AJCN EB Program 2010
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF 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
Right arrow Citation Map
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 Venables, M. C
Right arrow Articles by Jeukendrup, A. E
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Venables, M. C
Right arrow Articles by Jeukendrup, A. E
Agricola
Right arrow Articles by Venables, M. C
Right arrow Articles by Jeukendrup, A. E
American Journal of Clinical Nutrition, Vol. 87, No. 3, 778-784, March 2008
© 2008 American Society for Nutrition

ORIGINAL RESEARCH COMMUNICATION

Green tea extract ingestion, fat oxidation, and glucose tolerance in healthy humans1,2

Michelle C Venables, Carl J Hulston, Hannah R Cox and Asker E Jeukendrup

1 From the Human Performance Laboratory, School of Sport and Exercise Sciences, The University of Birmingham, Birmingham, United Kingdom

2 Reprints not available. Address correspondence to AE Jeukendrup, School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom. E-mail: a.e.jeukendrup{at}bham.ac.uk.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Background: Green tea consumption is reportedly associated with various health-promoting properties. For example, it has been shown to promote fat oxidation in humans at rest and to prevent obesity and improve insulin sensitivity in mice.

Objective: We investigated the effects of acute ingestion of green tea extract (GTE) on glucose tolerance and fat oxidation during moderate-intensity exercise in humans.

Design: Two studies were performed, both with a counter-balanced crossover design. In study A, 12 healthy men performed a 30-min cycling exercise at 60% of maximal oxygen consumption (VO2max) before and after supplementation. In study B, 11 healthy men took an oral-glucose-tolerance test before and after supplementation. In the 24-h period before the experimental trials, participants ingested 3 capsules containing either GTE (total: 890 ± 13 mg polyphenols and 366 ± 5 mg EGCG) or a corn-flour placebo (total: 1729 ± 22 mg).

Results: Average fat oxidation rates were 17% higher after ingestion of GTE than after ingestion of placebo (0.41 ± 0.03 and 0.35 ± 0.03 g/min, respectively; P < 0.05). Moreover, the contribution of fat oxidation to total energy expenditure was also significantly higher, by a similar percentage, after GTE supplementation. The insulin area under the curve decreased in both the GTE and placebo trials (3612 ± 301 and 4280 ± 309 µIU/dL · 120 min, respectively; P < 0.01), and there was a concomitant increase of 13% in insulin sensitivity.

Conclusions: Acute GTE ingestion can increase fat oxidation during moderate-intensity exercise and can improve insulin sensitivity and glucose tolerance in healthy young men.

Key Words: Tea catechins • substrate metabolism • oral-glucose-tolerance test • moderate-intensity exercise • men


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The prevalence of obesity is reaching epidemic proportions in many Western countries, with recently published data suggesting that, in some states in the United States, the prevalence of obesity is >30%. Because obesity and insulin resistance are major risk factors for the development of type 2 diabetes mellitus and cardiovascular disease, any potential treatment can have far-reaching economic and medical implications.

Green tea contains a class of polyphenolic flavonoids known as catechins, which comprise epigallocatechin gallate (EGCG), epicatechin gallate, and gallocatechin gallate; EGCG is thought to be the most pharmacologically active of the catechins. Several experimental studies have indicated that chronic consumption of green tea extract (GTE) can improve exercise performance, increase fat oxidation, and prevent obesity in C57BL/6J mice (1-4). It has been suggested that GTE exerts these effects through its action on the sympathetic nervous system, more specifically on the breakdown of the catecholamine noradrenaline. EGCG is a known inhibitor of the enzyme catechol O-methyltransferase (5), which degrades noradrenaline, and therefore EGCG can exert a regulatory effect on sympathetic activation and lipolysis.

Although most studies with green tea have been performed in animal models, Dulloo et al (6) showed that, in healthy young men, a similar effect can be observed with acute GTE ingestion. In their study, resting 24-h energy expenditure (EE) and the contribution of fat oxidation to total EE were elevated.

During moderate-intensity exercise, EE is several times higher than that during rest, and absolute rates of lipolysis and fat oxidation also are higher (7, 8). To date, it remains unclear whether EGCG can elevate fat oxidation and lipolysis during exercise when fatty acid (FA) metabolism is already stimulated.

