Acute effects of epigallocatechin gallate from green tea on oxidation and tissue incorporation of dietary lipids in mice fed a high-fat diet.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 21750518.
- Also identified by DOI 10.1038/ijo.2011.136.
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Abstract
To examine in mice the acute effects of epigallocatechin gallate (EGCG), a green tea bioactive polyphenol on substrate metabolism with focus on the fate of dietary lipids. Male C57BL/6 mice were fed high-fat diets supplemented with EGCG extracted from green tea (TEAVIGO, DSM Nutritional Products Ltd, Basel, Switzerland) at different dosages up to 1% (w/w). Effects of EGCG on body composition (quantitative magnetic resonance), food intake and digestibility, oxidation and incorporation of exogenous lipids (stable isotope techniques: (13)C-labeled palmitate and diet supplemented with corn oil as a natural source of (13)C-enriched lipids) as well as gene expression (quantitative real-time PCR) in liver and intestinal mucosa were investigated. Short-term supplementation (4-7 days) of dietary EGCG increased energy excretion, while food and energy intake were not affected. Fecal energy loss was accompanied by increased fat and nitrogen excretion. EGCG decreased post-prandial triglyceride and glycogen content in liver, increased oxidation of dietary lipids and decreased incorporation of dietary 13C-enriched lipids into fat tissues, liver and skeletal muscle. EGCG dose dependently reversed high-fat diet-induced effects on intestinal substrate transporters (CD36, FATP4 and SGLT1) and downregulated lipogenesis-related genes (ACC, FAS and SCD1) in liver in the post-prandial state. Anti-obesity effects of EGCG can be explained by a decreased food digestibility affecting substrate metabolism of intestinal mucosa and liver, leading to increased post-prandial fat oxidation and reduced incorporation of dietary lipids into tissues.
Medical subject headings
- Adipose Tissue
- Antioxidants
- Catechin
- Dietary Supplements
- Intestinal Absorption
- Intestinal Mucosa
- Lipid Metabolism
- Lipid Peroxidation
- Liver