Journal of Nutrition LabDiet, Your World of Nutritional Answers

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wang, S.
Right arrow Articles by Koo, S. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, S.
Right arrow Articles by Koo, S. I.
© 2006 American Society for Nutrition J. Nutr. 136:2791-2796, November 2006

Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Epigallocatechin Gallate and Caffeine Differentially Inhibit the Intestinal Absorption of Cholesterol and Fat in Ovariectomized Rats1

Shu Wang3,4, Sang K. Noh2,5 and Sung I. Koo2,5,*

2 Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269 and 3 Department of Human Nutrition, Kansas State University, Manhattan, KS 66506

* To whom correspondence should be addressed. E-mail: sung.koo{at}uconn.edu.


   ABSTRACT
TOP
 ABSTRACT
Introduction
 Materials and Methods
 Results
 Discussion
 LITERATURE CITED
 
We conducted this study to determine whether green tea constituents, (-)-epigallocatechin gallate (EGCG) and caffeine, affect the intestinal absorption of cholesterol (CH), fat, and other fat-soluble compounds. Ovariectomized rats with lymph cannula were infused intraduodenally with a lipid emulsion containing 14C-labeled CH (14C-CH), {alpha}-tocopherol ({alpha}TOH), triolein, and sodium taurocholate, without (control) or with EGCG, caffeine, or EGCG plus caffeine, in PBS, pH 6.5. The lymphatic total 14C-CH was significantly lowered by EGCG (21.1 ± 2.1% dose), caffeine (27.9 ± 1.7% dose), and EGCG plus caffeine (19.3 ± 0.9% dose), compared with the control (32.4 ± 1.6% dose). The lymphatic output of esterified CH also was significantly lower in rats infused with EGCG (7.9 ± 0.7 µmol), caffeine (7.6 ± 0.2 µmol), and EGCG plus caffeine (7.5 ± 0.6 µmol) than rats in the control group (11.6 ± 1.7 µmol). Also, EGCG and caffeine significantly lowered the absorption of {alpha}TOH, another highly hydrophobic lipid. However, the lymphatic outputs of oleic acid (exogenous fatty acid marker) and other fatty acids of endogenous origin were not affected by EGCG but were markedly lowered by caffeine and EGCG plus caffeine. Caffeine significantly lowered the amount of lymph flow, regardless of whether it was infused alone (14.2 ± 3.9 mL) or with EGCG (18.6 ± 2.0 mL), compared with EGCG (22.2 ± 2.2 mL) alone and the control group (23.2 ± 3.8 mL). The caffeine-induced decline in lymph flow was associated with the lowering of lipid absorption. The results indicate that both EGCG and caffeine inhibit lipid absorption and that the inhibitory effects of the 2 tea constituents are not synergistic but mediated by distinctly different mechanisms.


   Introduction
TOP
 ABSTRACT
 Introduction
Materials and Methods
 Results
 Discussion
 LITERATURE CITED
 
Evidence from animal, human, and epidemiological studies (1–3) suggests that consumption of green tea may reduce the risk of coronary heart disease (CHD)6. Considerable attention has been directed to the role of green tea catechins in reducing CHD risk, because they possess antioxidant and antiinflammatory properties. Studies have shown that green tea catechins effectively inhibit lipid peroxidation and LDL oxidation in vitro (4–6). However, it remains controversial whether green tea consumption in humans results in inhibition of LDL oxidation or lipid peroxidation in vivo. Studies with human subjects showed that the majority of the plasma catechins are present mainly in the nonlipoprotein protein-rich fraction, with <10% of the total plasma catechins found in LDL (7). The level of green tea intake ranging from 5–8 cups/d was not effective in increasing the resistance to LDL oxidation ex vivo in adult humans (7) or inhibiting lipid peroxidation in vivo, as measured by urinary excretion of F2-isoprostanes (8).

Numerous animal studies showed that green tea or its catechins lower the blood levels of cholesterol (CH) in rats, mice, and hamsters (9–11), and triglyceride in animals fed a high-fat diet (12) or fed a high-fructose diet (13). Evidence suggests that green tea and its catechins may lower the plasma levels of lipids in part by inhibiting their intestinal absorption (14–16). At present, however, the mechanism underlying the inhibition of lipid absorption by green tea is yet to be determined. Green tea is derived from the tea plant, Camellia sinensis, by treating fresh tea leaves with hot steam and air, which results in the inactivation of polyphenol oxidase, producing its peculiar green color in comparison to black and oolong tea (17). The polyphenols in green tea are largely catechins constituting about one-third of its total dry weight (17). The major catechins present in green tea are (-)-epigallocatechin gallate (EGCG), (-)-epicatechin gallate, (-)-epigallocatechin, and (-)-epicatechin. Green tea catechins, particularly EGCG, are not readily absorbed, with small percentages of orally ingested catechins appearing in the blood in rats (18) and humans (19,20). Due to their rather poor absorption and greater availability in the intestinal lumen, catechins likely influence the luminal processes involved in lipid digestion and absorption (14–16). In addition to catechins, green tea contains a significant amount of caffeine in the range of 10–20 mg/g (21). In contrast to catechins, caffeine is rapidly absorbed from the intestine and known to affect intestinal absorptive and secretory functions (22). An earlier study (23) suggested that caffeine may lower intestinal CH absorption in rats. This suggestion was based on the observation that the amounts of labeled CH appearing in serum and tissues were significantly lower following oral doses of caffeine and 14C-labeled CH (14C-CH). However, no direct evidence exists that caffeine affects the intestinal absorption of CH or any other lipids. It is also unknown whether catechins and caffeine interactively influence the intestinal processes of lipid absorption.

