Effect of feed restriction on hepatic estradiol metabolism and liver function in cows

Abstract

In this study, the effects of restriction feeding on the liver function, hepatic uridine diphosphate glucuronosyltransferase (UGT) activity, hepatic insulin-like growth factor (IGF)-1 mRNA expression and response to high-dose estradiol-17β (E 2) administration were investigated in non-lactating cows. Cows were assigned to either restricted feeding (30% of total digestible nutrient requirement) or ad libitum feeding of a dent corn-based concentrate and roughage for a 2-week feeding trial (Day 1 = day of beginning the feeding trial). On day 14, a high-dose E 2 administration study was carried out to examine plasma E 2 levels as an indicator of hepatic E 2 metabolism. Plasma E 2 concentration in the restricted feeding group was consistently higher after high-dose E 2 administration than in the control group. In addition, indocyanine green half-life value was prolonged by restricted feeding for 13 days, and increased liver triglyceride concentration and decreased liver UGT activity were caused by this restriction over 14 days. Restricted feeding did not affect plasma IGF-1 concentration or hepatic IGF-1 mRNA expression. These results suggest that two weeks of restriction feeding led to accumulation of triglyceride, decreased liver blood flow, and slightly impaired liver function, which in turn slowed down the hepatic metabolism of E 2 without significantly impacting hepatic IGF-1 production.

Maternal Nutrient Restriction Disrupts Gene Expression and Metabolites Associated with Urea Cycle, Steroid Synthesis, Glucose Homeostasis, and Glucuronidation in Fetal Calf Liver

“…These results indicate that MUN affects glucuronidation, which potentially leads to a deficiency in drug and steroid catabolism. Although the effect of MUN on fetal liver UGT activity has never been examined, the nutrient restriction has been shown to affect UGT activity in the livers of adult cows [ 52 ]. For example, alterations in nutritional level and high fat content can affect the expression of UGT1A1 and UGT1A6 in the liver, possibly through proliferator-activated receptor α [ 53 ].…”