Green Coffee Bean Extract in Human Health by Debasis Bagchi Hiroyoshi Moriyama & Anand Swaroop

Author:Debasis Bagchi, Hiroyoshi Moriyama & Anand Swaroop
Language: eng
Format: epub
Publisher: CRC Press

FIGURE 6.1 Effects of coffee polyphenols (CPP) on body fat accumulation (a); mean body weight of 10 mice at each time point (b, c); hepatic lipids were extracted from the liver and quantified. Values are means ± SE of 10 mice, *p < .05, **p < .01 vs. high-fat control group. (Modified from Murase T. et al., Am. J. Endocrinol. Metab., 2011, 300, E122–E133.)

FIGURE 6.2 Effects of coffee polyphenols (CPP) on mRNA levels in the liver (a), dipose tissue (b), and skeletal muscle (c). Values are means ± SE of 10 mice, *p < .05, **p < .01 vs. high-fat control group. (Modified from Murase T. et al., Am. J. Endocrinol. Metab., 2011, 300, E122–E133.)

Furthermore, Murase et al. [14] also investigated CPP-induced changes in energy metabolism–related gene expression using cultured hepatocytes. As observed in mice, mRNA expression of SREBP-1c and its associated proteins significantly decreased with exposure to CPP. The main polyphenols found in coffee, caffeoylquinic acids (3-/4-/5-caffeoylquinic acid [CQA]), feruloylquinic acids (3-/4-/5-feruloylquinic acid [FQA]), and dicaffeoylquinic acids (3,4-/3,5-/4,5-dicaffeoylquinic acid [diCQA]), were individually purified, isolated, and assessed for their effects on gene expression in vitro. The expression of SREBP-1c and its associated proteins was strongly inhibited by CQA and diCQA. Because total CPP, CQA, FQA, and diCQA did not activate AMP-activated protein kinase (AMPK) or peroxisome proliferator–activated receptor PPARα, PPARδ, or PPARγ, the CPP effects observed may not be mediated via these pathways.

Murase et al. [14] proposed CPP’s mechanism of action based on these findings as follows: when CPP is ingested, ACC1, FAS, and SCDl expression decreases in the liver due to the inhibition of SREBP-1c expression, and fatty acid synthesis is inhibited. It is also known that the inhibition of SCDl increases energy utilization [19]. Reduced ACC2 expression decreases malonyl-CoA production, which enhances CPT-I activity and promotes fatty acid oxidation. On the other hand, glucose utilization increases due to the inhibition of PDK4 expression. CPP-induced inhibition of fat synthesis and an increase in energy utilization may prevent body fat accumulation.

Several animal studies have reported the effects of GCBE and CPP on obesity (Table 6.1). Mubarak et al. [25] reported that supplementation of chlorogenic acid in a high-fat diet did not reduce body weight when compared with mice fed a high-fat diet alone. Moreover, Li Kwok Cheong et al. [27] also reported that GCE, rich in chlorogenic acid, did not attenuate high-fat diet–induced obesity. Although explanations for these discrepancies had not been presented, one explanation may be that the dosage of the CPP varied due to the difference in sources. Significant differences in CPP composition have been described between roasted and unroasted coffee beans [30]. The use of different strains of mice may have also contributed to these differences. Further work using CPP with varying composition and in various strains of experimental animals is required to determine the effects of GCE and CPP on obesity.

Medium- to long-term CPP ingestion increases energy utilization via changes in gene expression, whereas a single ingestion of CPP induces changes in the blood hormone levels and the ratios of utilized energy substrates by inhibiting digestive enzymes.

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