In this study, we used ovariectomized rats as a model to mimic the physiologic conditions of ovarian hormone deficiency or the postmenopausal state in which serum levels of lipids are elevated with increased CHD risk. Using an in vivo animal model with lymph cannula, our study compared the effects of EGCG, caffeine, and EGCG plus caffeine on the intestinal absorption of CH, fat, and other lipids.


   Materials and Methods
TOP
 ABSTRACT
 Introduction
 Materials and Methods
Results
 Discussion
 LITERATURE CITED
 
    Animals and diet. Twenty female Sprague-Dawley rats (Harlan Sprague Dawley) initially weighing 228 ± 12 g were placed individually in plastic cages with stainless-steel wire bottoms in a windowless room maintained at 22 to 24°C, with a 12-h-light/-dark cycle (the light period from 0330 to 1530 h). All rats were cared for in an animal care facility in accordance with a protocol approved by the Institutional Animal Care and Use Committee of Kansas State University. The rats were given free access to deionized water and a diet formulated by Dyets according to the AIN-93 recommendations (24,25) as used in our previous study (14).

    Ovariectomy and cannulation of mesenteric lymph duct. At the end of 2 wk, rats were food deprived for 12 h and ovariectomized (26) under halothane anesthesia. Seven wk after ovariectomy, rats weighing 325–342 g were food deprived for 16 h, the major mesenteric lymph duct was cannulated with polyethylene tubing for lymph collection, and a silicone catheter was inserted into the proximal duodenum for lipid infusion, as described previously in detail (27). After closure of the abdominal incision by suture, the rats were placed in restraining cages and housed in a recovery chamber controlled at 30°C for 20 h. During the postoperative recovery period, a maintenance solution (277.0 mmol/L glucose in PBS containing 6.8 mmol/L Na2HPO4, 16.5 mmol/L NaH2PO4, 115 mmol/L NaCl, and 5 mmol/L KCl, pH 6.5) was infused at 3.0 mL/h through the intraduodenal catheter by an infusion pump (Harvard Apparatus, Model 935).

    Measurement of 14C-CH absorption. After the overnight postoperative recovery, each rat was infused at 3.0 mL/h via the duodenal catheter with a lipid emulsion with or without EGCG and/or caffeine. The lipid emulsion, prepared by sonication, consisted of 27.4 kBq [4-14C]-CH (14C-CH; specific activity, 1.9 GBq/mmol; Dupont-New England Nuclear) and the following (in µmol): 20.7 CH (99%; Sigma Chemical), 451.8 triolein (95%; Sigma Chemical), 3.1 all-rac-{alpha}-tocopherol ({alpha}TOH) (97%; Aldrich Chemical), 396.0 sodium taurocholate, with 123.6 EGCG (99%; Sigma Chemical), caffeine (99.5%; Sigma Chemical), or EGCG plus caffeine (123.6 µmol each), in 24 mL PBS, pH 6.5. A control lipid emulsion was prepared in the same manner but without EGCG and caffeine. The amount of EGCG in the lipid emulsion, set at 123.6 µmol in 24 mL, was to reflect the amount of catechins/g of popular green teas (21). The dosage of caffeine in the lipid emulsion was set on an equimolar basis for comparison with EGCG. On the basis of the rats' food intake of 20 g/d providing 334 kJ (AIN-93G diet), the dosages were equivalent to 0.17 mg EGCG/kJ and 0.072 mg caffeine/kJ, respectively. For a person consuming 8,360 kJ/d, the total amounts of EGCG and caffeine infused were equivalent to 3 cups (6 g dry green tea leaves) and 2 cups of coffee, respectively.

Lymph was collected hourly for 8 h into preweighed conical tubes containing 25 mmol/L disodium EDTA cooled in ice-filled beakers under subdued light. From the hourly lymph samples, the 14C-radioactivity was determined in 100-µL aliquots after mixing with scintillation liquid (Scinti Verse; Fisher Scientific) by scintillation spectrometry (Beckman LS-8100; Beckman Instruments). 14C-radioactivities appearing in hourly lymph samples were expressed as percentage of the total 14C-CH infused.

