Caffeic acid ameliorates hepatic steatosis and decreased endoplasmic reticulum stress in high-fat diet-induced obese mice by regulating autophagy

Hong Min Kim, Yuna Kim, Eun Soo Lee, Ji Hye Huh, Choon Hee Chung

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Objective: Non-alcoholic fatty liver disease is characterized by high hepatic triacylglycerol contents, which is associated with endoplasmic reticulum (ER) stress and insulin resistance. Caffeic acid (CA) has antioxidant, immunomodulatory, and antiinflammatory effects. We investigated the effects of CA on hepatic steatosis and its mechanism of action. 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.

Original languageEnglish
Pages (from-to)63-70
Number of pages8
JournalNutrition
Volume55-56
DOIs
Publication statusPublished - 2018 Nov 1

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Obese Mice
Endoplasmic Reticulum Stress
Autophagy
High Fat Diet
Liver
Palmitates
Hepatocytes
caffeic acid
Insulin Resistance
Lipids
Protein Deficiency
Fat-Restricted Diet
Lipogenesis
Glucose Intolerance

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

Cite this

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title = "Caffeic acid ameliorates hepatic steatosis and decreased endoplasmic reticulum stress in high-fat diet-induced obese mice by regulating autophagy",
abstract = "Objective: Non-alcoholic fatty liver disease is characterized by high hepatic triacylglycerol contents, which is associated with endoplasmic reticulum (ER) stress and insulin resistance. Caffeic acid (CA) has antioxidant, immunomodulatory, and antiinflammatory effects. We investigated the effects of CA on hepatic steatosis and its mechanism of action. 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.",
author = "Kim, {Hong Min} and Yuna Kim and Lee, {Eun Soo} and Huh, {Ji Hye} and Chung, {Choon Hee}",
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Caffeic acid ameliorates hepatic steatosis and decreased endoplasmic reticulum stress in high-fat diet-induced obese mice by regulating autophagy. / Kim, Hong Min; Kim, Yuna; Lee, Eun Soo; Huh, Ji Hye; Chung, Choon Hee.

In: Nutrition, Vol. 55-56, 01.11.2018, p. 63-70.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Caffeic acid ameliorates hepatic steatosis and decreased endoplasmic reticulum stress in high-fat diet-induced obese mice by regulating autophagy

AU - Kim, Hong Min

AU - Kim, Yuna

AU - Lee, Eun Soo

AU - Huh, Ji Hye

AU - Chung, Choon Hee

PY - 2018/11/1

Y1 - 2018/11/1

N2 - Objective: Non-alcoholic fatty liver disease is characterized by high hepatic triacylglycerol contents, which is associated with endoplasmic reticulum (ER) stress and insulin resistance. Caffeic acid (CA) has antioxidant, immunomodulatory, and antiinflammatory effects. We investigated the effects of CA on hepatic steatosis and its mechanism of action. 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.

AB - Objective: Non-alcoholic fatty liver disease is characterized by high hepatic triacylglycerol contents, which is associated with endoplasmic reticulum (ER) stress and insulin resistance. Caffeic acid (CA) has antioxidant, immunomodulatory, and antiinflammatory effects. We investigated the effects of CA on hepatic steatosis and its mechanism of action. 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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