Ong et al., 1995 [113]
|
Adipocytes from epididymal fat pads from male Wistar rats treated with gallic acid at 1–1000 µM for various times from 20 min to 2 h |
Tannic acid was used at 1–1000 µM for various times from 20 min to 2 h |
Tannic acid inhibited insulin stimulated lipogenesis through promoting activation of insulin-receptor-associated tyrosine kinase phosphorylation. Whereas, gallic acid showed no effect |
Ren et al., 2006 [114]
|
3T3-L1 pre-adipocytes incubated with 6-deoxytetra-O-galloyl-α-d-glucopyranose, tetra-O-galloyl-α-d-xylopyranose and 6-chloro-6-deoxy-1,2,3,4-tetra-O-galloyl-α-d-glucopyranose at 30 µM for 15 min |
None |
Improved glucose uptake |
Hsu and Yen, 2007 [96]
|
3T3-L1 adipocytes were treated with gallic acid at 1–250 μM for 72 h |
o-coumaric acid and rutin were used at with 1–250 μM for 72 h |
o-coumaric acid and rutin demonstrated better effect in inhibiting glycerol-3-phosphate dehydrogenase activity, and the expression of peroxisome proliferator activated receptor (PPAR)γ, CAAT/enhancer-binding proteins (C/EBPR) and leptin. While also upregulating adiponectin levels |
Hsieh et al., 2010 [97]
|
3T3-L1 and C3H10T1/2 adipocytes treated with gallic acid at 5–10 μM for 2 h |
Compound C, n-acetyl-l-cysteine, epigallocatechin gallate and other catechins, such as epicatechin, epigallocatechin, and epicatechin 3-gallate were used at 5–10 μM for 2 h |
Epigallocatechin gallate performed better than other compounds in inhibiting insulin stimulated glucose uptake, with mechanistic involvement of 5’ adenosine monophosphate -activated protein kinase (AMPK) pathways |
Totani et al., 2011 [22]
|
High fat diet fed male Wistar rats treated with gallic acid at 90 ppm in diet for 12 weeks |
(z)-3-(3,4,5-trihydroxybenzoyloxy) propane-1,2-diyl dioleate (DOGGA) and octyl gallate (OG) were both used at 90 ppm in diet for 12 weeks |
DOGGA showed pronounced effect than OG in reducing the body weight in rats. Gallic acid showed no effect |
Sergent et al., 2012 [115]
|
In vitro bioassays testing epigallocatechin-3-gallate at 0.8 µM |
Kaempferol and quercetin were effective at 13.4 and 21.5 µM, respectively |
Epigallocatechin-3-gallate presented pronounced pancreatic lipase inhibitory effect than both kaempferol and quercetin |
Park et al., 2014 [116]
|
3T3-L1 adipocytes treated with gallic acid at 30, 60 and 90 µM during differentiation period |
KMU-3, a derivative of gallic acid, was used at 1, 5 and 10 µM during differentiation period |
KMU-3 outperformed gallic acid in suppressing lipid accumulation in cells. Mechanistically, it inhibited expressions of C/EBP-A, PPARγ, and Fas, as well as some pro-inflammatory markers |
Yang et al., 2015 [117]
|
3T3-L1 pre-adipocyte treated with epigallocatechin 3-O-(3-O-methyl) gallate and epicatechin-3-gallate at 20, 40 and 80 μg/mL for 48 h |
None |
Epigallocatechin 3-O-(3-O-methyl) gallate presented higher activity than epicatechin-3-gallate in inhibiting adipogenesis and proliferation |
Jeon et al., 2016 [118]
|
3T3-L1 adipocytes treated with methyl gallate at 25, 50 and 75 µM for 48 h |
None |
Inhibited adipogenesis through stabilizing β-catenin suppression of PPARγ expression. Further stimulated canonical Wnt/β-catenin signaling |
Ediriweera et al., 2017 [14]
|
MCF-7 cells treated with gallic acid at 90 µM for 48 h |
Ascorbic acid (6.5 µM), catechin (583 µM), curcumin (3.5), epigallocatechin gallate (7.5 µM), and quercetin (70 µM) for 48 h |
Only quercetin, curcumin and epigallocatechin gallate showed significant protective effects against leptin-induced proliferation |
Zengin et al., 2017 [101]
|
In vitro docking experiments assessing lipase inhibitory effect of gallic acid |
p-OH-benzoic acid, catechin, epigallocatechin gallate, epicatechin, and rosmarinic acid |
Epigallogatechin gallate and rosmarinic acid displayed best docking scores for the inhibition of α-glucosidase, α-glucosidase and lipase activities |