Proceedings of The Physiological Society

University of Cambridge (2008) Proc Physiol Soc 11, C29

Oral Communications

Effects of undernutrition during mouse pregnancy on tissue glycogen content

S. Finn1, R. S. Apatu1, R. J. Barnes1, P. M. Coan1, A. L. Fowden1

1. Department of Physiology, Development and Neuroscience, University of cambridge, Cambridge, United Kingdom.

  • Table 1 hepatic glycogen (mg/g) and blood glucose (mmol/l) levels in the four groups of adult CT and UN mice

    Values within rows with different superscripts are significantly different from each other (P&lt;0.05 ANOVA) * significantly different from corresponding control (P&lt;0.05 t-test). &#8224; UN for 19 days.

Glycogen is a storage form of glucose found primarily in liver, which is used to provide oxidative substrates and circulating glucose in poor nutritional conditions. Pregnancy increases the glucose demand but its effects on tissue glycogen stores are unknown. This study examined tissue glycogen contents of non-pregnant, pregnant and lactating (L, day I postpartum) mice and of newborn pups in control and undernourished (UN) conditions. Individually housed pregnant (P, n = 44) and non-pregnant (NP, n= 14) C57B1/6J mice were fed a 23% casein diet either ad libitum (control, CT) or at 80% of control intake for 16 or 19 days or until delivery (term 20.5 days). Where possible, placenta and liver samples were collected from adults and neonates after cervical dislocation or decapitation. Glucose levels were measured in blood taken from the severed neck while tissue glycogen was determined enzymatically (1). Results are means ± SE. Statistical significance was assessed by one-way ANOVA or t-test. In CT adults, hepatic glycogen content was significantly lower at day 19 of pregnancy than at day 16 or in NP mice (Table 1). Undernutrition reduced hepatic glycogen content in NP, P and L adults (Table 1). In contrast, there was no significant difference in mean hepatic glycogen content between litters of CT (27.2 ± 5.3mg/g, n =7) and UN neonates (24.1 ± 6.2mg/g, n =6). Placental glycogen content was significantly lower in UN than CT mice at day 16 (UN 10.5 ± 0.3mg/g, n =7; CT 12.1 ± 0.4mg/g, n =6, P<0.02) but not at day 19 of pregnancy (UN 4.2 ± 0.4mg/g, n = 6; CT 4.4 ± 0.3mg/g, n = 7, P>0.05). Blood glucose levels were lower in control L than P mice and were reduced by undernutrition in NP and day 19 P mice but not in day 16 P or L mice (Table 1). Blood glucose levels were also significantly lower in UN (1.2 ± 0.1mmol/l, n = 6) than CT neonates (2.2 ± 0.1mmol/l, n = 7, P<0.01). The results show that, in controls, the increased glucose demand of late pregnancy and lactation reduces maternal hepatic glycogen content but has little effect on blood glucose levels compared to NP mice. Hepatic glycogen stores were adversely affected in all UN adults but appeared to be protected in UN neonates, despite the low glucose and hepatic glycogen levels of their mothers near term.

Where applicable, experiments conform with Society ethical requirements