Effect of Dexamethasone on Glycogen Deposition in Pregnant Rats and Their Fetuses¹)

Abstract

Glycogen deposition was determined in pregnant rats and their fetuses twenty four hrs after maternal treatment with dexamethasone in the final days of pregnancy. Dexamethasone increases glycogen accumulation in the fetal liver, heart, adrenal glands and thymus. Simultaneously, it increases the glycogen concentration in maternal liver. In this study, dexamethasone did not change the glycogen level in the fetal kidneys, brain, placenta, lung and maternal adrenal glands. These results show that dexamethasone accelerated glycogen deposition in some fetal tissues. It is possible that dexamethasone activated enzymes of glycogen synthesis or potentiated the action of fetal corticosterone on induction of glycogen accumulation in fetal rat tissues.

Corticosterone alters materno‐fetal glucose partitioning and insulin signalling in pregnant mice

“…Oral corticosterone treatment did not alter liver glycogen content or activity of glucose 6‐phosphate, in contrast to previous studies in pregnant animals using the synthetic glucocorticoid, dexamethasone (Klepac, ; Franko et al . ).…”

“…GLUT1 is also expressed at low levels in the liver, where it facilitates basal glucose uptake (Olson & Pessin, ). Synthetic glucocorticoids, such as dexamethasone, are known to increase hepatic glycogen content and activity of the final, rate‐limiting glucogenic enzyme, glucose 6‐phosphatase, in pregnant rats and sheep (Klepac, ; Franko et al . ).…”

“…GLUT1 is also expressed at low levels in the liver, where it facilitates basal glucose uptake (Olson & Pessin, 1996). Synthetic glucocorticoids, such as dexamethasone, are known to increase hepatic glycogen content and activity of the final, rate-limiting glucogenic enzyme, glucose 6-phosphatase, in pregnant rats and sheep (Klepac, 1985;Franko et al 2007). Moreover, placental GLUT expression is altered by maternal treatment with synthetic glucocorticoids in pregnant rats (Hahn et al 1999;Langdown & Sugden, 2001).…”

Chronic late-gestation hypoglycemia upregulates hepatic PEPCK associated with increased PGC1α mRNA and phosphorylated CREB in fetal sheep

“…In the sheep, like many mammalian species, liver glycogen content increases during the later part of gestation (61). The increase in hepatic glycogen during the last part of gestation is dependent on cortisol (1,51,64), and in fact exogenous cortisol can augment and accelerate late-gestation hepatic glycogen synthesis and deposition (3,16,30,64). These results have been confirmed with in vitro studies using fetal liver explants and primary fetal hepatocytes, which show that glucocorticoids are necessary for allowing insulin-stimulated glycogen synthesis and deposition (14,48,64).…”

Hormones as epigenetic signals in developmental programming

“…In sheep, the metabolic, endocrine and cardiovascular responses to hypoxaemia are altered by administration of dexamethasone to either the mother or the fetus (Fletcher et al 2003;Jellyman et al 2004a,b). Glucocorticoids prolong the bradycardic response, increase the femoral vasoconstrictor response and enhance the increments in plasma neuropeptide Y, glucose and lactate to hypoxaemia Fowden et al (1993) ↑ Argininosuccuate lipase, ↑ 11βHSD1 Renouf et al (1995); Sloboda et al (2002) ↑ GH & prolactin receptors Li et al (1996); Phillips et al (1997) ↓ AT 1 receptors Segar et al (1995) ↑ IGF-I, ↓ IGF-II gene expression Li et al (1996), (1998) ↑ CBG, ↑ IGFBP, ↑ erythropoietin Lim et al (1996) ↓ Angiotensinogen gene expression Olson et al (1991); Segar et al (1995) ↑ Deiodinase type 1 Forhead et al (2006Forhead et al ( , 2007 ↑ Glycogen deposition Barnes et al (1978); Klepac, (1985) during the period of steroid exposure (Fletcher et al 2000b(Fletcher et al , 2003Jellyman et al 2005). Some but not all of these effects persist after treatment (Fletcher et al 2003;Jellyman et al 2005).…”