Beneficial effects of prolactin and laminin on human pancreatic islet-cell cultures

Labriola, Letícia; Montor, Wagner Ricardo; Krogh, Karin; Lojudice, Fernando Henrique; Genzini, Tércio; Goldberg, Anna Carla; Eliaschewitz, Freddy Goldberg; Sogayar, Mari Cleide

doi:10.1016/j.mce.2006.09.011

Cited by 74 publications

(72 citation statements)

References 57 publications

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“…Beneficial effects of prolactin on b-cell physiology may also extend to the nonpregnant state. Specifically, in cell culture systems, prolactin has been shown to increase b-cell proliferation, inhibit key caspases of the extrinsic and intrinsic pathways that lead to islet apoptosis, and promote b-cell survival (27)(28)(29). Moreover, prolactin supplementation of pretransplant culture media can improve b-cell survival in human islet preparations (30).…”

Section: Discussionmentioning

confidence: 99%

Maternal Serum Prolactin and Prediction of Postpartum β-Cell Function and Risk of Prediabetes/Diabetes

Retnakaran

Kramer

et al. 2016

Diabetes Care

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OBJECTIVEThe insulin resistance of mid-to late pregnancy poses a physiologic stress test for the pancreatic b-cells, which must respond by markedly increasing their secretion of insulin. This response is achieved through an expansion of b-cell mass induced by the hormones prolactin and human placental lactogen (HPL). Conversely, the furan fatty acid metabolite 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) has recently emerged as a negative regulator of b-cell function in pregnancy. Given their respective roles in the b-cell response to the stress test of gestation, we hypothesized that antepartum prolactin, HPL, and CMPF may relate to a woman's underlying glucoregulatory physiology and hence to her metabolic status after pregnancy. RESEARCH DESIGN AND METHODSThree hundred and sixty-seven women underwent measurement of fasting serum prolactin, HPL, and CMPF in the late-2nd/early-3rd trimester, followed by an oral glucose tolerance test (OGTT) at 3 months postpartum that enabled assessment of glucose tolerance, insulin sensitivity/resistance, and b-cell function (Insulin Secretion-Sensitivity Index-2 [ISSI-2]). RESULTSThe postpartum OGTT identified 301 women with normal glucose tolerance (NGT) and 66 with prediabetes or diabetes. Serum prolactin in pregnancy was higher in women with postpartum NGT compared with those with postpartum prediabetes/ diabetes (mean 98.2 vs. 80.2 ng/mL, P = 0.0003), whereas HPL and CMPF did not differ between the groups. On multiple linear regression analyses, antepartum prolactin was an independent determinant of postpartum ISSI-2 (b = 0.0016, t = 2.96, P = 0.003). Furthermore, higher serum prolactin in pregnancy independently predicted a lower risk of postpartum prediabetes/diabetes (odds ratio 0.50, 95% CI 0.35-0.72, P = 0.0002). CONCLUSIONSSerum prolactin in pregnancy predicts postpartum b-cell function and risk of prediabetes/diabetes.

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Section: Discussionmentioning

confidence: 99%

Maternal Serum Prolactin and Prediction of Postpartum β-Cell Function and Risk of Prediabetes/Diabetes

Retnakaran

Kramer

et al. 2016

Diabetes Care

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“…Likewise, there are indications that beta cells do not form their own basement membrane, but rely on endothelial cells to form a vascular basement membrane containing LMs next to the beta cell [14]. LM-111 has been demonstrated to promote differentiation of pancreatic precursor cells into beta cells in vitro [24] and to promote glucose-stimulated insulin secretion in vitro [15,25,26]. Prostaglandins exert a number of effects on islet beta cells, although mostly negative [27,28].…”

Section: Discussionmentioning

confidence: 99%

“…Conversion of total RNA to cDNA was performed with reverse transcription system (Promega, Madison, WI, USA) using oligo (dT) 15 primers. The LightCycler System (Hoffman-La Roche), and detection with SYBR Green (SYBR Green JumpStart Taq ReadyMix), was used to amplify and analyse generated cDNA.…”

