PUBLICATION

Effect of Melatonin on the Reduction of Hepatic Steatosis and Intestinal Leptin Expression in Zebrafish Exposed to Fructose

Authors
Schneider, A.C.R., de Moura, A.C., Carvalho, F.B., Alves, T., Meurer, F., Porawski, M., da Silveira, T.R.
ID
ZDB-PUB-210514-8
Date
2021
Source
Zebrafish   18(3): 184-189 (Journal)
Registered Authors
Keywords
appetite, fatty liver, fructose, melatonin, zebrafish
MeSH Terms
  • Animals
  • Fructose/adverse effects
  • Fructose/metabolism
  • Intestines
  • Leptin/metabolism
  • Liver/metabolism
  • Melatonin*/pharmacology
  • Zebrafish*/metabolism
PubMed
33983041 Full text @ Zebrafish
Abstract
Melatonin is a hormone related to circadian rhythms and has potential clinical applications. Our objectives were to verify the effect of melatonin on the liver of zebrafish exposed to fructose and evaluate the expression of appetite-related genes (leptin, ghrelin, and melanocortin receptor 4 [MC4R]). Animals were divided into three groups: control (CG, n = 25), fructose (FG, n = 25), and fructose+melatonin (FMG, n = 25). The study was carried out in 8 weeks. FG and FMG were exposed to 2% fructose and FMG treated with 1 μM of melatonin. Histological liver studies and gene expression analyses of Leptin, Ghrelin, and MC4R (liver and intestines) were performed. FG developed hepatic steatosis, which did not occur with CG and FMG. Genetic expression of hepatic leptin and MC4R did not show significant difference among the groups. Animals exposed to fructose (FG) presented an increased expression of intestinal leptin compared to those administered with melatonin. Animals exposed to fructose gained weight and developed an important hepatic steatosis, but melatonin reduced significantly the hepatic damage. Intestinal leptin showed increased expression in the group exposed to fructose.
Genes / Markers
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Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping