Aged green tea reduces high-fat diet-induced fat accumulation and inflammation via activating the AMP-activated protein kinase signaling pathway

Abstract

Background: Obesity is a global public health concern and increases the risk of metabolic syndrome and other diseases. The anti-obesity effects of various plant-derived bioactive compounds, such as tea extracts, are well-established. The mechanisms underlying the anti-obesity activity of Jinxuan green tea (JXGT) from different storage years are still unclear.

Objective: The aim of this study was to evaluate the effects of JXGTs from three different years on the high fat diet (HFD)-fed mouse model.

Design: The mice were divided into six groups, the control group received normal diet and the obese model group received HFD. We analyzed the effects of JXGTs from 2005, 2008, and 2016 on HFD-fed obese mice over a period of 7 weeks.

Results: The JXGTs reduced the body weight of the obese mice, and also alleviated fat accumulation and hepatic steatosis. Mechanistically, JXGTs increased the phosphorylation of AMP-activated protein kinase (p-AMPK)/AMP-activated protein kinase (AMPK) ratio, up-regulated carnitine acyl transferase 1A (CPT-1A), and down-regulated fatty acid synthase (FAS), Glycogen synthase kinase-3beta (GSK-3β), Peroxisome proliferator-activated receptor-gamma co-activator-1alpha (PGC-1α), Interleukin 6 (IL-6), and Tumour necrosis factor alpha (TNFα). Thus, JXGTs can alleviate HFD-induced obesity by inhibiting lipid biosynthesis and inflammation, thereby promoting fatty acid oxidation via the AMPK pathway.

Discussion: The anti-obesity effect of three aged JXGTs were similar. However, JXGT2016 exhibited a more potent activation of AMPK, and JXGT2005 and JXGT2008 exhibited a more potent inhibiting glycogen synthase and inflammation effect. Furthermore, the polyphenol (-)-epicatechin (EC) showed the strongest positive correlation with the anti-obesity effect of JXGT.

Conclusions: These findings demonstrate that JXGT treatment has a potential protection on HFD-induced obesity mice via activating the AMPK/CPT-1A and down-regulating FAS/GSK-3β/PGC-1α and IL-6/TNFα. Our study results also revealed that different storage time would not affect the anti-obesity and anti-inflammation effect of JXGT.

Keywords: AMPK; aged green tea; anti-inflammation; anti-obesity; metabolism.

Fig. 1

Effect of JXGTs on the body weight (A), weight gain (B), diet consumption (C), and water consumption (D) of HFD-fed obese mice. Data are presented as means ± SD (n = 8). **P < 0.01 and *P < 0.05.

Fig. 2

JXGTs attenuate fatty liver and adiposity in HFD-induced obese mice. Representative images of whole body (A), fatty liver (B), abdominal (C), and perirenal (D) white fat in all groups. The indices of total (E), abdominal (F), intestinal (G), and perirenal (H) white fat relative to body weight. Data are presented as the means ± SD (n = 8). **P < 0.01 and *P < 0.05.

Fig. 3

JXGTs activate AMPK phosphorylation. (A) Immunoblot showing AMPK protein levels in the liver of differentially treated mice and (B) densitometric quantification. Data are presented as means ± SD (n = 3). **P < 0.01 and *P < 0.05.

Fig. 4

JXGTs upregulate CPT-1 and inhibit FAS expression. (A) Immunoblot showing expression levels of CPT-1 and FAS protein in mouse liver and densitometric quantification of (B) CPT-1 and (C) FAS. Data are presented as the means ± SD (n = 3). **P < 0.01, and *P < 0.05.

Fig. 5

JXGTs upregulate PGC-1α and inhibit GSK-3β expression. (A) Immunoblot showing expression levels of GSK-3β and PGC-1α protein in mouse liver and densitometric quantification of (B) GSK-3β and (C) PGC-1α. Data are presented as means ± SD (n = 3). **P < 0.01 and *P < 0.05.

Fig. 6

JXGTs inhibit IL-6 and TNF-α expression. (A) Immunoblot showing IL-6 and TNF-α protein levels in mouse liver and densitometric quantification of (B) IL-6 and (C) TNF-α. Data are presented as means ± SD (n = 3). **P < 0.01 and *P < 0.05.

Fig. 7

The correlation between the phytochemicals and obesity parameters and inflammation indices in the different experimental groups. (−)-epicatechin (EC), (−)-epigallocatechin (EGC), (−)-epicatechin gallate (ECG), (−)-epigallocatechin gallate (EGCG), (+)-catechin (C) and (+)-gallocatechin (GC), (−)-catechin gallate (CG) and (−)-gallocatechin gallate (GCG). Significant correlations are annotated by **P < 0.01 and *P < 0.05.