Twenty multiparous cows were fed additional concentrate during the final 30
d prepartum to cause susceptibility to fatty liver. From 14 to 42 d postpa
rtum, all cows were subjected to a protocol to induce fatty liver and ketos
is. To test glucagon as a treatment for fatty liver, either glucagon at 10
mg/d or excipient was infused via the jugular vein from 21 to 35 d postpart
um. All cows had fatty liver at 14 d postpartum and became ketonemic and hy
poglycemic during the induction of ketosis. Glucagon increased plasma gluco
se to 142% of that of controls throughout the 14-d treatment. The hypoinsul
inemia present in cows with fatty liver was not affected by glucagon. Plasm
a beta-hydroxybutyrate and nonesterified fatty acids were decreased by gluc
agon. At 6 d postpartum, liver triacylglycerol averaged 12.9% of liver (wet
weight basis). Glucagon had decreased triacylglycerol content of livers by
71% at d 35. Glycogen was 1.0% of the wet weight of livers at 6 d in milk,
but it was decreased by glucagon to 0.5% at 2 d after glucagon began. Glyc
ogen then increased in cows treated with glucagon until at 38 d in milk liv
er glycogen was 3.7% versus 1.6% in controls. Our results document that glu
cagon decreases the degree of fatty liver in early lactation dairy cows, wh
ich also decreases the incidence of ketosis after alleviation of fatty live
r.