In addition to effects on fat metabolism, GTE may have an effect on glucose tolerance and insulin sensitivity. When Sprague-Dawley rats were fed a diet including 148 mg green tea catechins/d for 12 d, fasting plasma glucose and insulin concentrations and the insulin response to an oral glucose load (2 g glucose/kg body wt) were significantly reduced (9). In addition, when spontaneously hypertensive rats, which are often used as a genetic model of the metabolic syndrome, were fed a diet supplemented with 200 mg EGCG · kg–1 · d–1 for 3 wk, insulin sensitivity increased (10).

The first study presented in this report (study A) investigated whether acute ingestion of GTE can increase fat oxidation rates during moderate-intensity exercise. The second study (study B) investigated the effects of acute ingestion of GTE on glucose tolerance as assessed by a 2-h oral-glucose-tolerance test (OGTT). We hypothesized that the acute intake of GTE will increase fat oxidation during exercise and will improve glucose tolerance in healthy young men.


   SUBJECTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Participants
Twelve male participants [x ± SD age: 26 ± 2 y; weight: 75.1 ± 3.2 kg; body mass index (BMI; in kg/m2); 23.9 ± 0.8; maximal oxygen consumption (VO2max): 50.9 ± 2.1 mL · kg–1 · min–1] were recruited for study A. An additional 11 male participants (age: 23 ± 2 y; weight: 77.7 ± 4.5 kg; BMI: 24.1 ± 1.1; VO2max: 52.0 ± 2.8 mL · kg–1 · min–1) were recruited for study B. All participants were healthy according to results of a general health questionnaire.

All participants gave written informed consent to participate in the study. Both study A and study B were approved by the Ethics Subcommittee of the School of Sport and Exercise Sciences at the University of Birmingham.

Preliminary testing
At least 1 wk before the first experimental trial, all participants undertook an incremental exercise test, on an electronically braked cycle ergometer (Lode Excalibur Sport, Groningen, Netherlands), to volitional exhaustion. Participants started by cycling at 95W for 3 min and increased their effort by incremental steps of 35W every 3 min until they reached exhaustion. The Wmax was calculated by using the following equation (11):

Formula 1(1)
where Wout is the power output of the last completed stage, and t is the time (in s) spent in the final stage. Wmax values were used to determine the workload (50% Wmax) used in the later experimental trials for study A. Respiratory gas measurements were made by using the Douglas bag technique; oxygen consumption (Formula 1O2) and carbon dioxide production were calculated by using standard equations (12). Heart rate (HR) was measured continuously by using telemetry and an HR monitor (Polar S625X; Polar Electro Oy, Kempele, Finland). Formula 1O2 was considered to be maximal if 2 of the 3 following conditions were met: 1) a leveling off of Formula 1O2 with further increasing workloads (an increase of ≤2 mL · kg–1 · min–1); 2) an HR within 10 beats/min of the age-predicted maximum (220 bpm – age); and 3) a respiratory exchange ratio of >1.05.

General study designs
In a counter-balanced crossover design, each participant completed 2 trial days separated by ≥1 wk. In study A, each participant completed 30 min of cycling exercise at 50% of their previously determined Wmax; in study B, each participant underwent 2 OGTTs.

Diet and capsule content
In the 24-h period before the first trial, the participants were asked to produce a food diary; this was replicated before the second trial. During this 24-h period, participants ingested 3 capsules containing either GTE or a corn-flour placebo. The capsules were ingested with lunch and dinner on the day before the trial and in the morning, ≥1 h before the trial.

The GTE (Healthspan, St Peter Port, United Kingdom) consisted of a standardized GTE (total of 340 mg polyphenols and 136 mg EGCG), maltodextrin, microcrystalline cellulose, sodium croscarmellose, stearic acid, silicon dioxide, magnesium stearate (vegetable origin), hydroxypropylmethyl cellulose coating, and glycerine (vegetable origin). The capsule does not contain caffeine. The amount of GTE contained in each capsule is equivalent to {approx}3.5 cups green tea. The placebo capsule contained 1517 ± 48 mg of a gluten-free corn flour (Whitworths Ltd, Wellingborough, United Kingdom).

