2014
DOI: 10.1016/j.jff.2014.01.008
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Camellia sinensis fruit peel extract inhibits angiogenesis and ameliorates obesity induced by high-fat diet in rats

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Cited by 15 publications
(8 citation statements)
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“…The activation of AMPK modulates the expression of genes and proteins involved in lipid metabolism, downregulates the expression of fat synthesis proteins, and upregulates lipid catabolism proteins [ 2 ]. It was shown that EGCG inhibited the expressions of glucose 6-phosphatase (G6Pase, for gluconeogenesis), phosphoenolpyruvate carboxykinase, (PEPCK, for gluconeogenesis), fatty acid synthase (FAS, for fatty acid synthesis), acetyl-CoA carboxylase (ACC, for fatty acid synthesis), hydroxymethylglutaryl-CoA reductase (HMGR, for cholesterol), sterol regulatory element-binding proteins (SREBPs, for sterol synthesis), peroxisome proliferator-activated receptor gamma (PPAR γ , for lipid synthesis and storage), and CCAAT/enhancer-binding protein alpha (C/EBP α , for adipogenesis) as well as enhanced the expression of acyl-CoA oxidase (ACO, for fatty acid oxidation), peroxisome proliferator-activated receptor alpha (PPAR α , for fatty acid oxidation), carnitine palmitoyltransferase-1 (CPT-1, for fatty acid oxidation), acyl-CoA dehydrogenase (ACAD, for fatty acid oxidation), peroxisome proliferator-activated receptor gamma coactivator-1 α (PGC-1 α , for fatty acid oxidation), uncoupling proteins (UCPs, for thermogenesis), and adipose triglyceride lipase (ATGL, for triglyceride hydrolysis) [ 50 54 ].…”
Section: Health Benefitsmentioning
confidence: 99%
“…The activation of AMPK modulates the expression of genes and proteins involved in lipid metabolism, downregulates the expression of fat synthesis proteins, and upregulates lipid catabolism proteins [ 2 ]. It was shown that EGCG inhibited the expressions of glucose 6-phosphatase (G6Pase, for gluconeogenesis), phosphoenolpyruvate carboxykinase, (PEPCK, for gluconeogenesis), fatty acid synthase (FAS, for fatty acid synthesis), acetyl-CoA carboxylase (ACC, for fatty acid synthesis), hydroxymethylglutaryl-CoA reductase (HMGR, for cholesterol), sterol regulatory element-binding proteins (SREBPs, for sterol synthesis), peroxisome proliferator-activated receptor gamma (PPAR γ , for lipid synthesis and storage), and CCAAT/enhancer-binding protein alpha (C/EBP α , for adipogenesis) as well as enhanced the expression of acyl-CoA oxidase (ACO, for fatty acid oxidation), peroxisome proliferator-activated receptor alpha (PPAR α , for fatty acid oxidation), carnitine palmitoyltransferase-1 (CPT-1, for fatty acid oxidation), acyl-CoA dehydrogenase (ACAD, for fatty acid oxidation), peroxisome proliferator-activated receptor gamma coactivator-1 α (PGC-1 α , for fatty acid oxidation), uncoupling proteins (UCPs, for thermogenesis), and adipose triglyceride lipase (ATGL, for triglyceride hydrolysis) [ 50 54 ].…”
Section: Health Benefitsmentioning
confidence: 99%
“…Moreover, using experimental in vivo models, the effect of tea extracts and their bioactive compounds on changes in relevant biomarkers for obesity have been demonstrated. Green tea extract supplementation has anti-obesity effects by reducing body weight, white adipose tissue fat, liver fat accumulation, and serum triglyceride levels and by increasing lysophospholipids levels and energy expenditure [83][84][85][86][87][88][89][90][91]. These anti-obesity properties of green tea are mainly attributed to its polyphenols (i.e., epigallocatechin gallate and epigallocatechin) and polysaccharides [12,15].…”
Section: Camellia Sinensis and Obesitymentioning
confidence: 99%
“…A recent study showed that not only the leaf of C. sinensis has anti-obesity effect, but also the fruit peel, which is considered an agricultural waste (Chaudhary et al, 2014[ 28 ]). The administration of ethanolic green tea fruit peel extract (100 mg/kg/d) on high-fat diet feed female Sprague-Dawley rats for 50 days significantly decreased the body weight (approx.…”
Section: Epidemiology Of Obesitymentioning
confidence: 99%