Prolactin treatment increases GLUT2 but not the G protein subunit content in cell membranes from cultured neonatal rat islets

Mazancourt, Philippe de; Carneiro, Everardo M.; Atwater, I; Boschero, Antônio Carlos

doi:10.1016/0014-5793(94)80305-6

Cited by 15 publications

(7 citation statements)

References 25 publications

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“…These data confirm prior observations that PRL treatment increases GLUT2 expression in pancreatic B-cells (7,8). Expression of GLUT2 was further enhanced with the combination of glucose and PRL.…”

supporting

confidence: 81%

Synergistic effect of glucose and prolactin on GLUT2 expression in cultured neonatal rat islets

Crepaldi-Alves

Carneiro²,

Bosqueiro³

et al. 1997

Braz J Med Biol Res

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We studied the synergistic effect of glucose and prolactin (PRL) on insulin secretion and GLUT2 expression in cultured neonatal rat islets. After 7 days in culture, basal insulin secretion (2.8 mM glucose) was similar in control and PRL-treated islets (1.84 ± 0.06% and 2.08 ± 0.07% of the islet insulin content, respectively). At 5.6 and 22 mM glucose, insulin secretion was significantly higher in PRL-treated than in control islets, achieving 1.38 ± 0.15% and 3.09 ± 0.21% of the islet insulin content in control and 2.43 ± 0.16% and 4.31 ± 0.24% of the islet insulin content in PRL-treated islets, respectively. The expression of the glucose transporter GLUT2 in B-cell membranes was dosedependently increased by exposure of the islet to increasing glucose concentrations. This effect was potentiated in islets cultured for 7 days in the presence of 2 µg/ml PRL. At 5.6 and 10 mM glucose, the increase in GLUT2 expression in PRL-treated islets was 75% and 150% higher than that registered in the respective control. The data presented here indicate that insulin secretion, induced by different concentrations of glucose, correlates well with the expression of the B-cell-specific glucose transporter GLUT2 in pancreatic islets. Key wordsThe first step in glucose-induced insulin secretion is the entry of the sugar into the Bcells, which is mediated by the glucose transporter GLUT2, located on the B-cell plasma membrane. Alteration in the expression of GLUT2 has been implicated in the reduction of the secretory response to glucose (1,2). Since growth and differentiation of the endocrine pancreas are controlled by glucose and the somatolactogenic hormones, growth hormone (GH) and prolactin (PRL) (3), we determined the effect of glucose on insulin secretion and GLUT2 expression in neonatal rat islets cultured in the presence or absence of PRL.We have used islets from neonatal rats (2 to 48 h old) obtained by collagenase digestion and cultured for 7 days, as described previously (4). After 7 days, the culture medium was discarded and the islets were incubated for 90 min at 37 o C in a bicarbonatebuffered solution containing different concentrations of glucose. The supernatant was withdrawn for insulin measurements and the

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supporting

confidence: 81%

Synergistic effect of glucose and prolactin on GLUT2 expression in cultured neonatal rat islets

Crepaldi-Alves

Carneiro²,

Bosqueiro³

et al. 1997

Braz J Med Biol Res

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“…Table 2 summarizes the reported actions of GH-related hormones in various types of insulin-secreting cells. In addition to their mitogenic effect [4][5][6][7][8][9][10][11], these hormones are known to stimulate insulin biosynthesis [6,9,[12][13][14], to promote oxidative metabolism of glucose [7,9], and to increase GLUT2 expression [15], thereby contributing to the functional maturation (increase in sensitivity to glucose for the stimulation of insulin secretion) of /3-cells [14][15][16]. In view of these various effects of GH-related peptides in /3-cells, to study their mode of action might reveal crucial mechanisms for the regulation of growth and the function of these cells, which are only partially understood [2,17].…”