Experimental protocol
Study A
All participants reported to the Human Performance Laboratory between 0700 and 0900 after a 10-h overnight fast and having avoided strenuous exercise, alcohol, and caffeinated beverages for the preceding 24 h. On their arrival, standard measures of height and weight (Seca Alpha, Hamburg, Germany) were taken. A flexible 20-gauge Teflon catheter (Venflon; Becton Dickinson, Plymouth, United Kingdom) was then inserted into an antecubital vein. A 3-way stopcock (PVB Medizintechnik, Kirchseean, Germany) was attached to the catheter to allow repeated blood sampling during the test period. The participants then mounted the cycle ergometer, and a resting blood sample (5 mL) was collected in EDTA-containing tubes (Becton Dickinson) and stored on ice for later centrifugation. Additional blood samples, expiratory breath samples (2 min), and ratings of perceived exertion were collected at 10-min intervals throughout the exercise period. We kept the catheter patent by flushing it with 2–3 mL isotonic saline (0.9%; Baxter, Norfolk, United Kingdom) after each blood sample collection. HR was recorded continuously by telemetry with the use of a Polar S625X HR monitor, and averages were taken of the final 5 min of each 10-min interval.

Study B
All participants reported to the Human Performance Laboratory between 0700 and 0900 after a 10-h overnight fast and having avoided strenuous exercise, alcohol, and caffeinated beverages for the preceding 24 h. On their arrival, standard measures of height and weight (Seca Alpha) were taken. A flexible 20-gauge Teflon catheter (Venflon; Becton Dickinson) was then inserted into an antecubital vein. A 3-way stopcock (PVB Medizintechnik) was attached to the catheter to allow repeated blood sampling during the test period. A resting blood sample (5 mL) was taken, immediately after which the participants ingested a 25% glucose beverage consisting of 75 g glucose made up with water to a volume of 300 mL (Meritose-200; Amylum UK Ltd, London, United Kingdom). Further blood samples (5 mL) were collected at 15, 30, 45, 60, 90, and 120 min while the participants were seated. We kept the catheter patent by flushing it with 2–3 mL isotonic saline (0.9%; Baxter) after each blood sample collection and at 75 and 105 min. Of the 5-mL blood sample, 3 mL was collected into chilled EDTA-containing tubes (Becton Dickinson) and stored on ice; 2 mL was collected into serum tubes and left to clot at room temperature.

Blood variables
All tubes were centrifuged at 1700 x g for 10 min at 4 °C. Aliquots of plasma and serum were immediately frozen in liquid nitrogen and stored at –80 °C for later analysis. Where appropriate, plasma glucose (Glucose HK; ABX Diagnostics, Chicksands, United Kingdom), free FAs [(FFA) NEFA-C; Wako Chemicals, Neuss, Germany], and glycerol (Raisio Diagnostics UK Ltd, Worksop, United Kingdom) were analyzed on a COBAS MIRA semi-automatic analyzer (La Roche, Basel, Switzerland). Serum insulin was analyzed by using an enzyme-linked immunosorbent assay (DX EIA-2935 ELISA; IDS Ltd, Bolden, United Kingdom).

Calculations
Study A
From the rate of carbon dioxide production and Formula 1O2 (L/min), total carbohydrate and fat oxidation rates (g/min) were calculated by using the following stoichiometric equations of Jeukendrup and Wallis (13), working under the assumption that protein oxidation during exercise is negligible:

Formula 2(2)
and

Formula 3(3)

Study B
From plasma glucose and serum insulin concentrations during the 2-h OGTT, the whole-body insulin sensitivity index (ISI) was calculated by using the following equation of Matsuda and DeFronzo (14):

Formula 4(4)
where FPG is the fasting plasma glucose concentration, FPI is the fasting serum insulin concentration, and 10 000 represents a constant that allows numbers ranging between 1 and 12 to be obtained. The square root conversion is used to correct the nonlinear distribution of values.

Statistical analysis
Data analysis was performed by using SPSS for WINDOWS software (version 12.0.1; SPSS Inc, Chicago, IL). Data are expressed as means ± SEs unless otherwise stated. Blood variables over the course of the experimental trials were compared by using a 2-factor (time x trial) repeated-measures analysis of variance. Paired-sample t tests compared the contribution of substrate to total EE, the areas under the curve (AUCs) for glucose and insulin, and the ISI in the different trials. Significance was set at P < 0.05.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Study A
Workload and exercise intensities
The workload of 50% Wmax (133 ± 7W) used during the 30-min exercise trials elicited an average absolute Formula 4O2 of 2300 ± 99 and 2351 ± 94 mL/min for the placebo and GTE trials, respectively. Consequently, the average relative exercise intensity (61 ± 1% and 62 ± 1% Formula 4O2max) and EE (11.35 ± 0.48 and 11.57 ± 0.45 kcal/min) between trials in the placebo and GTE trials, respectively, did not differ significantly. In addition, there were no significant differences in HR (134 ± 4 and 136 ± 4 bpm), rate of perceived exertion (12 ± 1 and 12 ± 1), or self-selected cadence (85 ± 2 and 87 ± 3 rpm) between trials in the placebo and GTE trials, respectively.

