(-)-Epigallocatechin-3-gallate increases the expression of genes related to fat oxidation in the skeletal muscle of high fat-fed mice

Sudathip Sae-Tan, Kimberly A. Grove, Mary J. Kennett, Joshua D. Lambert

Research output: Contribution to journalArticle

56 Citations (Scopus)

Abstract

(-)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, has been shown to prevent the development of obesity in rodent models. Here, we examined the effect of EGCG on markers of fat oxidation in high fat-fed C57bl/6J mice. High fat-fed mice treated with 0.32% dietary EGCG for 16 weeks had reduced body weight gain and final body weight (19.2% and 9.4%, respectively) compared to high fat-fed controls. EGCG-treatment decreased fasting blood glucose, plasma insulin, and insulin resistance by 18.5%, 25.3%, and 33.9%, respectively. EGCG treatment also reduced markers of obesity-related fatty liver disease in high fat-fed mice. Gene expression analysis of skeletal muscle showed that EGCG increased mRNA levels of nuclear respiratory factor (nrf)1, medium chain acyl coA decarboxylase (mcad), uncoupling protein (ucp)3, and peroxisome proliferator responsive element (ppar)α by 1.4-1.9-fold compared to high fat-fed controls. These genes are all related to mitochondrial fatty acid oxidation. In addition, EGCG increased fecal excretion of lipids in high fat-fed mice. In summary, it appears that EGCG modulates body weight gain in high fat-fed mice both by increasing the expression of genes related fat oxidation in the skeletal muscle and by modulating fat absorption from the diet.

Original languageEnglish (US)
Pages (from-to)111-116
Number of pages6
JournalFood and Function
Volume2
Issue number2
DOIs
StatePublished - Feb 1 2011

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epigallocatechin
skeletal muscle
Skeletal Muscle
Fats
oxidation
Gene Expression
gene expression
mice
lipids
Body Weight
Weight Gain
Nuclear Respiratory Factor 1
body weight
Obesity
obesity
epigallocatechin gallate
Peroxisome Proliferators
weight gain
Carboxy-Lyases
beta oxidation

All Science Journal Classification (ASJC) codes

  • Food Science

Cite this

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title = "(-)-Epigallocatechin-3-gallate increases the expression of genes related to fat oxidation in the skeletal muscle of high fat-fed mice",
abstract = "(-)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, has been shown to prevent the development of obesity in rodent models. Here, we examined the effect of EGCG on markers of fat oxidation in high fat-fed C57bl/6J mice. High fat-fed mice treated with 0.32{\%} dietary EGCG for 16 weeks had reduced body weight gain and final body weight (19.2{\%} and 9.4{\%}, respectively) compared to high fat-fed controls. EGCG-treatment decreased fasting blood glucose, plasma insulin, and insulin resistance by 18.5{\%}, 25.3{\%}, and 33.9{\%}, respectively. EGCG treatment also reduced markers of obesity-related fatty liver disease in high fat-fed mice. Gene expression analysis of skeletal muscle showed that EGCG increased mRNA levels of nuclear respiratory factor (nrf)1, medium chain acyl coA decarboxylase (mcad), uncoupling protein (ucp)3, and peroxisome proliferator responsive element (ppar)α by 1.4-1.9-fold compared to high fat-fed controls. These genes are all related to mitochondrial fatty acid oxidation. In addition, EGCG increased fecal excretion of lipids in high fat-fed mice. In summary, it appears that EGCG modulates body weight gain in high fat-fed mice both by increasing the expression of genes related fat oxidation in the skeletal muscle and by modulating fat absorption from the diet.",
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(-)-Epigallocatechin-3-gallate increases the expression of genes related to fat oxidation in the skeletal muscle of high fat-fed mice. / Sae-Tan, Sudathip; Grove, Kimberly A.; Kennett, Mary J.; Lambert, Joshua D.

In: Food and Function, Vol. 2, No. 2, 01.02.2011, p. 111-116.

Research output: Contribution to journalArticle

TY - JOUR

T1 - (-)-Epigallocatechin-3-gallate increases the expression of genes related to fat oxidation in the skeletal muscle of high fat-fed mice

AU - Sae-Tan, Sudathip

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AU - Lambert, Joshua D.

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