Changes in rates of glucose utilization and regulation of glucose disposal by fast-twitch skeletal muscles in late pregnancy

Abstract

Glucose utilization indices (GUI) were measured in vivo in conjunction with active pyruvate dehydrogenase complex (PDH(a) and glycogen synthase (GS) activities in fast-twitch skeletal muscles [extensor digitorum longus (EDL), tibialis anterior and gastrocnemius] of late-pregnant rats and age-matched virgin control rats in the fed state, after 24 h starvation and at 2 h after re-feeding with standard laboratory chow ad libitum after 24 h starvation. As demonstrated previously [Holness and Sugden (1990) Biochem. J 277, 429-433], GUI values of fast-twitch skeletal muscles of virgin rats were low in the fed ad libitum and the 24 h-starved states, but dramatically increased after subsequent chow re-feeding. GUI values of fast-twitch skeletal muscles of late-pregnant rats were also low in the fed and starved states and were increased by re-feeding, but the increase in GUI values elicited by re-feeding was greatly attenuated. PDHa activities in EDL, tibialis anterior and gastrocnemius in the fed state were unaffected by late pregnancy, and skeletal-muscle PDHa activities were decreased after 24 h of starvation in both groups. Whereas re-feeding of virgin rats with standard diet for 2 h restored PDHa activities in fast-twitch skeletal muscles to values for rats continuously fed ad libitum, PDHa activities in fast-twitch skeletal muscles of late-pregnant rats, although increased in response to re-feeding, remained considerably less than the corresponding fed ad libitum values after 2 h of re-feeding. In contrast, neither skeletal-muscle GS re-activation nor rates of skeletal-muscle glycogen deposition after re-feeding were markedly affected by late pregnancy. The results are discussed in relation to the specific targeting of individual pathways of glucose disposal in fast-twitch skeletal muscles during re-feeding in late pregnancy.

Decreased contraction-stimulated glucose transport in isolated epitrochlearis muscles of pregnant rats

“…Accord- ingly, we assessed glycogen levels and found that pregnancy was associated with a nonsignificant trend for 13% increase in resting glycogen concentrations in epitrochlearis muscles, a result similar to the data of Holness and Sugden (17,18). Our results also indicated that pregnancy did not alter the amount of contraction-induced glycogen depletion.…”

“…Results from several studies suggest that late pregnancy may increase skeletal muscle resting glycogen concentrations (17,18,28), and previous studies have implicated precontraction glycogen concentration as a regulator of contraction-induced glycogen depletion and glucose transport (15,22,23). Accord- ingly, we assessed glycogen levels and found that pregnancy was associated with a nonsignificant trend for 13% increase in resting glycogen concentrations in epitrochlearis muscles, a result similar to the data of Holness and Sugden (17,18).…”

“…In this study, isolated epitrochlearis muscles from pregnant and nonpregnant rats were stimulated to contract by the same stimulation protocol. In addition, insulin-stimulated glucose uptake was determined for epitrochlearis muscles so that the magnitude of pregnancy effects on the two major pathways for activating muscle glucose transport could be compared in the same study.Under resting conditions, skeletal muscle glycogen concentration is similar or higher for pregnant compared with nonpregnant rats (17,18,28). However, the effect of contractile activity on glycogen depletion during pregnancy has apparently not been previously reported.…”

“…Under resting conditions, skeletal muscle glycogen concentration is similar or higher for pregnant compared with nonpregnant rats (17,18,28). However, the effect of contractile activity on glycogen depletion during pregnancy has apparently not been previously reported.…”

Re-feeding after starvation involves a temporal shift in the control site of glycogen synthesis in rat muscle

“…Also in this muscle there was a transient increase in the fractional velocity of the enzyme above basal (48 h-starved) levels between 1 and 6 h re-feeding before returning to basal levels at 8 h (Figures 1 and 2). Others have also presented evidence for the dephosphorylation of glycogen synthase during the starved-to-fed transition in rodents [2,25,26]. An important aspect of our results, however, is that, in muscles other than the white quadriceps, the increase in glycogen synthesis observed during re-feeding was not accompanied by any increase in the fractional velocity of glycogen synthase, implying that the phosphorylation state of the enzyme was unchanged.…”