Acute Metabolic Responses of Postpartal Dairy Cows to Subcutaneous Glucagon Injections, Oral Glycerol, or Both

Abstract

This study examined the effects of multiple subcutaneous glucagon injections with or without co-administration of oral glycerol on energy status-related blood metabolites and hormones of Holstein dairy cows in the first 2 wk postpartum. Twenty multiparous cows were fed a dry cow ration supplemented with 6 kg of cracked corn during the dry period to increase the likelihood of developing postpartal fatty liver syndrome. Cows with a body condition score of >or=3.5 points (1- to 5-point scale) were assigned randomly to 1 of 4 treatment groups: saline, glucagon, glycerol, or glucagon plus glycerol. Following treatment, serial blood samples were collected over an 8-h period to determine the effects of glucagon and glycerol on blood metabolites and hormones. Treatment effects were determined by comparing the concentrations of metabolites and hormones during the first 4-h period and the entire 8-h period after treatment administration (time 0) with the concentration of the same compounds at time 0 on d 1, 7, and 13 postpartum. Administration of glucagon alone increased concentrations of plasma glucagon and insulin on d 1, 7, and 13 and increased plasma glucose and decreased plasma nonesterified fatty acids (NEFA) on d 7 and 13 postpartum relative to the saline group. Administration of glycerol alone increased plasma glucose on d 7 and plasma triacylglycerols on d 1 postpartum. Glycerol administration also decreased plasma glucagon and NEFA on d 1, 7, and 13 and plasma beta-hydroxybutyrate (BHBA) on d 1 postpartum relative to the saline group. Administration of glucagon plus glycerol increased and sustained concentrations of plasma glucagon, glucose, and insulin on d 1, 7, and 13 and decreased plasma NEFA on d 1, 7, and 13 and BHBA on d 1 and 7. Early postpartal treatment of dairy cows with glucagon plus glycerol increased plasma glucose and insulin, decreased plasma NEFA and BHBA, and increased secretion of liver NEFA as plasma triacylglycerols. This suggests that glucagon and glycerol, when co-administered, act to decrease the likelihood of metabolism-related syndrome development in dairy cows.

Major Metabolic Diseases Affecting Cows in Transition Period

“…The results demonstrated that subcutaneous injections of glucagon of 7.5 and 15 mg/d starting at 2 d postpartum are sufficient for fatty liver prevention; however, some cows developed fatty liver already at d 2 postpartum. Previous results confirm (Osman et al, 2008) showing that prenatally and subcutaneously injected glucagon will decrease markedly the accumulation of lipid in the liver of the post parturient dairy cow. Daily administration of the same amount (15 mg/day) of glucagon for several days prenatally in a limited number of cows was effective in preventing fatty liver during the early post parturient period.…”

Influence of fish oil, palm oil and glycerol on milk fatty acid composition and metabolism in cows during early lactation

“…Fish oil and glycerol given to cows in TMR dose in the present study caused a successive increase in blood glucose concentration. Glycerol administered orally for the first two weeks postpartum caused an increase in blood glucagon, NEFA and and BHBA levels in 7th and 13th day (Osman et al 2008). More intense, profitable influence on metabolism was observed in the case of a joint subcutaneous application of glycerol and glucagon injection.…”

Precursors for liver gluconeogenesis in periparturient dairy cows

“…However, glucagon treatment in the study by She et al (1999) was initiated when the post partum metabolic adaptations have essentially occurred (Drackley et al, 2001). In post partum transition cows, glucagon injections have been observed to increase the glucogenic status of cows with high body condition scoring (Nafikov et al, 2008;Osman et al, 2010). Yet, to which extent glucagon is directly involved in changing liver AA metabolism is uncertain as the periparturient pattern of circulating concentrations of glucagon is not well described.…”

“…Yet, to which extent glucagon is directly involved in changing liver AA metabolism is uncertain as the periparturient pattern of circulating concentrations of glucagon is not well described. However, available data indicate that circulating concentrations in essence do not change from late pregnancy to the first few days after parturition, followed by an increase as lactation is progressing (Herbein et al, 1985;Holtenius et al, 1993;Osman et al, 2010;Park et al, 2010). Thus, periparturient changes in glucagon levels do not appear to be directly involved in the rapid post partum increase in liver glucose release (Table 1), but may be linked to the reduced insulin : glucagon ratio caused by the decreased circulating insulin level associated with parturition (Aschenbach et al, 2010).…”