Table 1.
Effect of green tea catechins on obesity in cell studies
| First author, yr [ref] |
Exerimental design and treatments | Results |
|---|---|---|
| Chan, 2011 [17] |
3T3-L1 cells treated with EGCG (0–10 µM) for 18 days. |
↓ Cell viability ↓ Adipose conversion ↓ C/EBPα and PPARγ ↓ Fat accumulation in a dose-dependent manner |
| Furuyashiki, 2004 [18] |
3T3-L1 cells treated with EGCG (0–30 µM) for 5–8 days. |
↓ C/EBPα and PPARγ protein levels in a dose-dependent manner |
| Hung, 2005 [19] |
3T3-L1 cells treated with EC, EGC, ECG, or EGCG (0–400 µM) for 1–6 days or 2 hours pretreat. |
↓ Preadipocyte proliferation ↓ Phospho-ERK1/2, Cdk2, and cyclin D1 proteins, Cdk2 activity ↑ G0/G1 growth arrest, p21waf/cip, and p27kip1 |
| Hung, 2005 [19] |
3T3-L1 cells treated with EC, EGC, ECG, or EGCG (0–400 µM) for 24 or 48 hours. |
↑ Apoptosis and caspase-3 activity |
| Hwang, 2005 [20] |
3T3-L1 cells treated with EGCG (0 and 100 µM) for 48 hours. |
↑ AMPK activation ↑ Phosphorylated ACC |
| Kim, 2010 [21] |
3T3-L1 cells treated with EGCG (0–200 µM) for 2 days. |
↓ Fat accumulation in a dose-dependent manner ↓ Transcriptional activity of FOXO1 and SREBP-1c ↑ Phosphorylated FOXO1 protein levels |
| Ku, 2009 [22] |
3T3-L1 cells treated with EGCG (0–50 µM) for 1.5 hours. |
↓ Preadipocyte proliferation and mitogenesis ↓ Phosphorylation of IR-β, IRS1, IRS2, and MAPK proteins, RAF1, MEK1/2, and ERK1/2 |
| Ku, 2012 [23] |
3T3-L1 cells treated with EGCG (0–50µM) for 48 hours. |
↓ IGF-I-stimulated and IGF-I-stimulated mitogenesis |
| Lee, 2009 [24] |
3T3-L1 cells treated with EGCG (0, 1 or 10 µM) for 24 hours. |
↔ Cell viability At 10 µM EGCG: ↓ Intracellular TG accumulation ↑ Glycerol release ↑ HSL mRNA levels |
| Lee, 2009 [25] |
3T3-L1 cells treated with EGCG (0, 1, 5 or 10 µM) for 24 hours. |
↑ UCP-2 mRNA levels ↑ UCP-2 promoter activity |
| Lin, 2005 [26] |
3T3-L1 cells treated with EGCG (0, 50, 100, and 200 µM) for 0–24 hours. |
↓ Preadipocyte proliferation ↑ Apoptosis ↓ Fat accumulation in a dose-dependent manner |
| Liu, 2006 [27] |
3T3-L1 cells treated with EGCG (20 and 100 µM) for 0–2 hours. |
↓ Steady-state levels of Rstn ↓ Rstn mRNA and protein expression ↓ Phospho-ERK1/2 |
| Moon, 2007 [28] |
3T3-L1 cells treated with EGCG (0, 10, 50 and 100 µM) for 0–12 days. |
↓ Cell viability at ≥ 50 µM ↑ Increased generation of reactive oxygen species ↑ Phosphorylated AMPK levels and AMPK activation ↑ Phosphorylated ACC ↓ C/EBPα and PPARγ expression ↓ Fat accumulation in a time- and dose-dependent manner |
Abbreviations: ACC, acetyl-Coenzyme A carboxylase; AMPK, AMP-activated protein kinase; C/EBP, CCAAT/enhancer-binding protein; Cdk2, cyclin-dependent kinase 2; EC, epicatechin; ECG, epicatechin gallate; EGC, epigallocatechin; EGCG, epigallocatechin gallate; ERK1/2, extracellular signal-regulated protein kinases 1 and 2; FOXO1, forkhead box protein O1; HSL, hormone sensitive lipase; IGF-I, insulin like growth factor-I; IR, insulin resistance; IRS, insulin receptor substrate; MAPK, mitogen-activated protein kinase; PPAR, peroxisome proliferators-activated receptor; Rstn, rat resistin; SREBP-1c, sterol regulatory element-binding protein-1c; UCP, uncoupling protein; ↑, increase; ↓, decrease; ↔, no change.