Caffeine reduces hepatic lipid accumulation through regulation of lipogenesis and ER stress in zebrafish larvae
Zheng X, Dai W, Chen X, Wang K, Zhang W, Liu L, Hou J
Journal of biomedical science · 71 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- Animal study (classified by our AI screen)
- Studied in
- Animals
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Funding not disclosed
Publication
- Published
- 2015-11-13 · J Biomed Sci · vol. 22 · issue 1 · p. 105
- Publisher
- BioMed Central
- Cited
- 96 citations · more than 95% of similar papers · 5.0× the field average
- Impact
- Top 10% most cited in its field
- References
- 59 works
- Access
- Open access (free to publish) · CC-BY
- Research areas
- Coffee research and impacts · Adenosine and Purinergic Signaling · Sirtuins and Resveratrol in Medicine
- Keywords
- Lipogenesis, Internal medicine, Endocrinology, Fatty liver, Downregulation and upregulation, Hepatoprotection, Steatosis, ATF6, Zebrafish, Unfolded protein response, Caffeine, CD36, Biology, Lipid metabolism, Chemistry, Medicine, Biochemistry, Endoplasmic reticulum, Gene
- MeSH
- liver, animals, zebrafish, humans, caffeine, lipids, zebrafish proteins, lipogenesis, endoplasmic reticulum stress, non-alcoholic fatty liver disease
7 authors
From CN
- Xinchun ZhengNanfang Hospital; Southern Medical University
- Wencong DaiNanfang Hospital; Southern Medical University
- Xiaohui ChenSouthern Medical University
- Kunyuan WangNanfang Hospital; Southern Medical University
- Wenqing ZhangSouthern Medical University
- Li Liu · correspondingNanfang Hospital; Southern Medical University
Abstract
Background
Caffeine, the main component of coffee, has showed its protective effect on non-alcoholic fatty liver disease (NAFLD) in many studies. However, the hepatoprotection of caffeine and its mechanisms in zebrafish were unexplored. Thus, this study's intentions are to establish a NAFLD model of zebrafish larvae and to examine the role of caffeine on fatty liver with the model.
Results
Growth and the incidence of fatty liver of zebrafish larvae increased with the increased amount of feeding in a dose-dependent manner. The degree of hepatic steatosis of larvae also gradually aggravated with the increased quantity and duration of feeding. Triglyceride contents of zebrafish fed for 20 days significantly increased in model group (180 mg/d) compared with control group (30 mg/d) (P < 0.001). Significant decreases in body weight and hepatic steatosis rate were observed in 2.5, 5, 8 % caffeine treatment group compared with model group (P < 0.05). Hepatic lipid accumulation was also significantly reduced in caffeine treatment larvae. Moreover, caffeine treatment was associated with upregulation of lipid β-oxidation gene ACO and downregulation of lipogenesis-associated genes (SREBP1, ACC1, CD36 and UCP2), ER stress-associated genes (PERK, IRE1, ATF6 and BIP), the inflammatory cytokine genes (IL-1beta and TNF-alpha) and autophagy associated genes (ATG12 and Beclin-1). Protein expression of CHOP, BIP and IL-1beta remarkably reduced in caffeine treatment group compared with model group.
Conclusions
We induced hepatoteatosis in zebrafish by overfeeding regimen and demonstrated caffeine have a role in suppression of hepatosteatosis by downregulation of genes associated with lipogenesis, ER stress, inflammatory response and enhancement of lipid oxidation, indicating zebrafish model may be used to identify putative pharmacological targets and to test novel drugs for human NAFLD treatment.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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