    Analysis of total CH, free CH, and esterified CH. For total CH (TC) analysis, lymph (120 µL) was added dropwise into a tube containing 300 µL of 33% KOH. After adding 3 mL ethanol to the mixture, lipids were saponified for 15 min at 60°C in a water bath. After cooling, 5 mL of hexane was added. The tube was capped, mixed well, then 1.5 mL of deionized water added and mixed. The upper solvent layer was transferred to another tube and dried under nitrogen. After drying under N2, 500 µL chloroform:methanol (1:3, v:v) was added. For free CH analysis, 200 µL of lymph was used for lipid extraction without saponification. CH in the extracts was separated by HPLC (Beckman HPLC with System Gold, Beckman Instruments) equipped with a C-18 reverse-phase column (Alltima C18, 5 µm, 4.6 x 150 mm; Alltech Associates). The mobile phase was isopropanol:acetonitrile:water (60:30:10) at 1.5 mL/min. Detection was monitored at 292 nm (Module 166; Beckman Instruments). Typical elution time for CH was 7.5 min. The esterified CH (EC) fraction was calculated by TC minus free CH.

    Analysis of fatty acids. Total lipids from 100 µL lymph were extracted by 2 mL of chloroform/methanol mixture (2:1, v:v) containing 10 mg of BHT/300 mL. An internal standard (17:0) was added during lipid extraction. For fatty acid analysis, the lipids were hydrolyzed with methanolic NaOH, and fatty acids were saponified and methylated simultaneously with BF3-methanol. The fatty acid methyl esters were analyzed by capillary GC (Hewlett-Packard, Model 6890) using an HP-INNOWax cross-linked polyethylene glycol phase capillary column (15 m, i.d. 0.53 mm; Resteck).

    Analysis of phospholipids and {alpha}TOH. From 100-µL aliquots of lymph samples, phospholipids (PL) were separated by a modification of the HPLC methods described by Kaduce (28) and Patton (29), as described in our previous study (30). {alpha}TOH in lymph was extracted with acetone with a slight modification of the procedure (31) and analyzed by HPLC, as described previously in detail (32).

    Statistics. All statistical analyses were performed using PC SAS (33). Repeated measures ANOVA was used with treatment as a between subjects factor and time as a within subjects factor. All analyses were performed using PROC MIXED procedure. At each time point, the means of different groups were compared by the Least Significant Difference test.


   Results
TOP
 ABSTRACT
 Introduction
 Materials and Methods
 Results
Discussion
 LITERATURE CITED
 
    Lymphatic outputs of 14C-radioactivity and CH. 14C-CH was used to determine the amount of exogenous CH taken up and released from intestine to mesenteric lymph. The total 14C-radioactivity appearing in the lymph collected for the 8-h period was lower (P < 0.01) in the rats infused with EGCG, caffeine, and EGCG plus caffeine than in the control rats (Table 1). Infusion of EGCG significantly decreased the hourly rates of 14C output at 2 h and thereafter, whereas caffeine alone did not affect the rate of 14C output until 6 h following its infusion, compared with controls, indicating that the effect of caffeine on14C output is not immediate but delayed (Fig. 1). Similarly, this delayed effect of caffeine was also observed with the simultaneous infusion of EGCG plus caffeine but with a more marked suppression of 14C output, as compared with EGCG alone (Fig. 1). Overall, EGCG was more effective in lowering the total amount and rate of 14C output than caffeine. The combined effect of EGCG and caffeine on 14C output was additive. However, no additive effect was noted with regard to the output of TC, which represents the total amount of CH from the exogenous source (lipid emulsion) and from bile and mucosal cells. EGCG and caffeine lowered the total output of CH, regardless of whether they were infused singly or in combination. Along with the decrease in TC output, there was a significant decrease in EC output with infusion of EGCG, caffeine, or both. The proportion of EC (%TC) did not differ between groups. The output of {alpha}TOH, another lipid of extreme hydrophobicity, was also significantly lowered by EGCG, caffeine, and EGCG plus caffeine (Fig. 2; Table 1). The combination of EGCG and caffeine additively lowered {alpha}TOH absorption but to a moderate extent.


View this table:
[in this window]
[in a new window]
  		TABLE 1 Total lymphatic outputs of various lipids and lymph flow in rats infused with EGCG, caffeine, or EGCG plus caffeine for 8 h1

 

Figure 1
View larger version (16K):
[in this window]
[in a new window]
  		Figure 1  The lymphatic absorption of 14C-CH at hourly intervals for 8 h during intraduodenal infusion of lipid emulsion without (control) or with caffeine, EGCG, or EGCG plus caffeine. Values are means ± SD, n = 5. Means at a time without a common letter differ, P < 0.05.

