Table 1.
Effects of coffee and its components on NAFLD.
| Parameter | Compound | Model | Results | Ref. | |
|---|---|---|---|---|---|
| In Vitro | In Vivo | ||||
| Steatosis | Caffeine, green coffee extracts (GCE) | Female Sprague Dawley rats (HFD) 4.2–5.8 mg/kg/day |
Neither caffeine nor GCE alleviated hepatic steatosis, but GCE-treated rats showed lower hepatic triglyceride levels | [49] | |
| Caffeine, chlorogenic acid | 100 subjects with T2DM and NAFLD 200 mg caffeine with/without chlorogenic acid/day |
Liver steatosis was not attenuated by caffeine or chlorogenic acid | [50] | ||
| Coffee | 2819 subjects with NAFLD or ALFD categorized consumption 0, 1, 2, and ≥3 cup/day |
Coffee intake was not associated with any lower odds of hepatic steatosis | [51] | ||
| Caffeine | Zebrafish in HFD 1–8% caffeine |
Caffeine suppressed diet-induced hepatic steatosis by downregulation of genes associated with lipogenesis, ER stress, and inflammatory response | [52] | ||
| Caffeine | HepG2 cells 2 mM |
Male C57Bl/6 mice with HFD 10 and 20 mg/kg |
Caffeine ameliorated hepatic steatosis by suppressing fatty acid synthesis and promoting β-oxidation | [52] | |
| Colombian coffee extracts | 40 male Wistar rats (8–9 weeks old 30–70 mg/kg caffeine/day |
Coffee extract attenuated diet-induced changes in structure and function of the liver and heart without changing the abdominal fat deposition | [53] | ||
| Coffee | 1452 subjects Caffeinated beverage consumption |
No association between caffeine consumption and either the prevalence of fatty liver or serum ALT concentrations | [54] | ||
| Caffeic acid | HepG2 cells 0–200 µM |
Caffeic acid reduced lipid accumulation and increased AMPK phosphorylation, which reduced the expression of the genes involved in hepatic lipogenesis and increased those related to hepatic lipolysis | [33] | ||
| Caffeic acid | AML12 cells 0–200 µM |
Mice with HFD 50 mg/kg/day |
Caffeic acid ameliorated hepatic steatosis, increasing autophagy and reducing ER stress | [45] | |
| Oxidative stress | Caffeine | Male Wistar rats 20–30 mg/kg/day |
Caffeine improved HFD-induced hepatic injury, suppressing inflammatory response, oxidative stress, and regulating lipogenesis and β-oxidation | [55] | |
| Caffeic acid | HepG2 cells 1, 5, and 10 µM |
Polyphenols decreased ROS generation by oleic acid treatment, increasing the expression of markers of mitochondrial respiratory complex subunits and mitochondrial biogenesis | [37] | ||
| Caffeic acid, other phenolic compounds | FaO cells 25 µM/24 h |
Polyphenols ameliorated fatty acid accumulation and endothelial and hepatic lipid-dependent oxidative imbalance | [38] | ||
| Chicoric acid | HepG2 cells 50–200 µM/24 h |
Chicoric acid enhanced Akt/GSK3b signaling pathways and modulated the expression of downstream genes related to lipid metabolism in a BMAL1-dependent manner | [48] | ||
| Inflammation | Caffeine | Hepa 1-6, C2C12, and 3T3L1 cells 0.5 mg/mL |
Male C57Bl/6 HFD | Caffeine ameliorated NAFLD via crosstalk between IL-6 production in muscle and liver STAT3 activation | [28] |
| Caffeic acid | Male C57Bl/6 HFD 0.08–0.16% caffeic acid supplementation HFD |
Caffeic acid reverted the imbalance in the gut microbiota and related LPS-mediated inflammation, contributing to normalizing the dysregulation expression of lipid-metabolism-related genes | [36] | ||
| Chicoric acid | HepG2 cells 10–20 µM/24 h |
Male C57Bl/6 HFD 15–30 mg/kg/day |
Chicoric acid modified gut microbiota toward a healthier microbial profile, ameliorating oxidative stress and inflammation via the AMPK/Nrf2/NF-κB signaling pathway | [46] | |
| Fibrosis | Caffeine | 195 severely obese subjects 0–5 g/wk total caffeine intake |
Regular coffee consumption was an independent protective factor for liver fibrosis | [20] | |
| Caffeine | 306 NAFLD subjects 0–822 (averaged 288 mg/day) mg/day total caffeine |
Coffee consumption was associated with a significant reduction in the risk of fibrosis among NASH patients | [56] | ||
| Caffeine, chlorogenic acid | Male TSOD mice spontaneous development of metabolic syndrome and NASH with liver tumors. 0.25 mg/caffeine day orally, 1.5 mg chlorogenic acid |
Coffee consumption was associated with the prevention of metabolic syndrome; antifibrotic effects appeared to be due to the polyphenols rather than the caffeine | [57] | ||
| Chicoric acid | HepG2 and AML12 cells 20 or 40 µM/24 h |
Male C57BL/6 MCD diet 10–30 mg/kg/day |
Chicoric acid reduced apoptosis, expression of lipogenesis-related genes, and fibrosis both in vivo and in vitro. | [45] | |