Maturation of pancreatic β-cell function in the fetal horse during late gestation

Abstract

At birth, the endocrine pancreas becomes more directly involved in the control of glycaemia than in utero. However, compared with other tissues, relatively little is known about the maturational changes that occur in the fetal endocrine pancreas in preparation for extrauterine life. This study examined the pancreatic -cell response to exogenous administration of glucose and arginine in fetal horses with respect to their gestational age and concentration of cortisol, the hormone responsible for prepartum maturation of other fetal tissues. Glucose administration had no effect on fetal insulin secretion between 175 and 230 days of gestation but evoked a rapid insulin response in fetuses closer to term (290-327 days). In late gestation, the -cell response was more rapid and greater in magnitude in fetuses with basal cortisol levels higher than 15 ng/ml than in those with lower cortisol values at the time of glucose administration. The fetal -cell response to arginine was unaffected by the rise in fetal plasma cortisol towards term. These findings show that there are maturational changes in pancreatic -cell function in fetal horses as cortisol levels rise close to term. Primarily, these prepartum maturational changes were in the mechanisms of glucose-stimulated insulin secretion, which would enable the cells to regulate glycaemia at the higher glucose levels observed postnatally.

Maternal Nutrition during Pregnancy Affects Testicular and Bone Development, Glucose Metabolism and Response to Overnutrition in Weaned Horses Up to Two Years

“…In sheep, offspring born to dams underfed in late gestation were shown to be glucose intolerant at 1 year of age, although, in that study, birth weight and post-natal growth did not differ from controls [56]. In the horse, pancreatic maturation takes place near term (290–327 days of gestation) [57]. In the present study, maternal undernutrition occurred from 200 to 321 days of gestation [31] when the foal’s pancreas was maturing.…”

Similar Developmental Patterns of Ghrelin- and Glucagon-Expressing Cells in the Human Pancreas

“…Therefore, it seems that insulin-, glucagonand ghrelin-producing cells together play a pivotal role in the regulation of plasma glucose concentrations. Although the endocrine pancreas becomes more directly involved in the control of glycemia shortly after birth, it is also functional before birth [Silver et al, 1986;Dunne et al, 2004;Fowden et al, 2005], and the ability of glucagon and ghrelin to enhance plasma glucose levels points toward their synergistic effects on glucose homeostasis as well as a possible developmental role for these hormones in the prevention of hypoglycemia. However, studies in pregnant rats have demonstrated that maternal fasting does not affect fetal plasma ghrelin levels, but causes a 2-to 3-fold increase in both pancreas and stomach acylghrelin concentrations [Chanoine and Wong, 2004], suggesting a paracrine role for fetal ghrelin.…”

Insulin resistance in pregnant mares: the influence of body condition

“…IR may develop for the first day after foaling (Holdstock et al, 2004). Fowden et al (2005) also found that premature foals have decreased insulin secretion in the immediate post natal period compared to full-term foals. Although it has been reported that, in Standardbreds, new-born foals are more insulin resistant than mature horses (Ralston, 1996), while other studies reported that the decreases in Si with increasing age were related to the environment, diet, genetics and other acquired factors (Barbieri et al, 2001).…”

“…Others have reported a contrary view that the neonatal foal naturally has IR due to the development of the pancreas at this age (Fowden et al, 2005, Holdstock et al, 2004.…”

“…Others studying on the insulin-glucose correlation in foetus have demonstrated that IR may change naturally in relation to age and species. Glucose administration has been reported to have no significant effect on foetus in early pregnancy, but the response by β cell to glucose dose increases with foetal age (Fowden et al 2005). IR may develop for the first day after foaling (Holdstock et al, 2004).…”