 

Figure 2
View larger version (17K):
[in this window]
[in a new window]
  		Figure 2  The lymphatic absorption of {alpha}TOH at hourly intervals for 8 h in rats during intraduodenal infusion of lipid emulsion without (control) or with caffeine, EGCG, or EGCG plus caffeine. Values are means ± SD, n = 5. Means at a time without a common letter differ, P < 0.05.

 
    Lymphatic outputs of fatty acids and PL. Oleic acid (OA) was the sole fatty acid included in the lipid emulsion in the form of triolein and used as a marker for fat absorbed from the exogenous source. EGCG did not significantly affect the output of OA compared with controls, whereas caffeine singly or in combination with EGCG significantly lowered its output (Table 2). Also, EGCG did not influence the outputs of other fatty acids of endogenous origin, such as 16:0, 18:0, 18:2, 18:3, and 20:4, whereas caffeine significantly lowered their outputs. When caffeine was administered along with EGCG, no such effect of caffeine was observed. Data on the hourly rate of fatty acid outputs showed that the effect of caffeine, singly or with EGCG, was late onset and only noticeable at 5 h and thereafter (data not shown). EGCG and caffeine, singly or in combination, significantly lowered the outputs of phosphatidylcholine (PC), lysophosphatidylcholine (LPC), and total PL (Table 1).


View this table:
[in this window]
[in a new window]
  		TABLE 2 Cumulative lymphatic fatty acid outputs in rats infused with EGCG, caffeine, or EGCG plus caffeine for 8 h1

 
    Lymph flow. The total volume of lymph secreted for 8 h was not affected by EGCG but markedly reduced by caffeine and EGCG plus caffeine, compared with controls (Table 1). In the rats infused with caffeine and EGCG plus caffeine, the hourly rate of lymph flow was significantly slower throughout the 8-h period of lipid infusion starting at 5 h, relative to EGCG and controls (Fig. 3). However, EGCG, when infused along with caffeine, ameliorated the suppressive effect of caffeine on lymph flow. The timing of the reduced rates of lymph flow in response to caffeine infusion coincided with that of the lower lymphatic absorption of 14C and {alpha}TOH (Figs. 1 and 2) and outputs of OA and other fatty acids of endogenous origin (Table 2).


Figure 3
View larger version (18K):
[in this window]
[in a new window]
  		Figure 3  The rate of lymph flow at hourly intervals for 8 h during intraduodenal infusion of lipid emulsion without (control) or with caffeine, EGCG, or EGCG plus caffeine. Values are means ± SD, n = 5. Means at a time without a common letter differ, P < 0.05.

 

   Discussion
TOP
 ABSTRACT
 Introduction
 Materials and Methods
 Results
 Discussion
LITERATURE CITED
 
This study provides evidence that EGCG and caffeine, whether infused singly or in combination, significantly inhibit the intestinal absorption of lipids. Our data here suggest that EGCG and caffeine differentially inhibit the absorption of lipids. The inhibitory effect of EGCG on CH and {alpha}TOH absorption is noticeable from the early phase of absorption, whereas the effect of caffeine is observed only during the late phase. In addition, EGCG has no effect, whereas caffeine has a strong inhibitory effect, on the absorption of fat (fatty acids). Also, caffeine significantly decreases the rate of mesenteric lymph flow, whereas EGCG does not. These findings suggest that the effects of EGCG and caffeine on lipid absorption are mediated via distinctly different mechanisms and vary depending on types of lipids.

