ARS | Publication request: Green Tea Extract Improves the Postprandial Overproduction of Intestinal Apolipoprotein B-containing Lipoproteins in Fructose-Fed Hamsters

Submitted to: BARC Poster Day
Publication Type: Abstract Only
Publication Acceptance Date: March 25, 2008
Publication Date: March 25, 2008
Citation: Qin, B., Dawson, H.D., Anderson, R.A. 2008. Green Tea Extract Improves the Postprandial Overproduction of Intestinal Apolipoprotein B-containing Lipoproteins in Fructose-Fed Hamsters . BARC Poster Day.

Technical Abstract: Green tea has putative medicinal properties that may be useful in preventing the metabolic syndrome since increased consumption of green tea extract (GTE) is associated with improved lipid and glucose homeostasis in human and animals. The acute effect of GTE on postprandial intestinal apoB48 production in fructose-fed, insulin-resistant Syrian golden hamsters was measured. Acute GTE oral treatment (200mg per kg BW) inhibited the overproduction of total apoB48 and triglyceride rich lipoprotein (TRL), free fatty acid levels, and triglyceride levels in a three-hour olive oil loading study. The effect of GTE (100ug per mL) on the expression of insulin signaling pathway genes IRS1, IRS2, Akt1, and PI3K, microsomal triglyceride transfer protein (MTP), sterol regulatory element-binding protein (SREBP)1c, and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) of lipid metabolism in fresh isolated primary enterocytes of fructose-fed hamsters was determined by quantitative real-time PCR. GTE increased IR, IRS1, IRS2, Akt1, and PI3K mRNA levels of enterocytes by 100, 55, 65, 80, and 47%, respectively; GTE inhibited the increased MTP, SREBP1c, and PTEN mRNA levels of enterocytes by 35, 60, and 25%, respectively. In summary, these data suggest that the postprandial overproduction of intestinal-derived apoB48 can be acutely inhibited by GTE through improved insulin sensitivity of intestinal enterocytes and regulation of MTP, SREBP1c, and PTEN mRNA levels. We conclude that GTE mimics the metabolic action of insulin to improve insulin resistance and oppose the overproduction of postprandial apoB-48 containing lipoproteins.