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Modulation of Hepatic Mineral Concentrations in Bile Acid‐Induced Fatty Liver
Author(s) -
HORI SHOTA,
Tanaka Yasutake,
Tsuneki Ikuya,
Hanai Taketo,
Hara Hiroshi,
Shimizu Hidehisa,
Ishizuka Satoshi
Publication year - 2017
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.31.1_supplement.887.10
Subject(s) - medicine , cholic acid , endocrinology , fatty liver , chemistry , bile acid , deoxycholic acid , fatty acid , taurocholic acid , cecum , biochemistry , biology , disease
Background & Aims Bile acids (BAs) promote lipid absorption as a detergent and a high fat diet consumption promotes its secretion. In our previous study, we found that a diet supplemented with cholic acid (CA), a major primary BA increasing during aging, induces non‐obese fatty liver in rats. The CA‐induced fatty liver seems represent some symptoms at an early stage of fatty liver. On the other hand, hepatic iron is associated with severity of fatty liver disease but little is known about the roles of iron in the early stage of fatty liver development. Thus, we investigated whether distribution of minerals in the body is involved in the CA‐induced fatty liver. Methods Rats were fed diets either with or without CA‐supplementation for 13 weeks. BAs were analyzed in portal vein, liver, and cecum with LC‐MS. Mineral concentrations (Fe, Ca, Mg, Mn, Zn, and Cu) in liver, aorta plasma, renal cortex, and feces were analyzed with ICP‐MS. Several parameters associated with fatty liver were analyzed. Results Cecal concentration of deoxycholic acid, the secondary BAs from CA, increased significantly in the CA‐fed rats. In the portal plasma, significant increases in CA and taurocholic acid (TCA) levels were observed in the CA‐fed rats. Prominent increases in the concentration of TCA and taurodeoxycholic acid as well as lipid accumulation were found in the liver of the CA‐fed rats. A significant decrease was observed in hepatic Fe in the CA‐fed rats, whereas there were significant increases of Ca, Mg, and Mn in the liver. Principal component analysis indicated hepatic iron concentration was closely associated with the lipid accumulation in the liver. No significant difference was observed in concentration of ferritin in aorta plasma between two groups although Fe concentration in aorta plasma decreased significantly in the CA‐fed rats, suggesting decrease in the amount of functional iron in the CA‐fed rats. Conclusion Iron deficiency is reported to cause a variety of changes in host energy metabolism such as increases of glucose uptake and lipogenesis as well as decreases of β‐oxidation in the liver. Therefore, the decrease of hepatic functional iron in the CA‐fed rats may be involved in the development of the lipid accumulation.