Pregnancy toxemia was induced in nine pregnant goat does with twins by the stress of fasting with access to water in late
pregnancy to investigate the effect of pregnancy toxemia on immunoglobulins (IgA, IgM, and IgG), cortisol, insulin, thyroid,
and growth hormones and their correlations with the plasma levels of glucose and β-Hydroxybutyrate. Plasma samples were
collected at 0, 12, 24, 36, 48, and 72 hours after induction of pregnancy toxemia. The result revealed that experimental animals
developed neurological findings with convulsions and acetone odor from the mouth with recumbency after 72 hours. Laboratory
findings showed a significant increase in β-Hydroxybutyrate, cortisol, and insulin while there were significant decreases in glucose,
thyroid, and immunoglobulins (IgA, IgM, and IgG). Plasma glucose concentrations had significant negative correlations with
β-hydroxybutyrate, cortisol, and insulin while the correlations were significantly positive with immunoglobulins and thyroid
hormone. Plasma β-hydroxybutyrate concentration was significantly positively correlated with cortisol and negatively correlated
with immunoglobulins, insulin, and thyroid hormone. From this study we can conclude that pregnancy toxemia might affect
humoral immune responses as well as insulin, cortisol, and thyroid hormones. Moreover, insulin might have a compensatory role
to increase suppressive effect on ketogenesis in experimentally pregnant toxemic goats.
1. Introduction
Pregnancy represents one of the most anabolic periods of
the female life cycle, and pregnancy toxemia is a disease
caused by a negative energy balance in late gestation and seen
commonly in ewes, guinea pigs, rabbits, and occasionally in
cows, ferrets, sows, and many other species. Predisposing
causes include stress and food deprivation or negative
energy balance in late pregnancy [1–5]. Pregnancy toxemia
frequently develops during the last 4 to 6 weeks of gestation
in sheep and goat, primarily in pregnancies with more than
one fetus. About 60% of fetal growth takes place in this
last gestation period [6], and during this time approximately
33%–36% of the circulating glucose is directed into fetoplacental
unit to satisfy its energetic demands [7].
The endocrine system especially the pancreas probably is
intimately involved in the development of ruminant ketosis
[8]. Insulin inhibits ketogenesis when free fatty acids levels
are high [9], as well as growth