Green tea catechins, particularly EGCG, are not readily absorbed in rats (34) and humans (35,36). Due to its presence in the intestinal lumen in high concentrations, EGCG likely influences the initial luminal processes of lipid hydrolysis and micelle formation, steps critical to the transfer of hydrolyzed lipids to the enterocyte for uptake. Under in vitro conditions, green tea and mixtures of catechins interfere with the luminal hydrolysis and micellar solubilization of lipids (15,37–40). Evidence shows that EGCG effectively precipitates CH from bile salt micelles, whereas it does not significantly affect the micellar solubility of fatty acids and monoacylglycerol, products of triglyceride hydrolysis by pancreatic lipase in the intestinal lumen (15,16). This observation is consistent with the present finding that EGCG is effective in lowering CH absorption but with no effect on fat (fatty acid) absorption. Our recent study (40) suggests that EGCG may also influence the micellar solubilization of lipids partly by inhibiting pancreatic phosholipase A2 (PLA2) activity. The study showed that EGCG, among the major green tea catechins, was most effective in inhibiting pancreatic PLA2 activity under in vitro conditions. When EGCG was intraduodenally infused in a lipid emulsion containing labeled PC in rats with lymph cannula, a large amount of the labeled PC remained unhydrolyzed in the small intestinal lumen, resulting in a significant decrease in the lymphatic output of the tracer (40). The initial action of pancreatic PLA2 is critical to the formation of mixed micelles and subsequent transfer of micellar lipids to the enterocyte (41,42). Homan and Hamelehle (43) demonstrated that the presence of unhydrolyzed PC in bile salt micelles markedly reduces the uptake of CH, a lipid of extreme hydrophobicity, whereas it did not interfere with the cell uptake of less hydrophobic lipids such as OA, monoacylglycerol, and retinol. Thus, the inhibition of luminal PC hydrolysis by EGCG may explain the strong inhibition of the lymphatic absorption of CH and {alpha}TOH and no significant effect on the absorption of fatty acid (fat), as observed here and in other studies (15,16,37,40). How EGCG inhibits PC hydrolysis is not clear, but EGCG may form complexes with PC in the intestinal lumen, hindering access to the substrate by pancreatic PLA2 (39) or directly with the enzyme protein (44,45) and thereby altering its conformation and catalytic activity. At present, it is unknown whether catechins may influence the cell uptake of CH and {alpha}TOH via the brush border membrane transporters (46–48) and intracellular processing and secretion of lipids via chylomicrons.

To our knowledge, these data provide the first direct evidence that caffeine inhibits the intestinal absorption of lipids. From our data, it is evident that the inhibitory effect of caffeine is not immediate but delayed. A previous study (23) showed that an oral dose of caffeine with 14C-CH in rats caused a 200% increase in 14C-radioactivity in the small intestinal tissue with significantly lower amounts of the tracer in serum, liver, and adipose tissues. This finding suggests that caffeine may not interfere with the luminal processes leading to the cell uptake of CH but delays the intracellular movement of the absorbed lipid from the enterocyte into the lymphatics. Unlike EGCG, caffeine is rapidly absorbed from the stomach and small intestine (22) and may have little impact on the luminal hydrolysis and micellar solubilization of lipids, but influence the intracellular events of lipid processing and transport involving chylomicrons. Methylxanthines, including caffeine, are known to elevate the intracellular levels of cAMP by inhibiting phosphodiesterase, which is responsible for the hydrolytic inactivation of cAMP (49). Previously, a study using hepatocytes in vitro (50) showed that the intracellular cAMP concentration rose when cells were cultured in the presence of isobutyl-methylxanthine. The rise in cAMP was accompanied by a decrease in the secretion of triacylglycerol, CH, and apoprotein B via VLDL. Thus, the possibility exists that caffeine may elicit a similar response in the enterocyte and interfere with the packaging and secretion of lipids via chylomicrons. Furthermore, studies showed that the mucosal accumulation of cAMP, as induced by caffeine, stimulates the intestinal secretion of fluid into the lumen with a decrease in net fluid absorption in rats (51) and humans (52). The cAMP-induced secretion of fluid may explain the marked decrease in lymph flow in the rats intraluminally infused with caffeine. A study by Tso (53) demonstrated that lymph flow has a profound effect on intestinal chylomicron transport from the enterocyte in rats. When the rate of intestinal lymph flow dropped to a critical level (30–40 µL/min), the appearance of chylomicrons into the lacteal was greatly delayed (53). Our data here indicate that during caffeine infusion, the rate of lymph flow rapidly fell to 20–25 µL/min, far below the critical threshold, at 5 h and thereafter. The decline in lymph flow rate coincided with the sharp decrease in lipid absorption. If caffeine inhibits lipid absorption by limiting lymph flow and chylomicron secretion, its inhibitory effect may be transient, because the lipids taken up by the enterocyte can be eventually released into the lymphatics after caffeine is withdrawn or fluid absorption is restored. Further studies are warranted to determine the exact mechanism underlying the effect of EGCG and caffeine and their potential interactive effect on intracellular packaging, transport, and secretion of lipids from the enterocyte.

In summary, this study provides direct evidence that EGCG and caffeine, when intraluminally administered, inhibit the intestinal absorption of lipids. The inhibition of lipid absorption by EGCG and caffeine may be mediated via distinctly different mechanisms. EGCG may interfere with luminal lipid hydrolysis and micellar solubilization, whereas caffeine may adversely affect the intracellular processing and secretion of lipids via chylomicrons from the enterocyte. Our findings suggest that intakes of EGCG and caffeine, at levels attainable by green tea or coffee consumption, may lower the absorption of CH and other lipids in humans. Further studies are necessary to investigate the exact mechanisms causing their inhibitory effects on lipid absorption and metabolism.


