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Galectin‐3 Levels in Hepatic Tissue from Lean and Obese Zucker Rats
Author(s) -
Schuster Jane E,
Motawe Zeinab Y.,
Trujillo Andrea N.,
Breslin Jerome W.
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.753.9
Subject(s) - medicine , endocrinology , fibrosis , obesity , nonalcoholic fatty liver disease , galectin 3 , metabolic syndrome , fatty liver , adipose tissue , immune system , liver disease , biology , disease , immunology
Obesity and metabolic syndrome are of major concern for physicians worldwide. Galectin‐3 is a β‐galactoside‐binding protein that has been shown to have regulatory functions in inflammatory responses as well as fibrosis of the liver, lung, heart and blood vessels. Galectin‐3 is widely expressed in multiple types of immune cells as well as epithelial and endothelial cells, and its properties have been explored as a therapeutic target for nonalcoholic fatty liver disease liver fibrosis, heart disease and other obesity‐associated diseases. We previously observed elevation of galectin‐3 in mesenteric fat from male and female 12‐week‐old obese Zucker rats compared to their lean counterparts. We hypothesized that galectin‐3 expression levels would be elevated in the liver in obese animals. Livers were collected from 20 Zucker rats (5 male, 5 female lean rats and 5 male, 5 female obese Zucker rats) for histology and protein analysis. After protein lysates were collected and total protein levels were normalized, galectin‐3 levels were quantified with the Wes Simple Western capillary electrophoresis assay. The results showed that livers of obese rats of both sexes display typical fatty liver pathology and have a significantly higher level of Galectin‐3 expression. The results show that increased galectin‐3 expression accompanies fatty liver in obese rats. Galectin‐3 may represent a future target for preventing tissue dysfunction in obesity and metabolic syndrome Support or Funding Information APS Frontiers in Physiology Fellowship This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .