Abstract
Background Cinnamic acid (CA) has been shown to have many beneficial effects including regulating lipid metabolism and reducing obesity. However, its effect on nonalcoholic fatty liver disease (NAFDL) has not been investigated in detail. Thus, we performed this study in order to explore CA's effect on hepatic lipid metabolism and the underlying mechanisms. Method Oleic acid (OA) was used to induce lipid accumulation in HepG2 cells. After coincubation with CA, the cells were stained with oil red O and the triglyceride (TG) content was assessed. Key genes in lipogenesis and fatty acid oxidation pathways were tested. Additionally, db/db and wt/wt mice were divided into three groups, with the wt/wt mice representing the normal group and the db/db mice being divided into the NAFLD and CA groups. After 4 weeks of oral treatment, all mice were sacrificed and the blood lipid profile and liver tissues were assessed. Results CA treatment reduced the lipid accumulation in HepG2 cells and in db/db mouse livers. ACLY, ACC, FAS, SCD1, PPARγ, and CD36 were significantly downregulated, while CPT1A, PGC1α, and PPARα were significantly upregulated. Conclusion CA's therapeutic effect on NAFLD may be attributed to its ability to lower hepatic lipid accumulation, which is mediated by suppression of hepatic lipogenesis and fatty acid intake, as well as increased fatty acid oxidation.
Highlights
Nonalcoholic fatty liver disease (NAFLD), the incidence of which often parallels the trends in obesity, type II diabetes, dyslipidemia, and other metabolic diseases, has become a major health problem worldwide and the most common chronic liver disease in recent years [1]. e global prevalence of NAFLD is approximately 25.24% [2] and the rate continues to increase [3]
de novo lipogenesis (DNL) is mediated by several lipogenic enzymes, the transcription of which is governed by transcription factors such as carbohydrate-responsive element-binding protein (ChREBP), sterol regulatory elementbinding protein 1c (SREBP1c), and liver X receptors (LXRs) [6]
Cinnamic acid (CA) has exhibited hypolipidemic effects in both in vivo and in vitro experiments, the underlying mechanisms of CA’s effect on NAFLD are still poorly understood. us, we investigated the effect of CA on Oleic acid (OA)-stimulated HepG2 cells and db/db mice, a commonly used genetic model for NAFLD [26, 27], and we explored the alterations in the expression of transcription factors and key enzymes in the lipogenesis and fatty acid oxidation pathways in cells and mice after CA treatment
Summary
Nonalcoholic fatty liver disease (NAFLD), the incidence of which often parallels the trends in obesity, type II diabetes, dyslipidemia, and other metabolic diseases, has become a major health problem worldwide and the most common chronic liver disease in recent years [1]. e global prevalence of NAFLD is approximately 25.24% [2] and the rate continues to increase [3]. NAFLD begins with simple hepatic steatosis and can develop into nonalcoholic steatohepatitis, potentially leading to hepatic fibrosis and cirrhosis and causing severe complications such as hepatocellular carcinoma [1] It reflects disrupted body energy homeostasis, which is the common pathological change in metabolic diseases. High IHTG levels in individuals with NAFLD may be attributed to increased de novo lipogenesis (DNL) and decreased fatty acid oxidation. Us, regulating energy metabolism, especially the fatty acid synthesis and oxidation pathways in hepatocytes, plays an important role in controlling excess IHTG levels and, eventually, improves the condition of NAFLD. CA’s therapeutic effect on NAFLD may be attributed to its ability to lower hepatic lipid accumulation, which is mediated by suppression of hepatic lipogenesis and fatty acid intake, as well as increased fatty acid oxidation
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