   FOOTNOTES
 
1 Supported in part by NIH R21AT001363-01A2 from the National Center for Complementary and Alternative Medicine (NCCAM). Back

4 Present address: Cardiovascular Nutrition Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA. Back

5 Present address: Department of Food and Nutrition, Changwon National University, Changwon, Kyongnam, 641-773, Korea. Back

6 Abbreviations used: 14C-CH, 14C-labeled cholesterol; CH, cholesterol; CHD, coronary heart disease; EC, esterified cholesterol; EGCG, (-)-epigallocatechin gallate; LPC, lysophosphatidylcholine; OA, oleic acid; PC, phosphatidylcholine; PL, phospholipid(s); PLA2, phosholipase A2; {alpha}TOH, {alpha}-tocopherol; TC, total cholesterol. Back

Manuscript received 28 June 2006. Initial review completed 2 August 2006. Revision accepted 23 August 2006.


   LITERATURE CITED
TOP
 ABSTRACT
 Introduction
 Materials and Methods
 Results
 Discussion
 LITERATURE CITED
 

1. Crespy V, Williamson G. A review of the health effects of green tea catechins in in vivo animal models. J Nutr. 2004;134:S3431–40.[Abstract/Free Full Text]

2. Cooper R, Morré DJ, Morré DM. Medicinal benefits of green tea: Part I. Review of noncancer health benefits. J Altern Complement Med. 2005;11:521–8.[Medline]

3. Cabrera C, Artacho R, Gimenez R. Beneficial effects of green tea: a review. J Am Coll Nutr. 2006;25:79–99.[Abstract/Free Full Text]

4. Da Silva EL, Piskula M, Terao J. Enhancement of antioxidative ability of rat plasma by oral administration of (-)-epicatechin. Free Radic Biol Med. 1998;24:1209–16.[Medline]

5. Ishikawa T, Suzukawa M, Ito T, Yoshida H, Ayaori M, Nishwaki M, Yonemura A, Hara Y, Nakamura H. Effect of tea flavonoid supplementation on the susceptibility of low-density lipoprotein to oxidative modification. Am J Clin Nutr. 1997;66:261–6.[Abstract/Free Full Text]

6. Vinson JA, Jang J, Yang J, Dabbagh Y, Liang X, Serry M, Proch J, Cai S. Vitamins and especially flavonoids in common beverages are powerful in vitro antioxidants which enrich lower density lipoproteins and increase their oxidative resistance after ex vivo spiking in human plasma. J Agric Food Chem. 1999;47:2502–4.[Medline]

7. van het Hof KH, Wiseman SA, Yang CS, Tijburg LBM. Plasma and lipoprotein levels of tea catechins following repeated tea consumption. Proc Soc Exp Biol Med. 1999;220:203–9.[Medline]

8. Hodgson JM, Croft KD, Mori TA, Burke V, Beilin LJ, Puddey IB. Regular ingestion of tea does not inhibit in vivo lipid peroxidation in humans. J Nutr. 2002;132:55–8.[Abstract/Free Full Text]

9. Muramatsu K, Fukuyo M, Hara Y. Effect of green tea catechins on plasma cholesterol level in cholesterol-fed rats. J Nutr Sci Vitaminol (Tokyo). 1986;32:613–22.[Medline]

10. Yang TTC, Koo MWL. Hypocholesterolemic effects of Chinese tea. Pharmacol Res. 1997;35:505–12.[Medline]

11. Suzuki H, Ishigaki A, Hara Y. Long-term effect of a trace amount of tea catechins with perilla oil on the plasma lipids in mice. Int J Vitam Nutr Res. 1998;68:272–4.[Medline]

12. Chan PT, Fong WP, Cheung YL, Huang Y, Ho WKK, Chen ZY. Jasmine green tea epicatechins are hypolipidemic in hamsters (Mesocricetus auratus) fed a high fat diet. J Nutr. 1999;129:1094–101.[Abstract/Free Full Text]

13. Yang MH, Wang CH, Chen HL. Green, oolong and black tea extracts modulate lipid metabolism in hyperlipidemia rats fed high-sucrose diet. J Nutr Biochem. 2001;12:14–20.[Medline]

14. Löest HB, Noh SK, Koo SI. Green tea extract inhibits the lymphatic absorption of cholesterol and {alpha}-tocopherol in ovariectomized rats. J Nutr. 2002;132:1282–8.[Abstract/Free Full Text]

15. Ikeda I, Imasato Y, Sasaki E, Nakayama M, Nagao H, Takeo T, Yayabe F, Sugano M. Tea catechins decrease micellar solubility and intestinal absorption of cholesterol in rats. Biochim Biophys Acta. 1992;1127:141–6.[Medline]

16. Ikeda I, Kobayashi M, Hamada T, Tsuda K, Goto H, Iamizumi K, Nozawa A, Sugimoto A, Kakuda T. Heat-epimerized tea catechins rich in gallocatechin gallate and catechin gallate are more effective to inhibit cholesterol absorption than tea catechins rich in epigallocatechin gallate and epicatechin gallate. J Agric Food Chem. 2003;51:7303–7.[Medline]

