the
dyslipidemia induced by
TNF-alpha in
Triton WR-1339 treated hamsters, and whether CE inhibits the oversecrection of apoB48-induced by
TNF-alpha in enterocytes in a 35S labeling study. In vivo, oral treatment of
Cinnulin PF (50 mg per kg BW), inhibited the postprandial overproduction of apoB48-containing
lipoproteins and serum
triglyceride levels. In ex vivo 35S labeling studies, CE (10 and 20 microg/ml) inhibited the oversecretion of
apoB48 induced by
TNF-alpha treated enterocytes into the media. To determine the molecular mechanisms,
TNF-alpha treated primary enterocytes isolated from chow-fed hamsters, were incubated with CE (10 microg/ml), and the expression of the inflammatory factor genes, IL1-beta,
IL-6, and
TNF-alpha,
insulin signaling pathway genes,
insulin receptor (IR), IRS1, IRS2,
phosphatidylinositol 3-kinase (PI3-K), Akt1 and
phosphatase and
tensin homology (PTEN), as well as the key regulators of lipid metabolism, cluster of differentiation (CD)36,
microsomal triglyceride transfer protein (
MTTP), and
sterol regulatory element binding protein (SREBP)-1c were evaluated. Quantitative real-time PCR assays showed that CE treatment decreased the
mRNA expression of IL-1beta,
IL-6 and
TNF-alpha, improved the
mRNA expression of IR, IRS1, IRS2, PI3K and Akt1, inhibited CD36,
MTTP, and PTEN, and enhanced the impaired
SREBP-1c expression in
TNF-alpha treated enterocytes. These data suggest that a water extract of cinnamon reverses
TNF-alpha-induced overproduction of intestinal
apoB48 by regulating gene expression involving inflammatory,
insulin, and
lipoprotein signaling pathways. In conclusion, Cinulin PF improves
inflammation related intestinal
dyslipidemia.