Carbohydrate and fat oxidation
The ingestion of GTE increased whole-body fat oxidation significantly more than did that of the placebo trial (0.41 ± 0.03 and 0.35 ± 0.03 g/min, respectively; P < 0.01 for main effect of trial; Figure 1Go A). The relative contribution of substrates to total EE can be seen in Figure 1BGo. Fat oxidation contributed 30% in the placebo trial and 35% in the GTE trial, which represents a significant (P < 0.05) increase of 17%. Correspondingly, the contribution of carbohydrate was decreased by 17% after GTE ingestion (P < 0.05).


Figure 1
View larger version (11K):
[in this window]
[in a new window]

  		FIGURE 1.. Mean (±SEM) fat oxidation measured every 10 min in the placebo (PLA) (•) and green tea extract (GTE) ({circ}) trials (A) and contribution of substrate ({square}, fat; {blacksquare}, carbohydrate) to total energy expenditure over the course of the 30-min period in the PLA and GTE exercise trials (B). n = 12. Differences between trials were determined by using repeated-measures ANOVA (A) and a paired-sample t test (B). *P < 0.05. Figure 1AGo indicates that there was a main effect of the trial: ie, the GTE trial had significantly (P < 0.01) higher fat oxidation rates than did the PLA trial.

 
Plasma metabolites and insulin
The effects of time and supplementation with or without GTE on plasma glucose, insulin, FFAs, and glycerol can be seen in Figure 2Go. Plasma glucose concentration was unaffected by GTE, although there was a decrease with time in both trials (Figure 2AGo; P < 0.05). Plasma insulin concentrations displayed a similar pattern, being unaffected by GTE but decreasing over time (Figure 2BGo; P < 0.05). Plasma FFA concentrations after GTE ingestion were elevated, but th change was not significant (P = 0.06 for main effect of trial; Figure 2CGo). GTE ingestion elicited significantly higher plasma glycerol concentrations than did placebo ingestion (P < 0.05 for main effect of trial; Figure 2DGo).


Figure 2
View larger version (21K):
[in this window]
[in a new window]

  		FIGURE 2.. Mean (± SEM) plasma concentrations of glucose (A), insulin (B), free fatty acids (FFA) (C), and glycerol (D) over the course of the 30-min period in both the placebo (•) and green tea extract ({circ}) exercise trials. n = 12. Differences between trials were determined by using repeated-measures ANOVA. Figure 2DGo indicates that there was a main effect of trial: ie, the plasma glycerol concentrations were significantly (P < 0.05) higher in the green tea extract trial than in the placebo trial.

 
Study B
There were no significant differences in fasting plasma glucose (5.04 ± 0.08 and 5.12 ± 0.08 mmol/L) or serum insulin (8.16 ± 1.53 and 7.93 ± 1.40 µIU/mL) concentrations between trials in the placebo and GTE trials, respectively. However there was a significant time effect on plasma glucose (P < 0.01; Figure 3Go A) and also time and trial effects on serum insulin (P < 0.01 for both), such that the GTE trial had lower serum insulin concentrations than the did placebo trial during the 2-h OGTT (Figure 3BGo).


Figure 3
View larger version (24K):
[in this window]
[in a new window]

  		FIGURE 3.. Mean (± SEM) plasma glucose (A) and insulin (B) concentrations in the placebo (PLA) ({circ}) and green tea extract (GTE) ({circ}) trials and the area under the curve (AUC) for glucose (C) and insulin (D) over the course of a 2-h oral-glucose-tolerance test in the 2 trials. n = 11. Differences between trials were determined by using repeated-measures ANOVA (A and B) and paired-sample t tests (C and D). {dagger}P < 0.01. Figure 3BGo indicates that there was a main effect of trial: ie, the serum insulin concentrations were significantly (P < 0.01) lower in the GTE trial than in the PLA trial.

