Previously, our laboratory observed for the first time that at 130 days of age (young adulthood), LP offspring of both sexes showed signs of impaired glucose tolerance and this deterioration was gender specific. 2005).Īlthough both β-cell dysfunction and insulin resistance contribute to diabetes, it is unclear which is prevalent in this model of dietary restriction. 2009) and females ( Fernandez-Twinn et al. LP exposure during early life has also been shown to affect the expression and activation of key proteins involved in the insulin signaling cascade in peripheral tissues in adult males ( Ozanne et al. Male and female offspring of LP-fed mothers have been reported to exhibit altered hepatic expression of enzymes involved in the regulation of glucose homeostasis ( Desai et al. LP exposure during pregnancy and lactation affects insulin sensitivity in the adult offspring. 1995), suggesting that events in the fetal and early postnatal growth periods can predispose subjects to glucose intolerance and diabetes in adult life. 1995, Minana-Solis Mdel & Escobar 2008) and females ( Dahri et al.
Despite changing to a control diet after birth or after weaning, β-cell dysfunction (as shown by a lower insulin response after a glucose challenge) persists into late adulthood in males ( Dahri et al. Moreover, the insulin-secretory capacity of fetal β-cells in response to secretagogues from LP-fed rat mothers is also significantly reduced ( Dahri et al. Previously, we suggested that the increase in β-cell apoptosis and decrease in neogenesis are due to the decrease in insulin-like growth factor 2 (IGF2) expression ( Petrik et al. 1999), and altered islet vascularization ( Snoeck et al. 2002), reduced islet cell proliferation, increased islet cell apoptosis ( Snoeck et al.
1991) with reduced islet size and pancreatic insulin content ( Snoeck et al. Offspring of rats fed a LP diet during gestation and lactation have lower body weights and altered structure and function of the fetal endocrine pancreas ( Snoeck et al. Protein restriction (low-protein (LP), 8%) during pregnancy and lactation in rats has been used extensively to investigate the role of fetal environment to determine future susceptibility to adult disease. This has been supported by epidemiological and animal studies, which have shown a strong relationship between poor fetal growth and subsequent development of obesity and type 2 diabetes in adult life ( Hales & Barker 1992). A perinatal origin of adult disease has been suggested to contribute to the rapid rise in type 2 diabetes. Type 2 diabetes is a prevalent health concern worldwide and has been predicted to affect more than 438 million people by the year 2030 ( Shaw et al. We conclude that i) maternal Tau supplementation has persistent effects on improving glucose metabolism (β-cell function and insulin sensitivity) in adult rat offspring of LP-fed mothers and ii) increasing the amount of protein in the diet of offspring adapted to a LP diet after weaning may impair glucose metabolism (β-cell function) in a gender-specific manner. The LP-all life diet improved β-cell function in males. Tau supplementation improved insulin sensitivity in females and β-cell function in males. In both genders, LP exposure decreased β-cell function. Insulin sensitivity in the offspring of LP-fed mothers was reduced in females but not in males.
A fourth group consisting of offspring of LP-fed mothers, maintained on a LP diet following weaning, was also studied (LP-all life). Offspring were given a control diet following weaning.
Pregnant rats were fed i) control, ii) LP, and iii) LP+Tau diets during gestation and lactation. The objective of this study was to examine the relative contribution of β-cell dysfunction and insulin resistance to impaired glucose tolerance in 130-day-old rat offspring of LP-fed mothers and the effects of maternal Tau supplementation on β-cell function and insulin resistance in these offspring. The prevention of postnatal catch-up growth has been suggested to improve glucose tolerance in adult offspring of low-protein (LP)-fed mothers. Maternal taurine (Tau) supplementation during pregnancy in rats restores β-cell function and mass in neonates, but its long-term effects are unclear. Dietary protein restriction during pregnancy and lactation in rats impairs β-cell function and mass in neonates and leads to glucose intolerance in adult offspring.
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