17. Harbowy ME, Balentine D. Tea chemistry. CRC Crit Rev Plant Sci. 1997;16:415–80.

18. Chen L, Lee M-J, Li H, Yang CS. Absorption, distribution, and elimination of tea polyphenols in rats. Drug Metab Dispos. 1997;25:1045–50.[Abstract/Free Full Text]

19. Warden BA, Smith LS, Beecher GR, Balentine DA, Clevidence BA. Catechins are bioavailable in men and women drinking black tea throughout the day. J Nutr. 2001;131:1731–7.[Abstract/Free Full Text]

20. Lee M-J, Maliakal P, Chen L, Meng X, Bondoc FY, Prabhu S, Lambert G, Mohr S, Yang CS. Pharmacokinetics of tea catechins after ingestion of green tea and (-)- epigallocatechin-3-gallate by humans: formation of different metabolites and individual variability. Cancer Epidemiol Biomark Prev. 2002;11:1025–32.[Abstract/Free Full Text]

21. Khokhar S, Magnusdottir SGM. Total phenol, catechins, and caffeine contents of teas commonly consumed in the United Kingdom. J Agric Food Chem. 2002;50:565–70.[Medline]

22. Higdon JV, Frei B. Caffeine and health: a review of human research. Crit Rev Food Sci Nutr. 2006;46:101–23.[Medline]

23. Fears R. The hypercholesterolemic effect of caffeine in rats fed diets with and without supplementary cholesterol. Br J Nutr. 1978;39:363–74.[Medline]

24. Reeves PG, Nielsen FH, Fahey GC Jr. AIN-93 purified diets for laboratory rodents: final report of the American Institute of Nutrition Ad Hoc Writing Committee on the reformulation of the AIN-76A rodent diet. J Nutr. 1993;123:1939–51.[Abstract/Free Full Text]

25. Reeves PG. AIN-93 purified diets for the study of trace element metabolism in rodents. In: Watson RR, editor. Trace elements in laboratory rodents. Boca Raton (FL): CRC Press; 1996. p. 3–37.

26. Waynforth HB, Flecknell PA. Experimental and surgical technique in the rat. San Diego (CA): Academic Press; 1997. p. 276–7.

27. Koo SI, Noh SK. Phosphatidylcholine inhibits and lysophosphatidylcholine enhances the lymphatic absorption of {alpha}-tocopherol in adult rats. J Nutr. 2001;131:717–22.[Abstract/Free Full Text]

28. Kaduce TL, Norton KC, Spector AA. A rapid, isocratic method for phospholipid separation by high-performance liquid chromatography. J Lipid Res. 1983;24:1398–403.[Abstract]

29. Patton GM, Fasulo JM, Robins SJ. Separation of phospholipids and individual molecular species of phospholipids by high-performance liquid chromatography. J Lipid Res. 1982;23:190–6.[Abstract]

30. Noh SK, Koo SI. Milk sphingomyelin is more effective than egg sphingomyelin in inhibiting intestinal absorption of cholesterol and fat in rats. J Nutr. 2004;134:2611–6.[Abstract/Free Full Text]

31. Zaspel BJ, Csallany AS. Determination of alpha-tocopherol in tissues and plasma by high-performance liquid chromatography. Anal Biochem. 1983;130:146–50.[Medline]

32. Koo SI, Noh SK. Phosphatidylcholine inhibits and lysophosphatidylcholine enhances the lymphatic absorption of {alpha}-tocopherol in adult rats. J Nutr. 2001;131:717–22.[Abstract/Free Full Text]

33. SAS Institute, Inc. SAS user's guide: statistics, version 5. Cary (NC): SAS Institute; 1985. p. 433–506.

34. Chen L, Lee M-J, Li H, Yang CS. Absorption, distribution, and elimination of tea polyphenols in rats. Drug Metab Dispos. 1997;25:1045–50.[Abstract/Free Full Text]

35. Warden BA, Smith LS, Beecher GR, Balentine DA, Clevidence BA. Catechins are bioavailable in men and women drinking black tea throughout the day. J Nutr. 2001;131:1731–7.[Abstract/Free Full Text]

36. Lee M-J, Maliakal P, Chen L, Meng X, Bondoc FY, Prabhu S, Lambert G, Mohr S, Yang CS. Pharmacokinetics of tea catechins after ingestion of green tea and (-)- epigallocatechin-3-gallate by humans: formation of different metabolites and individual variability. Cancer Epidemiol Biomark Prev. 2002;11:1025–32.[Abstract/Free Full Text]

37. Raederstorff DG, Schlachter MF, Elste V, Weber P. Effect of EGCG on lipid absorption and plasma lipid levels in rats. J Nutr Biochem. 2003;14:326–32.[Medline]

