Binding of3H-progesterone by isolated rat islets of Langerhans

Green, I. C.; Howell, S. L.; Seifi, S. El; Perrin, David

doi:10.1007/bf03161001

Cited by 28 publications

(13 citation statements)

References 19 publications

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“…Sorenson et al demonstrated that progesterone counterregulates the effects of rat PRL on insulin secretion and B-cell proliferation of rat islets in a homologous in vitro system (22). The pancreatic B-cells in female rats are known to possess progesterone receptor (23,24). In the present study, the values of plasma progesterone remained relatively high during prolonged pregnancy and on day 19 of normal pregnancy.…”

Section: Discussionsupporting

confidence: 53%

Adaptation of pancreatic islet B-cells during the last third of pregnancy: regulation of B-cell function and proliferation by lactogenic hormones in rats

Kawai

Kishi²

1999

European Journal of Endocrinology

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In rodents, placental lactogen (PL)-I is considered to be the first trigger to enhance pancreatic islet B-cell function, and after its secretion is diminished at mid-pregnancy, PL-II takes over this role. However, little information is available on the regulation of islet B-cell function and proliferation by lactogenic hormones during the last third of pregnancy. This was the focus of the present study using rats in which pregnancy was forcibly prolonged. This rat possesses unique characteristics in that PL-I is re-secreted during the prolonged period of pregnancy and the peak concentrations in maternal circulation are comparable with those observed during mid-pregnancy in normal-pregnancy rats. Pregnancy was prolonged by successive administration of pregnant mare's serum gonadotropin (30 IU/rat, s.c. on day 12) and human chorionic gonadotropin (10 IU/rat, i.v. on day 14). When the insulin secretory responses to 10 mmol/l glucose in islets obtained from normal-pregnancy and prolonged-pregnancy rats were tested, each insulin secretory response correlated well with the values of plasma lactogenic activity throughout the period of pregnancy and lactation. Examination of B-cell proliferation in normal-pregnancy rats showed that 5-bromo-2 0 -deoxyuridine (BrdU) incorporation into dividing B-cells reached a maximum on day 15 and then decreased markedly towards term. No increase in B-cell proliferation was observed on day 19 when plasma lactogenic activity reached the maximum. In prolonged-pregnancy rats, BrdU incorporation also continued to decrease as observed in normal-pregnancy rats after day 15, and then no enhancement in B-cell proliferation was observed even when the plasma lactogenic activity, including re-secreted PL-I, reached maximum. These results suggest that, in the last third of pregnancy, B-cell proliferation is no longer stimulated by lactogenic hormones in contrast to the insulin secretory response which is sustained.

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Section: Discussionsupporting

confidence: 53%

Adaptation of pancreatic islet B-cells during the last third of pregnancy: regulation of B-cell function and proliferation by lactogenic hormones in rats

Kawai

Kishi²

1999

European Journal of Endocrinology

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“…Progesterone treatment stimulated islet-cell proliferation in both intact male and female rats, although only female rats possess significant amounts of pancreatic progesterone receptors (2)(3)(4). Moreover, the effect of progesterone on islet-cell proliferation was absent in TX male and OVX female rats, suggesting that the gonads play an essential role in the genesis of the proliferative effect of progesterone.…”

Section: Discussionmentioning

confidence: 98%

“…In extra-islet pancreatic tissue of intact female rats, progesterone treatment Figure 4 shows a pancreatic section of an intact female rat, not treated with progesterone, doublestained for insulin and cytokeratin 20. In intact female rats not treated with progesterone, the incidence of cytokeratin 20/insulin double-immunoreactive cells in pancreatic tissue was 0.18Ϯ0.06 cells/mm 2 . In progesterone-treated female rats, this incidence was 0.31Ϯ0.10 cells/mm 2 (NS).…”

Section: Identification Of Proliferating Cellsmentioning

confidence: 92%

“…A direct effect of progesterone on the islets of Langerhans may be possible in intact female rats, as both the pancreatic a and b cells of these animals possess progesterone receptors (2,3). Yet, a direct effect of progesterone on islet-cell proliferation is less likely in ovariectomized (OVX) rats, as ovariectomy causes loss of the progesterone receptors within the pancreatic islets; this loss can be prevented by oestradiol (E2) substitution (3).…”

Section: Introductionmentioning

confidence: 99%

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Progesterone stimulates pancreatic cell proliferation in vivo

Nieuwenhuizen

Schuiling²,

Liem³

et al. 1999

European Journal of Endocrinology

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Treatment of cyclic and pregnant rats with progesterone stimulates cell proliferation within the islets of Langerhans. It was investigated whether this effect of progesterone depends on sex and/or the presence of the gonads or the presence of oestradiol. For this purpose, Silastic tubes containing progesterone were inserted s.c. in intact and gonadectomized male and female rats, and in gonadectomized female rats treated with oestradiol. After 6 days of progesterone treatment, rats were infused for 24 h with 5-bromo-2 0 -deoxyuridine (BrdU) and dividing cells were identified in pancreatic sections by immunostaining for BrdU. Progesterone treatment increased islet-cell proliferation in intact male and female rats (P<0.05), but not in gonadectomized male and female rats or in gonadectomized female rats supplemented with oestradiol. Furthermore, in intact male and female rats, progesterone treatment also stimulated cell proliferation in extra-islet pancreatic tissue (P<0.05). Identification of the proliferating cells, by double-immunocytochemistry, revealed that progesterone treatment stimulated proliferation of both a and b cells within the pancreatic islets. In extra-islet pancreatic tissue, progesterone treatment stimulated proliferation in both duct (cytokeratin 20-immunoreactive) and non-duct cells. Progesterone treatment did not increase the number of single glucagon or insulincontaining cells outside the pancreatic islets, nor that of cytokeratin 20/insulin double-positive cells, suggesting that progesterone treatment did not stimulate differentiation of duct cells into endocrine cells. Progesterone treatment did not affect insulin responses to an i.v. glucose load (0.5 g/kg body weight). It is concluded that progesterone stimulates pancreatic cell proliferation indirectly; gonadal factor(s), not identical to oestradiol, is (are) probably involved.

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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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Binding of3H-progesterone by isolated rat islets of Langerhans

Cited by 28 publications

References 19 publications

Adaptation of pancreatic islet B-cells during the last third of pregnancy: regulation of B-cell function and proliferation by lactogenic hormones in rats

Adaptation of pancreatic islet B-cells during the last third of pregnancy: regulation of B-cell function and proliferation by lactogenic hormones in rats

Progesterone stimulates pancreatic cell proliferation in vivo

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

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