Tea catechins modulate the glucose transport system in 3T3-L1 adipocytes

Abstract

In this study, we investigated the effects of tea catechins on the translocation of glucose transporter (GLUT) 4 in 3T3-L1 adipocytes. We found that the ethyl acetate fraction of green tea extract, containing abundant catechins, most decreased insulin-induced glucose uptake activity in 3T3-L1 cells. When the cells were treated with 50 μM catechins in the absence or presence of insulin for 30 min, nongallate-type catechins increased glucose uptake activity without insulin, whereas gallate-type catechins decreased insulin-induced glucose uptake activity. (-)-Epicatechin (EC) and (-)-epigallocatechin (EGC), nongallate-type catechins, increased glucose uptake activity in the dose- and time-dependent manner, whereas (-)-catechin 3-gallate (Cg) and (-)-epigallocatechin 3-gallate (EGCg), gallate-type catechins, decreased insulin-induced glucose uptake activity in the dose- and time-dependent manner. When the cells were treated with 50 μM catechins for 30 min, EC and EGC promoted GLUT4 translocation, whereas Cg and EGCg decreased the insulin-induced translocation in the cells. EC and EGC increased phosphorylation of PKCλ/ζ without phosphorylation of insulin receptor (IR) and Akt. Wortmannin and LY294002, inhibitors for phosphatidylinositol 3'-kinase (PI3K), decreased EC- and EGC-induced glucose uptake activity in the cells. Cg and EGCg decreased phosphorylation of PKCλ/ζ in the presence of insulin without affecting insulin-induced phosphorylation of IR, and Akt. Therefore, EC and EGC promote the translocation of GLUT4 through activation of PI3K, and Cg and EGCg inhibit insulin-induced translocation of GLUT4 by the insulin signaling pathway in 3T3-L1 cells.

In vitro anti-hyperglycemic and antioxidant properties of extracts from the stem bark of Ceiba pentandra

“…This mechanism is similar to the action of insulin and could be attributed to the presence of catechin, which has been isolated from the stem bark of C. pentandra [22]. In fact, Ueda et al [23] showed that catechin induces glucose uptake in 3T3-L1 adipocytes by promoting the translocation of GLUT4 to the plasma membrane. This is likely the mechanism by which the stem bark decoction from C. pentandra increases glucose uptake in the skeletal muscle.…”

Cacao liquor procyanidin extract improves glucose tolerance by enhancing GLUT4 translocation and glucose uptake in skeletal muscle

“…In fact, we previously reported that catechins, particularly (−)-epigallocatechin-3-gallate, increased glucose uptake and enhanced GLUT4 translocation in L6 myotubes and in the skeletal muscle of rodents in vivo and ex vivo ( 19 ) . In 3T3-L1 cells, non-gallate-type catechins increased glucose uptake and GLUT4 translocation, whereas gallate-type catechins inhibited insulin-stimulated glucose uptake ( 42 ) . Similarly, the intake of green and black tea increased GLUT4 translocation in skeletal muscle and maintained GLUT4 and insulin receptor expression in high-fat diet-fed C57BL/6 mice ( 3 , 21 , 22 ) .…”

Studies on Mechanistic Role of Natural Bioactive Compounds in the Management of Obesity An Overview

“…2g), such as (−)-epicatechin, 3-O-galloyl-(−)-epicatechin, (−)-epigallocatechin and epigallocatechin 3-gallate (GEGC), are polyphenols present in high concentrations in tea [60]. Green tea and catechins have been demonstrated in cell culture (Table 1), human trials and crosssectional studies ( Table 2) that may reduce adipocyte differentiation and proliferation, lipogenesis [61][62][63], fat mass, body weight, oxidised LDL-c and blood pressure, and can improve glycemic control [64][65][66][67]. GEGC has been widely investigated for its possible body fat-reducing effects.…”

“…Evidences have shown that the anti-adipogenic effects of catechins are mediated by several mechanisms including the inhibition of cell proliferation, a decrease in PPAR-γ and C/EBP-α expression, an increase in glucose uptake [61][62][63], and the induction of thermogenesis via sympathetic nervous system through inhibition of the enzyme catechol-Omethyltransferase as well as noradrenaline enhancement [68]. Moreover, reduced body fat accumulation may also be explained by a decrease in the digestibility of the diet [69,70], higher faecal energy loss, increased post-prandial fat oxidation and a reduction in dietary lipid incorporation into adipose tissue, liver and skeletal muscle [70].…”

“…The potential of kaempferol to increase energy expenditure should not be dismissed because this flavonoid may contribute to an increase in skeletal myocyte oxygen consumption of up to 30%, can affect regulation of metabolically important genes and activate thyroid hormones [25]. ↓ glucose uptake Catechin 3T3-L1 adipocytes 50 μM 30 min translocation of GLUT4 through activation of PI3K [62] ↓, decrease; ↑, increase; STAT-1, signal transducers and activators of transcription; NF-kB, nuclear factor kappa B; iNOS, inducible nitric oxide synthase; COX-2, ciclooxigenase-2; AP-1, activator protein 1; PPAR-γ, peroxisome proliferator-activated receptors-γ; TNF-, tumour necrosis factor-; IL, interleukin; AMPk, AMP-activated protein kinase; MAPK, mitogen-activated protein kinase; ERK, extracellular signal-regulated kinases; JNK, c-Jun N-terminal protein kinases; C/EBPα, CCAAT/enhancer binding protein; SIRT1, sirtuin-1; FFA, free fatty acid. ↓, decrease; ↑, increase; COX-2, ciclo-oxygenase2; iNOS, inducible nitric oxide synthase; TNF-α , tumor necrosis factor-α; INF-γ, interferon-gamma; IL, interleukin; TEE, total energy expenditure; PPAR-γ, peroxisome proliferator-activated receptors-γ; 8-isso-PGF2α, prostaglandin2;AMPK, AMP-activated protein kinase; UCP1, mitochondrial uncoupling proteins; IGF-1, insulin-like growth factor 1; PGC-1 α , peroxisome proliferator-activated receptor-gamma coactivator 1 alpha; RMR, resting metabolic rate; Sirt1, sirtuin-1; GLP-1, glucagon-like peptide-1; SIRT1, sirtuin-1; HOMA, homeostasis model assessment; VEGF, vascular endothelial growth factor; VEGFR-2, vascular endothelial growth factor receptor 2 ↓, decrease; ↑, increase; BMI, body mass index, LDL-c, low-density-lipoprotein cholesterol It is noteworthy that most studies on these compounds have been performed In vitro with the aim to clarify mechanisms of action; they have been focused on elucidating implications for inflammation.…”