Direct effects of progesterone on rat islets of Langerhans in vivo and in tissue culture

Howell, S. L.; Tyhurst, M.; Green, Irene C.

doi:10.1007/bf01236310

Cited by 41 publications

(26 citation statements)

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“…In other experiments no changes in activity of this enzyme have been detected in islets taken from progesterone injected rats, or in islets which have been cultured with progesterone, and no direct effects of steroids on adenylate cyclase activity in vitro have been found [4]. The recent reports of raised cyclic AMP levels in islets from progesterone injected rats may therefore result from other actions of the hormone [23].…”

Section: Discussionmentioning

confidence: 88%

“…The nuclear events which lead to subse-Administration of certain steroids to rats will induce hyperinsulinism and islet hypertrophy [1], and combination of progesterone and estradiol will effect changes somewhat similar to that observed in late pregancy [2][3][4][5]. It has not been possible to observe short term direct effects of progesterone and estradiol on insulin secretion in vitro from isolated islets [2,4]. However, enhanced insulin secretory responses were observed when islets were cultured in the presence of combinations of different concentrations of progesterone and estradiol for a period of 18 h [4].…”

Section: Discussionmentioning

confidence: 99%

“…It has not been possible to observe short term direct effects of progesterone and estradiol on insulin secretion in vitro from isolated islets [2,4]. However, enhanced insulin secretory responses were observed when islets were cultured in the presence of combinations of different concentrations of progesterone and estradiol for a period of 18 h [4]. The purpose of the present paper was to investigate the mode of action of progesterone in exerting these effects by examining some of the characteristics of uptake and binding of 3H-progesterone to intact islets.…”

Section: Discussionmentioning

confidence: 99%

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Binding of3H-progesterone by isolated rat islets of Langerhans

et al. 1978

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Summary.Islets of Langerhans isolated from normal female rats have been used in studies of 3H-progesterone uptake by intact islet cells. The intracellular sites which are involved in binding of the hormones have been determined by subcellular fractionation and autoradiography. Uptake of 3H-progesterone into islets occurred in a temperature and concentration dependent manner. The uptake increased rapidly in the first 30 min, and could be partially displaced by addition of excess unlabelled progesterone. 3H-progesterone uptake was lowered by incubation of the islets in the absence of Ca ++, at 0 ° compared to 37 ° C, or to a much lesser extent when islet cycilic AMP levels were raised by addition of 3-isobutyl-1-methylxanthine. However, uptake was unaffected by prior treatment of the islets with neuraminidase or phydroxymercuribenzoate. Differential centrifugation of islets which had previously been incubated with 3H-progesterone showed the highest specific activity of binding in the nuclei and debris fraction. Isolation of a purified nuclear fraction by sedimentation through sucrose solutions confirmed that binding was present in the nuclear component of this heterogeneous fraction, while autoradiographic studies suggested both nuclear and cytosolic localisation of 3H-progesterone. In a separate series of experiments, evidence was obtained for the existence of saturable cytosolic binding of progesterone, and for movement of labelled hormone from the cytosol to the nuclear fraction.It is suggested that, in the islets of Langerhans as in other target tissues, the action of progesterone involves penetration into the cells, binding to a cytosolic receptor protein, and subsequent transfer to the nucleus. The nuclear events which lead to subse-

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Binding of3H-progesterone by isolated rat islets of Langerhans

et al. 1978

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“…The mechanism(s) by which plasma insulin is elevated in pregnancy is still largely unknown. The process for development of insulin resistance in normal pregnancy is complex and is associated, at least in part, with increasing maternal serum levels of both progesterone and 17 -estradiol (Howell et al 1977) or progesterone alone (Sutter-Dub & Dazey 1979).…”

Section: Introductionmentioning

confidence: 99%

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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“…Several lines of experimental evidence lend sup port to such an assumption. Specific receptors for estro gen [27] and progesterone [9] have already been described, and a direct effect of glucocorticoids [5], estrogen [ 13], progesterone [13,14], thyroid hormones [28] and testosterone (unpublished data) have also been found. Furthermore, we can now report that the lack of three different steroid hormones, namely adrenal, female and male sexual hormones, differently and speci fically affects both insulin release and B-cell ultrastructurc.…”

Section: Discussionmentioning

confidence: 99%

Effect of the Removal of Different Endocrine Glands upon Insulin Secretion and B-Cell Ultrastructure

Dumm¹,

García²,

Borelli³

et al. 1984

Cells Tissues Organs

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Glucose-induced insulin secretion and B-cell ultrastructure were studied in islets obtained from normal, adrenalectomized, radiothyroidectomized, ovariectomized and orchidectomized rats. Both parameters were also studied in the same experimental groups submitted to specific substitutive therapy. Insulin secretion in response to high glucose was significantly diminished in adrenalectomized, hypothyroid and male castrated rats. Conversely, this secretion was enhanced in ovariectomized rats. These abnormal insulin responses were restored to normal range by specific substitutive therapy. B-cell ultrastructure was markedly altered in hypothyroid and in female and male castrated rats. No significant changes were observed in the adrenalectomized rats. No conspicuous alterations were depicted in the other islet cell populations. The features of the morphological alterations were mainly related to changes in the B-granules and the rough endoplasmic reticulum. Modifications of the other B-cell organelles were less frequent. In the castrated rats, a distinctive feature was the appearance of a finely granulated colloid material. These B-cell alterations, consecutive to changes in the circulating levels of a given hormone, seemed to depend on the chemical structure of the hormone itself rather than on the changes induced in the B-cell secretory function. The ultrastructural changes described were reversed, as in the case of insulin release, by specific substitutive therapy. It is concluded that changes in the circulating levels of the hormones studied are followed by specific alterations in both B-cell secretion and ultrastructure.

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Direct effects of progesterone on rat islets of Langerhans in vivo and in tissue culture

Cited by 41 publications

References 14 publications

Binding of3H-progesterone by isolated rat islets of Langerhans

Binding of3H-progesterone by isolated rat islets of Langerhans

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

Effect of the Removal of Different Endocrine Glands upon Insulin Secretion and B-Cell Ultrastructure

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