Alleviation of Fatty Liver in Dairy Cows with 14-Day Intravenous Infusions of Glucagon

Abstract

Twenty multiparous cows were fed additional concentrate during the final 30 d prepartum to cause susceptibility to fatty liver. From 14 to 42 d postpartum, all cows were subjected to a protocol to induce fatty liver and ketosis. 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 postpartum. All cows had fatty liver at 14 d postpartum and became ketonemic and hypoglycemic during the induction of ketosis. Glucagon increased plasma glucose to 142% of that of controls throughout the 14-d treatment. The hypoinsulinemia present in cows with fatty liver was not affected by glucagon. Plasma beta-hydroxybutyrate and nonesterified fatty acids were decreased by glucagon. 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. Glycogen then increased in cows treated with glucagon until at 38 d in milk liver glycogen was 3.7% versus 1.6% in controls. Our results document that glucagon decreases the degree of fatty liver in early lactation dairy cows, which also decreases the incidence of ketosis after alleviation of fatty liver.

Studies on hepatic lipidosis and coinciding health and fertility problems of high‐producing dairy cows using the “Utrecht fatty liver model of dairy cows”. A review

“…It should be noted that the fatty liver induction protocol was more successful in experimental cows with a lower parity. The outcome of our studies is contrary to the idea that there might be a genetic basis to post partum fatty liver development or that a fatty liver protocol is more susceptible in cows that are naturally susceptible to fatty liver (24,25). Clearly, the development of fatty liver post partum can be counteracted by restricted feeding during the dry period.…”

Protein nutrition in late pregnancy, maternal protein reserves and lactation performance in dairy cows

“…This idea is consistent with the finding of Holtenius & Hjort (1990) that dry cows fed on diets high in energy but low in protein suffered a major increase in the severity of fatty liver at parturition compared with cows fed on high-energy high-protein or low-energy low-protein diets. A similar response was induced by Hippen et al (1999) who fed cows on a diet very high in energy but with only 120 g CP/kg for 30 d before calving. The hepatic supply of protein, or specific amino acids, may be limiting for synthesis of apolipoprotein B, and therefore hepatic lipid disposal via synthesis and secretion of VLDL.…”

Gluconeogenesis in dairy cows: The secret of making sweet milk from sour dough

“…Although the mechanisms leading to postparturient fatty liver and ketosis are not fully understood, it could be related in part to the drainage of OAA from the TCA cycle (74). Increases in PC mRNA, which coincides with increased clearance of lipid from liver in dairy cattle given glucagon infusions (76,77), support a role for PC in this process.…”