TY - JOUR
T1 - Lactoferrin interacts with bile acids and increases fecal cholesterol excretion in rats1
AU - Nakamura, Kanae
AU - Morishita, Satoru
AU - Ono, Tomoji
AU - Murakoshi, Michiaki
AU - Sugiyama, Keikichi
AU - Kato, Hisanori
AU - Ikeda, Ikuo
AU - Nishino, Hoyoku
N1 - Publisher Copyright:
© 2017 Published by NRC Research Press.
PY - 2017
Y1 - 2017
N2 - Lactoferrin (LF) is a multifunctional cationic protein (pI 8.2-8.9) in mammalian milk. We previously reported that enteric-LF prevented hypercholesterolemia and atherosclerosis in a diet-induced atherosclerosis model using Microminipig, although the underlying mechanisms remain unclear. Because LF is assumed to electrostatically interact with bile acids to inhibit intestinal cholesterol absorption, LF could promote cholesterol excretion. In this study, we assessed the interaction between LF and taurocholate in vitro, and the effect of LF on cholesterol excretion in rats. The binding rate of taurocholate to LF was significantly higher than that to transferrin (pI 5.2-6.3). When rats were administered a high-cholesterol diet (HCD) containing 5% LF, LF was detected using ELISA in the upper small intestine from 7.5 to 60 min after the administration. Rats were fed one of the following diets: control, HCD, or HCD + 5% LF for 21 days. Fecal neutral steroids and hepatic cholesterol levels in the HCD group were significantly higher than those in the control group. The addition of LF to a HCD significantly increased fecal neutral steroids levels (22% increase, p < 0.05) and reduced hepatic cholesterol levels (17% decrease, p < 0.05). These parameters were inversely correlated (R = -0.63, p < 0.05). These results suggest that LF promotes cholesterol excretion via interactions with bile acids.
AB - Lactoferrin (LF) is a multifunctional cationic protein (pI 8.2-8.9) in mammalian milk. We previously reported that enteric-LF prevented hypercholesterolemia and atherosclerosis in a diet-induced atherosclerosis model using Microminipig, although the underlying mechanisms remain unclear. Because LF is assumed to electrostatically interact with bile acids to inhibit intestinal cholesterol absorption, LF could promote cholesterol excretion. In this study, we assessed the interaction between LF and taurocholate in vitro, and the effect of LF on cholesterol excretion in rats. The binding rate of taurocholate to LF was significantly higher than that to transferrin (pI 5.2-6.3). When rats were administered a high-cholesterol diet (HCD) containing 5% LF, LF was detected using ELISA in the upper small intestine from 7.5 to 60 min after the administration. Rats were fed one of the following diets: control, HCD, or HCD + 5% LF for 21 days. Fecal neutral steroids and hepatic cholesterol levels in the HCD group were significantly higher than those in the control group. The addition of LF to a HCD significantly increased fecal neutral steroids levels (22% increase, p < 0.05) and reduced hepatic cholesterol levels (17% decrease, p < 0.05). These parameters were inversely correlated (R = -0.63, p < 0.05). These results suggest that LF promotes cholesterol excretion via interactions with bile acids.
KW - Bile acid
KW - Cholesterol
KW - Hypercholesterolemia
KW - Lactoferrin
KW - Rats
UR - http://www.scopus.com/inward/record.url?scp=85012082504&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85012082504&partnerID=8YFLogxK
U2 - 10.1139/bcb-2016-0052
DO - 10.1139/bcb-2016-0052
M3 - Article
C2 - 28165288
AN - SCOPUS:85012082504
VL - 95
SP - 142
EP - 147
JO - Biochemistry and Cell Biology
JF - Biochemistry and Cell Biology
SN - 0829-8211
IS - 1
ER -