Effects of pregnancy on the glucose-induced insulin release from cultivated pancreatic islets of the rat

Ziegler, B; Ziegler, M.; Fiedler, H

doi:10.1007/bf01921949

Cited by 6 publications

(7 citation statements)

References 10 publications

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“…This is in agreement with a previously reported cultured islet study (24), but at variance with some other in vitro studies, using the perifused islet technique (9,20), which reported that pregnancy increased insulin release in response to a glucose stimulus of 300 mg/dl. However, the first-phase insulin response of the pregnant group exceeded that in the nonpregnant group by 70%.…”

Section: Discussionsupporting

confidence: 93%

Synthesis-Secretion Coupling of Insulin

Baaziz

Curry

1993

Pancreas

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Synthesis-secretion coupling of insulin was determined using perfused pancreata taken from either control, pregnant, or lactating female Sprague-Dawley rats. The pancreata were stimulated for 3 h with one of the two glucose concentrations used: either 150 or 300 mg/dl. In the case of pregnancy, the pancreata exhibited a twofold hypersecretory activity in response to the physiological glucose level of 150 mg/dl. Net insulinogenesis did not occur in response to the normoglycemic glucose concentration, and, as with the controls, there was an overall depletion of insulin stores. There was no insulin hypersecretion at the hyperglycemic level of 300 rng/dl, but net insulinogenesis did occur; however, it matched that of the controls. Therefore, the hypersecretion of insulin ascribed to pregnancy appears to be a function of the secretory process only, to be most demonstrable under normoglycemic conditions, and not to be due to en-hanced synthesis-secretion coupling. In the case of pancreata from lactating rats, just the converse was observed. Compared with controls, there was no substantial difference in insulin secretion by pancreata from lactating rats at either glucose level or of insulinogenesis under normoglycemia conditions. However, when glucose was at a hyperglycemic load in the lactating group, not only was there no net insulinogenesis, but this condition actually resulted in a depletion of intrzcellular insulin stores (as opposed to both the control and the pregnant groups). This suggests that the hypoinsulinemia noted during lactation may be related to a reduced capacity of those p-cells to synthesize insulin in the face of prolonged hyperglycemic stimulation.

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Section: Discussionsupporting

confidence: 93%

Synthesis-Secretion Coupling of Insulin

Baaziz

Curry

1993

Pancreas

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“…Bone Kalkhoff & Kim 1978;Ziegler et al 1978) corresponding to the increased insulin level observed in vivo in pregnant rats (Sutter-Dub et al 1973) and man (Fisher et al 1980). These observations agree with the effect of normal pregnant human serum on isolated islets in organ culture which was characterized by in¬ creased insulin release and reduced insulin con¬ tent of islets after culture (Table 1) suggesting a direct effect of humoral factors on the ß-cells.…”

