Role of 17-β-estradiol and progesterone on glucose homeostasis: Effects of food restriction (50%) in pregnant and non pregnant rats

Cg, González; Fd, García; Sf, Fernández; Am, Patterson

doi:10.1007/bf03347991

Cited by 21 publications

(26 citation statements)

References 26 publications

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“…2). In spite of these levels, the profiles of both hormones in this group were similar to pregnancy, that is to say, similar plasma concentrations between days 6 and 11 and a significant increase between days 11 and 16, in agreement with previous studies in rats (Sutter-Dub et al 1978, Aerts et al 1980, González et al 1997. The level of 17 -estradiol was also higher in the E group than expected, but the profile of this hormone was also similar to pregnancy.…”

Section: Discussionsupporting

confidence: 91%

“…2. The plasma levels of progesterone in the P group were in concordance with normal pregnancy in the rat (González et al 1997). However, in the EP group these were higher than in normal pregnancy.…”

Section: Resultssupporting

confidence: 60%

“…However, in the EP group these were higher than in normal pregnancy. On the other hand, the plasma levels of 17 -estradiol were higher in the E and EP groups than in normal pregnancy in the rat (González et al 1997).…”

Section: Resultsmentioning

confidence: 77%

“…A control group (V) injected with vehicle (olive oil/ethanol 3:2, v/v) was followed in parallel. Different doses of 17 -estradiol and/or progesterone were injected (Sutter-Dub et al 1978, Aerts et al 1980 in order to simulate the plasma levels that we observed in normal pregnant rats (González et al 1997(González et al , 1998. Day 0 represents the start of hypothetic pregnancy.…”

Section: Experimental Designmentioning

confidence: 99%

“…These days were selected as changes were found in sensitivity to the action of insulin during pregnancy in the Wistar rat (González et al 1997).…”

Section: Experimental Designmentioning

confidence: 99%

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Role of 17beta-estradiol and/or progesterone on insulin sensitivity in the rat: implications during pregnancy

González¹,

Alonso²,

Álvarez³

et al. 2000

Journal of Endocrinology

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The mechanism for the development of insulin resistance in normal pregnancy is complex and is associated with serum levels of both progesterone and 17 -estradiol. However, it remains unclear whether estrogens alone or progestins alone can cause insulin resistance, or whether it is a combination of both which produces this effect. We attempted to determine the role played by progesterone and/or 17 -estradiol on the phenomena of sensitivity to insulin action that take place during pregnancy in the rat. Ovariectomized rats were treated with different doses of progesterone and/or 17 -estradiol in order to simulate the plasma levels in normal pregnant rats. A euglycemic/ hyperinsulinemic clamp was used to measure insulin sensitivity. At days 6 and 11, vehicle (V)-and progesterone (P)-treated groups were more insulin resistant than 17 -estradiol (E)-and 17 -estradiol+progesterone (EP)-treated groups. Nevertheless, at day 16, the V, EP and E groups were more resistant to insulin action than the P group. On the other hand, the V, EP and E groups were more insulin resistant at day 16 than at day 6, whereas the P group was more insulin resistant at day 6 than at day 16. Our results seem to suggest that the absence of female steroid hormones gives rise to a decreased insulin sensitivity. The rise in insulin sensitivity during early pregnancy, when the plasma concentrations of 17 -estradiol and progesterone are low, could be due to 17 -estradiol. However, during late pregnancy when the plasma concentrations of 17 -estradiol and progesterone are high, the role of 17 -estradiol could be to antagonize the effect of progesterone, diminishing insulin sensitivity.

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Section: Discussionsupporting

confidence: 91%

Section: Resultssupporting

confidence: 60%

Section: Resultsmentioning

confidence: 77%