 
The AUCs for plasma glucose (Figure 3CGo) did not differ between trials; however, the AUC for serum insulin was 15 ± 4% smaller during the GTE trial than during the placebo trial (3612 ± 301 and 4280 ± 309 µIU/mL · 120 min, respectively; P < 0.01; Figure 3DGo). When the ISI of Matsuda and DeFronzo was used, ISI was 13 ± 4% greater during the GTE trial than during the placebo trial (7.24 ± 0.61 and 6.52 ± 0.60, respectively; P < 0.05; Figure 4Go).


Figure 4
View larger version (10K):
[in this window]
[in a new window]

  		FIGURE 4.. Mean (± SEM) insulin sensitivity index in the placebo (PLA) and green tea extract (GTE) trials. n = 11. Differences between trials were determined by using paired-sample t tests. *P < 0.05.

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The study reported here is the first to show that GTE can increase fat oxidation during moderate-intensity cycling exercise in healthy young men. It also observed that the acute ingestion of GTE significantly reduced the insulin AUC during a 2-h OGTT and improved insulin sensitivity. The study observed a 17% greater fat contribution to total EE during moderate-intensity exercise when GTE was ingested than when placebo was ingested. This increase is in agreement with, yet not as great as, the 31% increase observed at rest by Dulloo et al (6). Several factors may explain this difference; first, the GTE used in the study by Dulloo et al contained 150 mg caffeine, a quantity that they observed to be sufficient to increase EE and the fat contribution to total EE by 7%. Second, evidence suggests that, during exercise in the fasted state, caffeine can increase fat oxidation (15, 16). Third, the present study investigated the effect of GTE on fat oxidation during exercise, rather than during rest, and it is known that, during moderate-intensity exercise, both lipolysis and fat oxidation already show marked increases compared with the values during rest (8, 17-19). The present study therefore shows that, even under conditions of elevated lipolysis and fat oxidation seen during moderate-intensity exercise, GTE can increase fat metabolism.

It is believed that GTE exerts its effects on fat oxidation through the inhibition of catechol O-methyltransferase (5, 6), an enzyme that degrades noradrenaline. This reduction in noradrenaline degradation could potentially prolong adrenergic drive and increase lipolysis. The higher plasma glycerol concentrations seen during the GTE trial than during the placebo trial in the present study have shown, albeit indirectly, that GTE can increase lipolysis.

In addition to adrenergic drive, insulin is a well-known regulator (ie, inhibitor) of lipolysis (20), and it could be conceived that, during the placebo trial, the corn flour may have elevated plasma glucose, which resulted in insulin release and which ultimately inhibited lipolysis. The difference between the 2 trials, therefore, is due to a lower rate of lipolysis in the placebo trial, rather than to a higher rate in the GTE trial. Thus, we rule out this potential mechanism, because the amount of corn flour ingested was minimal (1.5 g), and neither fasted glucose nor insulin concentrations differed significantly between trials.

Lipolysis during low-intensity exercise of this nature is not thought to limit fat oxidation (21), and it could be that GTE has additional effects on lipid metabolism. Chronic feeding of GTE to mice has been shown to elevate the mRNA content of important proteins involved in lipid transport and oxidation such as FA translocase/CD36 and medium-chain acyl-CoA dehydrogenase (1). In a similar study, GTE also reduced the content of malonyl CoA (2), and, thus, it could relieve the inhibition on and increase the activity of carnitine palmitoyl transferase 2. Whether this can occur with acute GTE feeding, either through a direct regulatory action of GTE or due to the transient increase in FA, remains to be seen. However, dietary manipulations that elevate plasma FA can up-regulate many genes encoding for proteins involved in fat metabolism (22). In addition, Watanabe et al (23) incubated 3T3-L1 adipocytes in a medium containing various concentrations of EGCG for 15 min and observed an inhibition in the enzyme acetyl CoA-carboxylase. EGCG could therefore alter the partitioning of lipid in such a way that lipid is directed away from storage and toward oxidation.

