Effects of slow-release insulin on production, liver triglyceride, and metabolic profiles of holsteins in early lactation

Abstract

The objective of this experiment was to determine whether there is a dose of slow-release insulin (SRI) that decreases concentrations of plasma nonesterified fatty acids (NEFA) and liver triglyceride (TG) without decreasing plasma glucose concentration, dry matter intake (DMI), and milk yield. Forty-three Holsteins weighing 765 ± 70 kg with body condition score of 3.29 ± 0.25 (mean ± SD) were fed for ad libitum consumption of the same diet from 2 wk before parturition through 6 d postpartum. Cows were blocked according to actual calving date and parity and then assigned randomly to intramuscular injection of a single dose of 0, 0.14, 0.29, or 0.43 IU of SRI per kilogram of body weight (BW) on d 3 postpartum. On the day of injection, cows were fed hourly to minimize fluctuations in blood hormones and metabolites due to feed intake pattern. Blood samples were collected via jugular catheter every hour from 0 to 24 h and every 6 h from 24 to 48 h postinjection. Pre-and postinjection period liver samples were taken on d 2 and 5 postpartum. One cow injected with 0.29 and two cows injected with 0.43 IU of SRI per kilogram of BW could not complete the trial due to severe hypoglycemia (<20 mg/dl). Both DMI and milk yield during d 3 to 5 postpartum tended to increase quadratically by increasing dose of SRI. Concentrations of serum insulin and glucagon increased linearly, concentration of plasma glucose decreased linearly, and concentrations of plasma NEFA and β-hydroxybutyrate decreased quadratically from 0 to 24 h postinjection by increasing dose of SRI. Serum insulin concentrations remained higher in cows injected with SRI (CISRI) than in cows injected with sterile water (CISW; 0 IU of SRI/kg of BW), the quadratic effect of SRI on plasma NEFA concentration continued, and the linear effect of SRI on plasma glucose concentration diminished from 24 to 48 h postinjection. Concentration of hepatic TG for CISRI tended to be lower than for CISW, and increasing dose of SRI quadratically decreased hepatic accumulation of TG. Increasing dose of SRI tended to increase concentration of hepatic glycogen (GLY) quadratically and decreased the ratio of TG to GLY quadratically. In conclusion, a low dose of SRI (0.14 IU/kg of BW) could be considered for prophylactic use against hepatic lipidosis and ketosis.