Section: Isolation Of Islet Endothelial Cellsmentioning

confidence: 99%

“…Indeed, the high islet vascular density and the vascular phenotype, with a great number of fenestrations, is induced and maintained by secretion of vascular endothelial growth factor from the beta cells [9][10][11]. Recently, we and others have shown that endothelial cells signal back and contribute to maintenance [12], and during certain conditions even expansion, of the adult beta cell mass [6,[13][14][15]. In the present study, we tested the hypothesis that islet endothelial cell products may directly influence beta cell function.…”

Section: Introductionmentioning

confidence: 99%

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Endothelial cell signalling supports pancreatic beta cell function in the rat

et al. 2009

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Aims/hypothesis The proximity of endothelial cells and beta cells in islets by necessity means that they are exposed to each other's products. Whereas islet endothelial cells require signals from beta cells to function properly, endothelin-1, thrombospondin-1 and laminins, among others, have been identified as endothelial-derived molecules, although their full effects on beta cells have not been explored. We tested the hypothesis that islet endothelialderived products affect beta cell function. Methods Endothelial cells from rat islets were proliferated and purified. Endothelium-conditioned culture medium (ECCM) was obtained by maintaining the endothelial cells in culture medium. Islet function was evaluated following exposure of cultured islets to standard culture medium or ECCM. Changes in mRNA levels for key beta cell metabolic enzymes were also measured in islets after ECCM exposure.Results Glucose-stimulated insulin release and islet insulin content were markedly enhanced by exposure to ECCM. This was at least partly explained by improved mitochondrial function, as assessed by glucose oxidation and an upregulation of the mitochondrial gene for glycerol-3-phosphate dehydrogenase (mGpdh [also known as Gpd2]), combined with upregulation of the rate-limiting enzyme in the glycolysis, glucokinase, in the islets. The intracellular degradation of insulin was also decreased in the islets. Islet endothelial cells produced laminins, and the positive effects of islet endothelial cells were prevented by addition of a neutralising antibody to the β1-chain of laminin. Addition of exogenous laminin stimulated islet function. Conclusions/interpretation This study provides proof of principle that endothelial cells can affect the function of beta cells in their vicinity and that this is at least partially mediated by laminins.

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“…A number of hormones such as insulin, glucagon, cortisol, epinephrine, leptin, adiponectin, GH and prolactin, which are involved in energy metabolism, are included in so-called "energy" axis by some authors [3,11,13,15,27,31]. A hormone inhibin was studied relatively later and it has been revealed that the hormone is glycoprotein consisting of alfa and beta dimers, which is produced in ovarian granulose cells in females and testicle Sertoli cells in males, its synthesis is stimulated with the increase of FSH in the blood and the hormone inhibits FSH release from pituitary gland [10,25,28 Production and secretion of prolactin is elevated during pregnancy, and this hormone has been recognized as a potent growth factor for pancreatic beta-cells [2,18]. Prolactin metabolism appears to differ between species.…”

Section: Introductionmentioning

confidence: 99%

Interrelationship of some hormonesbelonging to HPG and energy axes inhorses during various reproductive states

Batsaikhan¹,

Bayar-Enkh²,

Tuvshin³

2015

Mong. J. Agric. Sci.

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Beneficial effects of prolactin and laminin on human pancreatic islet-cell cultures

Cited by 74 publications

References 57 publications

Maternal Serum Prolactin and Prediction of Postpartum β-Cell Function and Risk of Prediabetes/Diabetes

Maternal Serum Prolactin and Prediction of Postpartum β-Cell Function and Risk of Prediabetes/Diabetes

Endothelial cell signalling supports pancreatic beta cell function in the rat

Interrelationship of some hormonesbelonging to HPG and energy axes inhorses during various reproductive states

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