Lanzamiento Enero 2027

Estudio2015Financiación no declaradaAcceso abierto

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 citas

Etiquetas de revisión

Financiación no declarada

Datos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.

Cómo se estudió

Diseño
Estudio en animales (clasificado por nuestro filtro de IA)
Estudiado en
Animales
Resultado principal
Marcadores de salud y funcionamiento

Quién lo pagó

Financiación
Financiación no declarada

Publicación

Publicado
2015-11-13 · J Biomed Sci · vol. 22 · número 1 · pág. 105
Editorial
BioMed Central
Citado
96 citas · más que el 95% de estudios similares · 5.0× el promedio de su campo
Impacto
Entre el 10 % más citado de su campo
Referencias
59 trabajos
Acceso
Acceso abierto (publicación gratuita) · CC-BY
Áreas de investigación
Coffee research and impacts · Adenosine and Purinergic Signaling · Sirtuins and Resveratrol in Medicine
Palabras clave
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 autores

  • Xinchun Zheng🇨🇳Nanfang Hospital; Southern Medical University
  • Wencong Dai🇨🇳Nanfang Hospital; Southern Medical University
  • Xiaohui Chen🇨🇳Southern Medical University
  • Kunyuan Wang🇨🇳Nanfang Hospital; Southern Medical University
  • Wenqing Zhang🇨🇳Southern Medical University
  • Li Liu🇨🇳 · autor de correspondenciaNanfang Hospital; Southern Medical University
  • Jinlin Hou🇨🇳 · autor de correspondenciaNanfang Hospital; Southern Medical University

Resumen

El texto original del estudio, en el idioma en que se publicó.

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.

Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).

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