Green Tea Supplementation Affects Body Weight, Lipids, and Lipid Peroxidation in Obese Subjects with Metabolic Syndrome

Abstract

Green tea beverage consumption (4 cups/d) or extract supplementation (2 capsules/d) for 8 weeks significantly decreased body weight and BMI. Green tea beverage further lowered lipid peroxidation versus age- and gender-matched controls, suggesting the role of green tea flavonoids in improving features of metabolic syndrome in obese patients.

Epigallocatechin-3-gallate (EGCG) activates AMPK through the inhibition of glutamate dehydrogenase in muscle and pancreatic ß-cells: A potential beneficial effect in the pre-diabetic state?

“…In this context, green tea has been widely investigated. It is rich in polyphenols including epigallocatechin-3-gallate (EGCG) and epicatechin-3-gallate (ECG), which cause weight reduction in various animal models (Sae-tan et al, 2011;Wang et al, 2014) and obese subjects (Basu et al, 2010 shown some inconsistencies in this regard probably due to the heterogeneity of both protocols and populations used (for review see (Wang et al, 2014;Hursel et al, 2009;Phung et al, 2010)). …”

Glutamate pathways of the beta-cell and the control of insulin secretion

“…In human pancreatic islets stimulated with high glucose, EGCG lowers insulin secretion along with a decrease of intracellular glutamate [23]. EGCG has been shown to reduce the body weight of obese subjects [24] and of various animal models [25,26], as well as to improve glucose tolerance in diabetic db/db mice [27]. However, the poor bioavailability of EGCG may limit its use and human trials have shown some inconsistencies [26,28].…”

Limited Sampling Estimates of Epigallocatechin Gallate Exposures in Cirrhotic and Noncirrhotic Patients With Hepatitis C After Single Oral Doses of Green Tea Extract

“…28 However, chronic moderate to high dose daily GTE and EGCG use in healthy human volunteers was not shown to cause severe adverse effects or impair liver function. [29][30][31][32] Prior pharmacokinetic studies have established peak blood concentrations and exposures of EGCG associated with its safety and tolerability in healthy subjects. [30][31][32][33][34] In a study by Chow et al, following a single 800mg dose of EGCG in five healthy volunteers, AUC (min·µg/ml) ±SD was 167.1 ± 57.0, C max (ng/mL) was 438.5 ± 28.4 and t 1/2 (min) was 114.0 ± 33.3.…”

“…[29][30][31][32] Prior pharmacokinetic studies have established peak blood concentrations and exposures of EGCG associated with its safety and tolerability in healthy subjects. [30][31][32][33][34] In a study by Chow et al, following a single 800mg dose of EGCG in five healthy volunteers, AUC (min·µg/ml) ±SD was 167.1 ± 57.0, C max (ng/mL) was 438.5 ± 28.4 and t 1/2 (min) was 114.0 ± 33.3. 35 In a multi-dose study by Chow et al, volunteers were randomly assigned to receive one of the five treatments for 4 weeks: 800 mg EGCG once/day, 400 mg EGCG twice/day, 800 mg EGCG as Polyphenon E once/day, 400 mg EGCG as Polyphenon E twice/day, or a placebo once/day (8 subjects/group).…”