COMPARISON OF OESTROGEN-INDUCED GLYCOGENESIS IN THE UTERUS OF THE RAT, RABBIT AND SHEEP

1967 ◽  
Vol 54 (3) ◽  
pp. 505-513 ◽  
Author(s):  
Joel Bitman ◽  
Helene C. Cecil ◽  
Joan R. Wood ◽  
T. Randall Wrenn

ABSTRACT Essentially similar 2- to 3-fold increases in glycogen concentration were observed in uteri of rats, rabbits and sheep in the first six to ten hours after administration of 17β-oestradiol. Rats and rabbits were treated with alloxan to assess the effect of high circulating levels of glucose upon uterine glycogen and upon uterine glucose shifts. Uterine glycogen was elevated to a level almost as high as that achieved under oestrogen stimulation. Oestrogen administration caused a further increase in glycogen concentration. Free uterine glucose was measured in each species to see whether an increase in glucose availability occurred. The relative expansion in glucose space was compared to chloride space (used as an index of extracellular volume) to determine if there was an influx of glucose into the uterine cell. In the rat uterus and in the sheep endometrium, increases in free uterine glucose were observed, but the rabbit uterus and sheep myometrium synthesized glycogen without showing an increase in free glucose in the tissue.

1962 ◽  
Vol 25 (1) ◽  
pp. 69-76 ◽  
Author(s):  
H. C. CECIL ◽  
J. BITMAN ◽  
M. R. CONNOLLY ◽  
T. R. WRENN

SUMMARY Glycogen was investigated in uteri of intact and progesterone-treated spayed rats with and without deciduomata. Samples of whole uterus, endometrium and myometrium were analysed. With development of deciduoma in intact animals the glycogen concentration of whole uterus increased from 68 to 125 mg./100 g. wet weight. There was no change in the myometrial glycogen concentration; i.e. 74 mg./100 g. without deciduoma and 73 mg./100 g. wet weight in the decidual myometrium. The endometrial glycogen content of decidual tissue was 221 mg./100 g. wet weight. Since myometrial glycogen was constant, the increases observed in the decidual tissue of whole uteri must be due to an increase in the amount of endometrium and/or an increase in the concentration of glycogen in the endometrium. As the deciduoma developed the proportion of endometrium increased from 9% in the uninjured horn to 34% in the injured horn. Thus, an increase in the amount of endometrium contributes to the increase in the glycogen concentration. Similar changes were observed in whole uterus, myometrium and endometrium of the spayed animals treated with progesterone. Previous work on uterine glycogen in rats indicated that oestrogens cause glycogen deposition and this occurs only in the myometrium, while progesterone exhibits no effect. The present results demonstrate that progesterone is responsible for the glycogen increase by stimulating the growth of endometrium—a glycogen-rich tissue. Since no endometrial tissue could be obtained from horns without decidual development, this study could not determine whether progesterone had any effect on glycogen deposition.


1967 ◽  
Vol 38 (1) ◽  
pp. 33-37 ◽  
Author(s):  
W. J. BO ◽  
L. E. MARASPIN ◽  
MAVIS S. SMITH

SUMMARY Glycogen synthetase, phosphorylase and glycogen were determined biochemically in the smooth muscle of the rat uterus following a single s.c. injection (10 μg.) of oestradiol dipropionate. The ovariectomized animals were killed 6, 12, 24, 48, 72 and 96 hr. after the hormone treatment. From 12 to 96 hr. glycogen synthetase activity was significantly greater than in the untreated control rats. Phosphorylase activity was significantly less than in the controls at 12 hr. and greater from 48 to 96 hr. After the initial drop, control phosphorylase values were obtained between 24 and 48 hr. From 12 to 96 hr. the glycogen concentration was greater than in the control animals. The results show that oestrogen increased glycogen synthetase activity in the smooth muscle of the uterus soon after the hormone treatment, and with the increase in enzymic activity the glycogen concentration was also increased. They indicate that, during the early phase of glycogen synthesis, oestrogen stimulates glycogenesis by increasing glycogen synthetase activity and suppresses glycogenolysis by inhibiting phosphorylase activity. The glycogen concentration at later stages did not alter significantly, and this may have been due to the build-up and breakdown of the carbohydrate by the action of glycogen synthetase and phosphorylase, respectively.


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