The present study also showed that GTE ingestion can increase insulin sensitivity by 13% and, therefore, can reduce the insulin response to a glucose load by 15%. Fructose-fed Sprague-Dawley rats exhibit insulin resistance and hypertension, pathologic conditions that resemble type 2 diabetes mellitus in humans. When these rats were supplemented with GTE in addition to fructose for 12 wk, they became more insulin sensitive. Fasting plasma glucose and insulin concentrations were reduced to control concentrations, and plasma insulin concentrations during the OGTT were significantly lower than those in the the rats fed fructose only at all time-points. In parallel with this, increases in adipocyte insulin–receptor binding and membrane GLUT 4 protein content were observed (9, 24). EGCG can also mimic insulin by increasing the tyrosine phosphorylation of both the insulin receptor and insulin receptor substrate-1 (25)—the first stage of insulin-stimulated glucose uptake.

A further mechanism by which GTE could enhance glucose tolerance may be the partitioning of lipid toward oxidation rather than storage. The present study has shown an increase in fat oxidation during moderate-intensity exercise, which could reduce the build-up of FA metabolites within the muscle. Such metabolites are known to interfere with the insulin-signaling cascade via the activation of novel isoforms of protein kinase C (nPKC β and {theta}) (26, 27). A reduction in the build-up of such metabolites could therefore relieve the inhibition of the signaling cascade and increase insulin-stimulated glucose uptake within the skeletal muscle.

In conclusion, acute ingestion of green tea can increase fat oxidation during moderate-intensity exercise, possibly through an increase in lipolysis and therefore an increased availability of fat as a fuel. Green tea ingestion can also improve glycemic control after an oral glucose load and could have the potential to reduce the risk of type 2 diabetes mellitus.


