Abstract | OBJECTIVE: METHODS: We treated CA (50 µM) with AML12 cells. We categorized mice into three groups as follows: low-fat diet mice (LFD, n = 10), high-fat diet-induced obese mice (HFD, n = 10), and HFD fed with CA (50 mg/kg/d, n = 10) for 10 wk. RESULTS: CA did not cause any cytotoxic effect on AML12 cell line within the range of concentrations tested (0-200 µM). We found that CA (50 µM) treatment in palmitate-treated AML12 hepatocytes reduced lipid accumulation and lipogenesis markers, decreased ER stress, and increased autophagy markers. However, there was no significant difference in lipid droplets of palmitate-treated AML12 hepatocytes and CA-treated autophagy-related protein 7 deficiency AML12 hepatocytes with palmitate. Similarly, CA significantly lowered body and liver weights. Lipid accumulation in the liver decreased in the HFD + CA group compared with the HFD group. Glucose intolerance and insulin sensitivity also were markedly improved in the HFD + CA group. Moreover, the levels of ER stress markers were decreased in the livers of the HFD + CA group. CONCLUSION: Autophagy markers were increased in the livers of the HFD + CA group. These results suggest that caffeic acid may ameliorate hepatic steatosis and decrease ER stress by increasing autophagy.
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Authors | Hong Min Kim, Yuna Kim, Eun Soo Lee, Ji Hye Huh, Choon Hee Chung |
Journal | Nutrition (Burbank, Los Angeles County, Calif.)
(Nutrition)
Vol. 55-56
Pg. 63-70
(11 2018)
ISSN: 1873-1244 [Electronic] United States |
PMID | 29960159
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2018 Elsevier Inc. All rights reserved. |
Chemical References |
- Antioxidants
- Caffeic Acids
- caffeic acid
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Topics |
- Animals
- Antioxidants
(pharmacology)
- Autophagy
(drug effects)
- Caffeic Acids
(pharmacology)
- Diet, High-Fat
(adverse effects)
- Endoplasmic Reticulum Stress
(drug effects)
- Mice
- Mice, Obese
- Non-alcoholic Fatty Liver Disease
(drug therapy, etiology)
- Obesity
(drug therapy, etiology)
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