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ARS Home » Northeast Area » Beltsville, Maryland (BHNRC) » Beltsville Human Nutrition Research Center » Diet, Genomics and Immunology Laboratory » Research » Publications at this Location » Publication #222810
Title: Green Tea Extract Improves the Post Prandial Overproduction of Intestinal Apolipoprotein B-containing Lipoproteins in Fructose Fed Hamsters

Author
item QIN, BOLIN - ARS RESEARCH ASSOICIATE
item Dawson, Harry
item Anderson, Richard

Submitted to: Diabetes
Publication Type: Abstract Only
Publication Acceptance Date: 3/12/2008
Publication Date: 6/10/2008
Citation: Qin, B., Dawson, H.D., Anderson, R.A. 2008. Green Tea Extract Improves the Post Prandial Overproduction of Intestinal Apolipoprotein B-containing Lipoproteins in Fructose Fed Hamsters. Diabetes. 57:A705.

Interpretive Summary:

Technical Abstract: Green tea has putative medicinal properties that may be useful in preventing the metabolic syndrome. However, little is known of the effects of green tea extract (GTE) on postprandial apoB-48 containing lipoproteins and its molecular mechanisms. In a three-hour olive oil loading study, acute GTE oral treatment (200mg per kg BW) inhibited the overproduction of total apoB48 and triglyceride rich lipoprotein (TRL), free fatty acid levels, as well as triglyceride levels. We also investigated the molecular mechanisms of the effect of GTE (100ug per mL) on the expression of insulin signaling pathways genes (insulin receptor (IR), IRS1, IRS2, Akt1, and PI3K), and the relative genes (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, using quantitative real-time PCR. GTE increased the impaired 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 in a process involving improvement of insulin sensitivity of intestinal enterocytes and regulation of MTP, SREBP1c, and PTEN mRNA levels. We conclude that GTE may mimic metabolic actions of insulin to improve insulin resistance in enterocytes and oppose the overproduction of postprandial apoB-48 containing lipoproteins. Thus, consumption of green tea may be a beneficial adjunct in the treatment of dyslipidemia.