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

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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 β-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.

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Abbreviations

A:

acidic

apoB:

apolipoprotein B

B:

basic

BCS:

body condition score

BHBA:

β-hydroxybutyrate

BW:

body weight

CPT-I:

carnitine palmitoyltransferase-I

C-peptide:

connecting peptide

DMI:

dry matter intake

FA:

fatty acid

G1P:

glucose-1-phosphate

G6P:

glucose-6-phosphate

GTT:

glucose tolerance test

GLUT:

glucose transporter

GLY:

glycogen

GH:

growth hormone

hCG:

human chorionic gonadotrophin

IRS:

insulin receptor substrate

LPL:

lipoprotein lipase

MW:

molecular weight

NEFA:

nonesterified fatty acid

NEL:

net energy for lactation

NFC:

non-fibre carbohydrates

PI3:

phosphoinositol phosphate kinase

RRI:

rapid-release insulin

RER:

rough endoplasmic reticulum

SRI:

slow-release insulin

TCA:

tricarboxylic acid

TG:

triglyceride

VFA:

volatile fatty acids

VLDL:

very low-density lipoprotein

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    A. Hayirli

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Hayirli, A. The Role of Exogenous Insulin in the Complex of Hepatic Lipidosis and Ketosis Associated with Insulin Resistance Phenomenon in Postpartum Dairy Cattle. Vet Res Commun 30, 749–774 (2006). https://doi.org/10.1007/s11259-006-3320-6

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