Section: Gh and Prl As Growth/differentiationmentioning

confidence: 99%

GH Signalling in Pancreatic β-Cells

1998

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Abstract. GH and its related peptide PRL are known to stimulate proliferation and insulin biosynthesis in pancreatic fl-cells, and assumed to be involved in their functional maturation. We investigated signal transduction of GH and PRL in insulin-secreting cells using the differentiated rat insulinoma cell line, INS-1. In these cells, both hormones stimulated proliferation and DNA synthesis, increased viability, cellular metabolism and insulin content. GH induced cytosolic Ca2+ ([Ca2+];) rises, which appear to be due to Ca2+-influx through voltage-gated Ca2+-channels. GH also promoted tyrosine phosphorylation of several proteins in INS-1 cells, one of which was identified as JAK2 tyrosine kinase. Moreover, GH caused changes in DNA binding of nuclear proteins to some interferon-'y-activated sites. Verapamil inhibited neither DNA synthesis nor JAK2 phosphorylation stimulated by GH, whereas a tyrosine kinase inhibitor, lavendustin A, blocked the mitogenic effect. Involvement of cAMP is also suggested because Rp-cAMPS, a competitive inhibitor of protein kinase A, abolished both [Ca2+]; rises and DNA synthesis stimulated by GH. The effects of GH and PRL on [Ca2+];, JAK2 phosphorylation and DNA binding of the STATs were virtually identical in INS-1 cells. Since both hormones failed to activate MAP kinase in these cells, it is strongly suggested that activation of the JAK-STAT pathway is the major signalling event for the mitogenic effects of GH and PRL in /3-cells. It remains to be clarified whether the [Ca2+]; rise mediates other effects of these hormones.

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“…PRL has been reported to enhance insulin secretion (5,6,7), to decrease the glucose threshold and to increase the gapjunctional coupling among B-cells (8) receptors on these cells (9). In neonatal islets, PRL treatment also induces B-cell proliferation and increases islet volume (10,11,12,13), enhances glucose oxidation (11) and cAMP metabolism (14), increases glucokinase activity (15), stimulates 3[Hjthymidine incorporation (13), increases GLUT2 membrane content (15,16), and potentiates the ability of glucose in reducing IC permeability (5). Since the maximal effects of PRL requires a few days to occur, it has recently been suggested that PRL receptors need to be upregulated in order for this response to be observed (9).…”

Section: Introductionmentioning

confidence: 99%

Long-Term Effect of Prolactin Treatment on Glucose-Induced Insulin Secretion in Cultured Neonatal Rat Islets

Crepaldi

Carneiro²,

Boschero³

1997

Horm Metab Res

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Insulin secretion and 45Ca2+ uptake and efflux were studied in neonatal rat islets maintained in culture for 7 or 19 days in the absence or presence of prolactin (PRL). Insulin secretion in response to glucose (G), leucine (Leu), arginine (Arg) and carbachol (Cch) was augmented after 7 and 19 days in culture, compared to basal secretion (G 2.8 mM), in both PRL-treated and control islets. However, the increase in insulin secretion induced by the above secretagogues was higher in islets cultured in the presence of PRL for 19 days. In PRL-treated islets, the 45Ca2+ content after a 5 min incubation in the presence of G, Leu, Arg and Cch was significantly higher than the control only in islets cultured for 19 days. Except with Arg, the 45Ca2+ uptake in PRL-treated islets after a 90 min incubation was also significantly higher than the control only in islets cultured for 19 days. Finally, Leu-induced alterations in the 45Ca2+ efflux were higher in PRL-treated than in control islets cultured for 7 or 19 days. In the absence of external Ca2+, the reduction in 45Ca2+ efflux induced by glucose was also significantly higher in PRL-treated than in control islets. This effect was slightly potentiated after 19 days in culture. These data further support the hypothesis that PRL treatment enhances maturation of the secretory mechanism in neonatal islets. This effect can be potentiated even more if the treatment is prolonged.

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Prolactin treatment increases GLUT2 but not the G protein subunit content in cell membranes from cultured neonatal rat islets

Cited by 15 publications

References 25 publications

Synergistic effect of glucose and prolactin on GLUT2 expression in cultured neonatal rat islets

Synergistic effect of glucose and prolactin on GLUT2 expression in cultured neonatal rat islets

GH Signalling in Pancreatic β-Cells

Long-Term Effect of Prolactin Treatment on Glucose-Induced Insulin Secretion in Cultured Neonatal Rat Islets

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