Section: Discussionmentioning

confidence: 99%

Effects of pregnancy hormones on pancreatic islets in organ culture

Nielsen¹,

Nielsen²,

Pedersen

et al. 1986

Acta Endocrinologica

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Pregnancy is associated with hyperinsulinaemia and decreased glucose tolerance which may lead to gestational diabetes. Sera from pregnant women in the last trimester were found to stimulate insulin secretion of mouse pancreatic islets maintained in organ culture suggesting a direct effect of pregnancy hormones and/or metabolites on the endocrine pancreas. Previous studies have shown that progesterone and human placental lactogen (hPL) had direct effects on isolated islets and in the present study the effects of combined addition of these hormones to the cultured islets were evaluated. hPL, 1 \g=m\g/ml was found to prevent the decrease in the islet insulin content due to progesterone 100 ng/ml, and hPL induced an increase in the DNA\x=req-\ content compared with the progesterone treated islets. The effect of the hormones on the DNA synthesis was evaluated by incorporation of [3H]thymidine into newborn rat islets. Progesterone in a high concentration, 1 \g=m\g/ml, inhibited while 0.1 and 1 \g=m\g/ml hPL stimulated the [3H]thymidine incorporation. These results indicate that progesterone may contribute to the increased glucose-induced insulin release during pregnancy and hPL to the \g=b\-cellhyperplasia. Since progesterone and hPL counteracted each other with regard to both insulin content and DNA-synthesis in the islets, the direct interaction between these two hormones on the \g=b\-cel l may be of importance for the changes in glucose metabolism during pregnancy.Alterations of glucose homeostasis take place dur¬ ing normal pregnancy as expressed by hyperinsulinaemia and decreased glucose tolerance (for a review see Freinkel 1980). Sometimes transient diabetes, gestational diabetes, or persisting insu¬ lin-dependent diabetes may occur (for a review see Kühl 1977). The precipitating factors for the latter pathological development are not known although hormonal disturbances are supposed to play a role (Kühl 1977; Freinkel 1980; Hornnes 1985). The major hormonal changes known to take place during pregnancy are the early transi¬ tional increase in chorionic gonadotrophin and the later increase in oestriol, oestrone, progester¬ one, prolactin and placental lactogen (for a review see Buster & Marshall 1979). In studies of the effects of the individual hormones, progesterone and placental lactogen seem to have profound direct influence on the pancreatic islets (for a review see Nielsen 1985). Therefore the aim of the present study was to compare the effect of pregnant human sera with that of the individual hormones on insulin release, insulin content, and DNA synthesis in isolated pancreatic islets in or¬ gan culture. Materials and MethodsSerum and hormones Serum samples from 10 women in the last trimester of pregnancy-were obtained from the Outpatient Preg¬ nancy Clinic, Rigshospitalet, Copenhagen, Denmark. None were overweight or had glucosuria. The contents of progesterone and placental lactogen were measured by standard methods at Frederiksberg Hospital. Clini¬ cal-Chemical Department, Copenhagen, Denmark. For compar...

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“…Thus, we tried to achieve a pronounced B-cell growth by a physiological stimulus, namely pregnancy. It is well known that pregnancy increases insulin demand and B-cell growth with corresponding enhancement of B-cell volume, insulin biosynthesis and release [1][2][3][4][5][6]. Our STZ-treated normoglycaemic rats are responsive to pregnancy as shown by a decrease of plasma glucose and an increase of peripheral and pancreatic insulin concentrations.…”

Section: Discussionmentioning

confidence: 68%

“…The normal endocrine pancreas responds to the metabolic changes of pregnancy with an enhancement of pancreatic B-cell volume and an increase of insulin synthesis and release [1][2][3][4][5]. Furthermore, it is well known that a pre-existing disturbance of the carbohydrate metabolism is generally aggravated by pregnancy [6].…”

mentioning

confidence: 99%

Pregnancy-associated changes in the endocrine pancreas of normoglycaemic streptozotocin-treated Wistar rats

et al. 1985

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The effect of pregnancy on pancreatic insulin content and relative B-cell volume has been studied in normoglycaemic Wistar rats treated with streptozotocin 14 days before mating. A single intravenous injection of streptozotocin (30 mg/kg body weight) caused a significant reduction of pancreatic insulin content and B-cell volume. The islet insulin content was 60% of control values. However, pregnancy-associated adaptation was preserved in these streptozotocin-treated animals. Plasma insulin levels, pancreatic insulin and Bcell volume were significantly enhanced compared with non-pregnant rats investigated on the same date. The incorporation of [3H]-thymidine into islets from pregnant rats (day 10.5) was higher than that in islets isolated from non-pregnant animals. After delivery insulin content and B-cell volume returned to pre-pregnant values. Also during a longer period after streptozotocin treatment (156 days), no measurable enhancement of B-cell volume and pancreatic insulin content was observed indicating the unresponsiveness of residual B cells to compensate spontaneously for the loss despite persisting norrnoglycaemia.

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Effects of pregnancy on the glucose-induced insulin release from cultivated pancreatic islets of the rat

Abstract: 7-day-cultured islets from pregnant Wistar rats released at 5.6 mM glucose significantly more insulin than islets from nonpregnant rats, whereas in vivo this heigthened glucose sensitivity is lost 48 h post partum.

Cited by 6 publications

References 10 publications

Synthesis-Secretion Coupling of Insulin

Synthesis-Secretion Coupling of Insulin

Effects of pregnancy hormones on pancreatic islets in organ culture

Pregnancy-associated changes in the endocrine pancreas of normoglycaemic streptozotocin-treated Wistar rats

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