38. Juhel C, Armand M, Pafumi Y, Rosier C, Vandermander J, Lairon D. Green tea extract (AR25) inhibits lipolysis of triglycerides in gastric and duodenal medium in vitro. J Nutr Biochem. 2000;11:45–51.[Medline]

39. Shishikura Y, Khokhar S, Murray BS. Effect of tea polyphenols on emulsification of olive oil in a small intestine model system. J Agric Food Chem. 2006;54:1906–13.[Medline]

40. Wang S, Noh SK, Koo SI. Green tea catechins inhibit pancreatic phospholipase A2 and intestinal absorption of lipids in ovariectomized rats. J Nutr Biochem. 2006;17:492–8.[Medline]

41. Thomson AB, Cleland L. Intestinal cholesterol uptake from phospholipid vesicles and from simple and mixed micelles. Lipids. 1981;16:881–7.[Medline]

42. Reynier MO, Lafont H, Crotte C, Sauve P, Gerolami A. Intestinal cholesterol uptake: comparison between mixed micelles containing lecithin or lysolecithin. Lipids. 1985;20:145–50.[Medline]

43. Homan R, Hamelehle KL. Phospholipase A2 relieves phosphatidylcholine inhibition of micellar cholesterol absorption and transport by human intestinal cell line Caco-2. J Lipid Res. 1998;39:1197–209.[Abstract/Free Full Text]

44. Hollman PC, Tijburg LB, Yang CS. Bioavailability of flavonoids from tea. Crit Rev Food Sci Nutr. 1997;37:719–38.[Medline]

45. Guharay J, Sengupta B, Sengupta PK. Protein-flavonol interaction: fluorescence spectroscopic study. Proteins. 2001;43:75–81.[Medline]

46. Cai L, Eckhardt ER, Shi W, Zhao Z, Nasser M, de Villiers WJ, van der Westhuyzen DR. Scavenger receptor class B type I reduces cholesterol absorption in cultured enterocyte CaCo-2 cells. J Lipid Res. 2004;45:253–62.[Abstract/Free Full Text]

47. Davis HR Jr, Zhu LJ, Hoos LM, Tetzloff G, Maguire M, Liu J, Yao X, Iyer SP, Lam MH, et al. Niemann-Pick C1 Like 1 (NPC1L1) is the intestinal phytosterol and cholesterol transporter and a key modulator of whole-body cholesterol homeostasis. J Biol Chem. 2004;279:33586–92.[Abstract/Free Full Text]

48. Reboul E, Klein A, Bietrix F, Gleize B, Malezet-Desmoulins C, Schneider M, Margotat A, Lagrost L, Collet X, et al. Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. J Biol Chem. 2006;281:4739–45.[Abstract/Free Full Text]

49. Howell LL, Coffin VL, Spealman RD. Behavioral and physiological effects of xanthines in nonhuman primates. Psychopharmacology (Berl). 1997;129:1–14.[Medline]

50. Bjornsson OG, Sparks JD, Sparks CE, Gibbons GF. Regulation of VLDL secretion in primary culture of rat hepatocytes: involvement of cAMP and cAMP-dependent protein kinases. Eur J Clin Invest. 1994;24:137–48.[Medline]

51. Brady PG, Bayless TM. Methylxanthine induced small intestinal secretion. Johns Hopkins Med J. 1975;136:251–3.[Medline]

52. Wald A, Back C, Bayless TM. Effect of caffeine on the human small intestine. Gastroenterology. 1976;71:738–42.[Medline]

53. Tso P, Pitts V, Granger DN. Role of lymph flow in intestinal chylomicron transport. Am J Physiol. 1985;249:G21–8.




This article has been cited by other articles:


Home page
 J. Nutr.Home page
S. Shrestha, S. J. Ehlers, J.-Y. Lee, M.-L. Fernandez, and S. I. Koo
Dietary Green Tea Extract Lowers Plasma and Hepatic Triglycerides and Decreases the Expression of Sterol Regulatory Element-Binding Protein-1c mRNA and Its Responsive Genes in Fructose-Fed, Ovariectomized Rats
J. Nutr., April 1, 2009; 139(4): 640 - 645.
[Abstract] [Full Text] [PDF]

Home page
 J. Nutr.Home page
R. S. Bruno, C. E. Dugan, J. A. Smyth, D. A. DiNatale, and S. I. Koo
Green Tea Extract Protects Leptin-Deficient, Spontaneously Obese Mice from Hepatic Steatosis and Injury
J. Nutr., February 1, 2008; 138(2): 323 - 331.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wang, S.
Right arrow Articles by Koo, S. I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, S.
Right arrow Articles by Koo, S. I.

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Copyright © 2006 by American Society for Nutrition