The Role of Exogenous Insulin in the Complex of Hepatic Lipidosis and Ketosis Associated with Insulin Resistance Phenomenon in Postpartum Dairy Cattle

Abstract

As a result of a marked decline in dry matter intake (DMI) prior to parturition and a slow rate of increase in DMI relative to milk production after parturition, dairy cattle experience a negative energy balance. Changes in nutritional and metabolic status during the periparturient period predispose dairy cattle to develop hepatic lipidosis and ketosis. The metabolic profile during early lactation includes low concentrations of serum insulin, plasma glucose, and liver glycogen and high concentrations of serum glucagon, adrenaline, growth hormone, plasma beta-hydroxybutyrate and non-esterified fatty acids, and liver triglyceride. Moreover, during late gestation and early lactation, flow of nutrients to fetus and mammary tissues are accorded a high degree of metabolic priority. This priority coincides with lowered responsiveness and sensitivity of extrahepatic tissues to insulin, which presumably plays a key role in development of hepatic lipidosis and ketosis. Hepatic lipidosis and ketosis compromise production, immune function, and fertility. Cows with hepatic lipidosis and ketosis have low tissue responsiveness to insulin owing to ketoacidosis. Insulin has numerous roles in metabolism of carbohydrates, lipids and proteins. Insulin is an anabolic hormone and acts to preserve nutrients as well as being a potent feed intake regulator. In addition to the major replacement therapy to alleviate severity of negative energy balance, administration of insulin with concomitant delivery of dextrose increases efficiency of treatment for hepatic lipidosis and ketosis. However, data on use of insulin to prevent these lipid-related metabolic disorders are limited and it should be investigated.

Inorganic phosphorus decrease after intravenous glucose tolerance test is associated with insulin resistance in dairy cows

“…During early lactation, a negative energy balance, ketosis and greater concentrations of NEFA and BHB in the blood of cows are noted (OETZEL, 2007;ŠAMANC et al, 2015;DJOKOVIĆ et al, 2015). Higher values of NEFA and BHB in the blood can cause insulin resistance by affecting pancreatic islands that secrete less insulin, as well as the fact that they negatively affect insulin receptors in peripheral tissue (HAYIRLI, 2006). This may serve as an explanation of our results which show that the correlation between Pi response and insulin and glucose response during IVGTT depends on the RQUICKI and RQUICKI-BHB insulin resistance indexes.…”

“…Greater lipolysis in tissues takes place in order to compensate for the negative energy balance, but insulin resistance is also needed. Insulin resistance in ketosis is characterized by lower concentrations of insulin and glucose, reduced responsiveness of insulin to glucose, greater lipolysis in peripheral tissues, ketone body production and lower RQUICKI index values (HAYIRLI, 2006;XU et al, 2014).…”

Intraday variation of metabolic key indicators in serum of dairy cows between week 2 antepartum and week 12 postpartum

“…No consistent circadian patterns have been found for the secretion of insulin (Trenkle, 1978), but ultradian oscillations have been reported to occur in ranges of 2, 10-15, and 100-150 min intervals (Sturis et al, 1991). Insulin levels vary in direct relation to feeding in most of the studies with cattle (Hayirli, 2006). Two peaks in insulin concentrations were found in cows associated with twice daily feeding (Hove and Blom, 1973).…”

Relaciones entre calcio, ácidos grasos no esterificados, e insulina sanguínea en preparto y leche bovina perdida en el inicio de la lactancia

“…La insulina ha demostrado que suprime la producción de glucosa a través de la inhibición de enzimas reguladoras involucradas en la gluconeogénesis (Hayirli, 2006). Sin embargo, en dicha acción también participa el ßHB (Zarrin et al 2013).…”