   ACKNOWLEDGMENTS
 
The authors' responsibilities were as follows—MCV: study design, data collection and analysis, and writing of the manuscript; CJH: data collection and critical review of the manuscript; HRC: data collection; and AEJ: study design and critical review of the manuscript. None of the authors had a personal or financial conflict of interest.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Murase T, Haramizu S, Shimotoyodome A, Nagasawa A, Tokimitsu I. Green tea extract improves endurance capacity and increases muscle lipid oxidation in mice. Am J Physiol Regul Integr Comp Physiol 2005;288:R708–15.[Abstract/Free Full Text]
  2. Murase T, Haramizu S, Shimotoyodome A, Tokimitsu I, Hase T. Green tea extract improves running endurance in mice by stimulating lipid utilization during exercise. Am J Physiol Regul Integr Comp Physiol 2006;290:R1550–6.[Abstract/Free Full Text]
  3. Murase T, Nagasawa A, Suzuki J, Hase T, Tokimitsu I. Beneficial effects of tea catechins on diet-induced obesity: stimulation of lipid catabolism in the liver. Int J Obes Relat Metab Disord 2002;26:1459–64.[Medline]
  4. Shimotoyodome A, Haramizu S, Inaba M, Murase T, Tokimitsu I. Exercise and green tea extract stimulate fat oxidation and prevent obesity in mice. Med Sci Sports Exerc 2005;37:1884–92.
  5. Lu H, Meng X, Yang CS. Enzymology of methylation of tea catechins and inhibition of catechol-O-methyltransferase by (-)-epigallocatechin gallate. Drug Metab Dispos 2003;31:572–9.[Abstract/Free Full Text]
  6. Dulloo AG, Duret C, Rohrer D, et al. Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans. Am J Clin Nutr 1999;70:1040–5.[Abstract/Free Full Text]
  7. Jeukendrup AE, Saris WH, Wagenmakers AJ. Fat metabolism during exercise: a review—part II: regulation of metabolism and the effects of training. Int J Sports Med 1998;19:293–302.[Medline]
  8. Romijn JA, Coyle EF, Sidossis LS, et al. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol 1993;265:E380–91.[Medline]
  9. Wu LY, Juan CC, Ho LT, Hsu YP, Hwang LS. Effect of green tea supplementation on insulin sensitivity in Sprague-Dawley rats. J Agric Food Chem 2004;52:643–8.[Medline]
  10. Potenza MA, Marasciulo FL, Tarquinio M, et al. EGCG, a green tea polyphenol, improves endothelial function and insulin sensitivity, reduces blood pressure, and protects against myocardial I/R injury in SHR. Am J Physiol Endocrinol Metab 2007;292:E1378–87.[Abstract/Free Full Text]
  11. Kuipers H, Verstappen FT, Keizer HA, Geurten P, van Kranenburg G. Variability of aerobic performance in the laboratory and its physiologic correlates. Int J Sports Med 1985;6:197–201.[Medline]
  12. McArdle W, Katch F, Katch V. Exercise physiology: energy, nutrition and human performance. Baltimore, MD: Lippincott Williams & Wilkins, 2001.
  13. Jeukendrup AE, Wallis GA. Measurement of substrate oxidation during exercise by means of gas exchange measurements. Int J Sports Med 2005;26(suppl):S28–37.[Medline]
  14. Matsuda M, DeFronzo RA. Insulin sensitivity indices obtained from oral glucose tolerance testing: comparison with the euglycemic insulin clamp. Diabetes Care 1999;22:1462–70.[Abstract/Free Full Text]
  15. Costill DL, Dalsky GP, Fink WJ. Effects of caffeine ingestion on metabolism and exercise performance. Med Sci Sports 1978;10:155–8.[Medline]
  16. Ivy JL, Costill DL, Fink WJ, Lower RW. Influence of caffeine and carbohydrate feedings on endurance performance. Med Sci Sports 1979;11:6–11.[Medline]
  17. Arner P, Kriegholm E, Engfeldt P, Bolinder J. Adrenergic regulation of lipolysis in situ at rest and during exercise. J Clin Invest 1990;85:893–8.[Medline]
  18. van Loon LJ, Greenhaff PL, Constantin-Teodosiu D, Saris WH, Wagenmakers AJ. The effects of increasing exercise intensity on muscle fuel utilisation in humans. J Physiol 2001;536:295–304.[Abstract/Free Full Text]
  19. Wolfe RR, Klein S, Carraro F, Weber JM. Role of triglyceride-fatty acid cycle in controlling fat metabolism in humans during and after exercise. Am J Physiol 1990;258:E382–9.[Medline]
  20. Campbell PJ, Carlson MG, Hill JO, Nurjhan N. Regulation of free fatty acid metabolism by insulin in humans: role of lipolysis and reesterification. Am J Physiol 1992;263:E1063–9.[Medline]
  21. Horowitz JF, Mora-Rodriguez R, Byerley LO, Coyle EF. Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise. Am J Physiol 1997;273:E768–75.[Medline]
  22. Cameron-Smith D, Burke LM, Angus DJ, et al. A short-term, high-fat diet up-regulates lipid metabolism and gene expression in human skeletal muscle. Am J Clin Nutr 2003;77:313–8.[Abstract/Free Full Text]
  23. Watanabe J, Kawabata J, Niki R. Isolation and identification of acetyl-CoA carboxylase inhibitors from green tea (Camellia sinensis). Biosci Biotechnol Biochem 1998;62:532–4.[Medline]
  24. Wu LY, Juan CC, Hwang LS, Hsu YP, Ho PH, Ho LT. Green tea supplementation ameliorates insulin resistance and increases glucose transporter IV content in a fructose-fed rat model. Eur J Nutr 2004;43:116–24.[Medline]
  25. Waltner-Law ME, Wang XL, Law BK, Hall RK, Nawano M, Granner DK. Epigallocatechin gallate, a constituent of green tea, represses hepatic glucose production. J Biol Chem 2002;277:34933–40.[Abstract/Free Full Text]
  26. Itani SI, Ruderman NB, Schmieder F, Boden G. Lipid-induced insulin resistance in human muscle is associated with changes in diacylglycerol, protein kinase C, and IkappaB-alpha. Diabetes 2002;51:2005–11.[Medline]
  27. Yu C, Chen Y, Cline GW, et al. Mechanism by which fatty acids inhibit insulin activation of insulin receptor substrate-1 (IRS-1)-associated phosphatidylinositol 3-kinase activity in muscle. J Biol Chem 2002;277:50230–6.[Abstract/Free Full Text]
Received for publication August 14, 2007. Accepted for publication September 21, 2007.




This article has been cited by other articles:


Home page
 J. Nutr.Home page
S. Egert, S. Wolffram, A. Bosy-Westphal, C. Boesch-Saadatmandi, A. E. Wagner, J. Frank, G. Rimbach, and M. J. Mueller
Daily Quercetin Supplementation Dose-Dependently Increases Plasma Quercetin Concentrations in Healthy Humans
J. Nutr., September 1, 2008; 138(9): 1615 - 1621.
[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
Right arrow Citation Map
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 Venables, M. C
Right arrow Articles by Jeukendrup, A. E
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Venables, M. C
Right arrow Articles by Jeukendrup, A. E
Agricola
Right arrow Articles by Venables, M. C
Right arrow Articles by Jeukendrup, A. E

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS