Artykuły w czasopismach: „Neuroendocrine signalling”

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Rogoza, Olesja, Kaspars Megnis, Marija Kudrjavceva, Aija Gerina-Berzina i Vita Rovite. "Role of Somatostatin Signalling in Neuroendocrine Tumours". International Journal of Molecular Sciences 23, nr 3 (27.01.2022): 1447. http://dx.doi.org/10.3390/ijms23031447.

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Somatostatin (SST) is a small peptide that exerts inhibitory effects on a wide range of neuroendocrine cells. Due to the fact that somatostatin regulates cell growth and hormone secretion, somatostatin receptors (SSTRs) have become valuable targets for the treatment of different types of neuroendocrine tumours (NETs). NETs are a heterogeneous group of tumours that can develop in various parts of the body, including the digestive system, lungs, and pituitary. NETs are usually slow growing, but they are often diagnosed in advanced stages and can display aggressive behaviour. The mortality rate of NETs is not outstandingly increased compared to other malignant tumours, even in the metastatic setting. One of the intrinsic properties of NETs is the expression of SSTRs that serve as drug targets for SST analogues (SSAs), which can delay tumour progression and downregulate hormone overproduction. Additionally, in many NETs, it has been demonstrated that the SSTR expression level provides a prognostic value in predicting a therapeutic response. Furthermore, higher a SSTR expression correlates with a better survival rate in NET patients. In recent studies, other epigenetic regulators affecting SST signalling or SSA–mTOR inhibitor combination therapy in NETs have been considered as novel strategies for tumour control. In conclusion, SST signalling is a relevant regulator of NET functionality. Alongside classical SSA treatment regimens, future advanced therapies and treatment modalities are expected to improve the disease outcomes and overall health of NET patients.

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Withers, D. J. "Insulin receptor substrate proteins and neuroendocrine function". Biochemical Society Transactions 29, nr 4 (1.08.2001): 525–29. http://dx.doi.org/10.1042/bst0290525.

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A family of insulin receptor substrate (IRS) proteins mediates the pleiotropic effects of insulin and insulin-like growth factor 1 (IGF-1) on cellular function by recruiting several intracellular signalling networks. Conventional murine knockout strategies have started to reveal distinct physiological roles for the IRS proteins. Deletion of Irsl produces a mild metabolic phenotype with compensated insulin resistance but also causes marked growth retardation. In contrast, mice lacking IRS-2 display nearly normal growth but develop diabetes owing to a combination of peripheral insulin resistance and β-cell failure. As well as the classical metabolic events regulated by insulin signalling pathways, studies in lower organisms have implicated insulin/IGF-1 signalling pathways in the control of food intake and reproductive function. Our analysis of IRS-2 knockout mice shows that female mice are infertile owing to defects in the hypothalamus, pituitary and gonad. IRS-2−1 mice have small, anovulatory ovaries with reduced numbers of follicles. Levels of the pituitary hormones luteinizing hormone and prolactin and gonadal steroids are low in these animals. Pituitaries of IRS-2−1 animals are decreased in size and contain reduced numbers of gonadotrophs. Additionally, IRS-2−1 females display increased food intake and develop obesity, despite elevated leptin levels, suggesting abnormalities in hypothalamic function. Coupled with recent observations that brain-specific deletion of the insulin receptor causes a similar phenotype, these findings implicate IRS signalling pathways in the neuroendocrine regulation of reproduction and energy homeostasis.

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Harada, Kenichi, Yasunori Sato, Hiroko Ikeda, Maylee Hsu, Saya Igarashi i Yasuni Nakanuma. "Notch1-Hes1 signalling axis in the tumourigenesis of biliary neuroendocrine tumours". Journal of Clinical Pathology 66, nr 5 (19.02.2013): 386–91. http://dx.doi.org/10.1136/jclinpath-2012-201273.

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AimsBiliary neuroendocrine tumours (NETs) are rare and mostly exist as a component of mixed adenoneuroendocrine carcinomas (MANECs). Although the NET component in biliary MANECs is generally more malignant and clinically more important to the prognosis than the ordinary adenocarcinomatous component, the histogenesis of biliary NET has not been clarified. In this study, the role of the Notch1-Hes1 signalling axis in the histogenesis of biliary NETs was examined.MethodsImmunohistochemistry for Notch1, its ligand Jagged1 and Hes1 was performed using surgical specimens from 11 patients with biliary MANEC. Moreover, after the knock-down of Notch1 mRNA expression in a cholangiocarcinoma cell line, the expression of chromogranin A (a neuroendocrine marker) and Ascl1 (a neuroendocrine-inducing molecule inhibited by activated Hes1) was examined by quantitative PCR.ResultsHistological examination revealed that the adenocarcinomatous components were predominately located at the luminal surface of the MANEC and the majority of stromal invasion involved NET components. Ordinary adenocarcinomas and non-neoplastic biliary epithelium constantly expressed Notch1, Jagged1 and Hes1, but the expression of Notch1 and Hes1 was decreased or absent in NET components, suggesting interference with the Notch1-Hes1 signalling axis in biliary NET. Moreover, in the cholangiocarcinoma cell line in which the expression of Notch1 mRNA was knocked down, the mRNA expression of Ascl1 and chromogranin A was increased.ConclusionsThe Notch1-Hes1 signalling axis suppresses neuroendocrine differentiation and maintains tubular/acinar features in adenocarcinoma and non-neoplastic epithelium in the biliary tree. Moreover, a disruption of this signalling axis may be associated with the tumourigenesis of NETs in biliary MANEC.

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Igaz, Péter. "Genetics of neuroendocrine tumours, hereditary tumour syndromes". Orvosi Hetilap 154, nr 39 (wrzesień 2013): 1541–48. http://dx.doi.org/10.1556/oh.2013.29706.

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Neuroendocrine tumours occur in some hereditary tumour syndromes, and the molecular pathophysiological mechanisms involved in these are also important in their sporadic counterparts which representing the majority of neuroendocrine tumours. These syndromes include multiple endocrine neoplasia type 1, von Hippel–Lindau syndrome, neurofibromatosis type 1 and tuberous sclerosis. All these follow an autosomal dominant inheritance. The primarily affected molecular pathways are Ras-MAPK signalling, hypoxia induced factor 1α, and mTOR signalling that are also involved in sporadic tumours and may even represent potential molecular targets of therapy. In this review, the major characteristics of hereditary tumour syndromes, their molecular genetics and the pathophysiological mechanisms involved in sporadic tumours are discussed. Orv. Hetil., 2013, 154, 1541–1548.

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Webber, Jonathan, i Ian A. Macdonald. "Signalling in body-weight homeostasis: neuroendocrine efferent signals". Proceedings of the Nutrition Society 59, nr 3 (sierpień 2000): 397–404. http://dx.doi.org/10.1017/s0029665100000446.

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Whilst a number of neuroendocrine afferent signals are implicated in body-weight homeostasis, the major efferent pathway is the sympathetic nervous system (SNS), which affects both energy expenditure and substrate utilization. Thyroid hormones and their interactions with the SNS may also have a role to play. Some of the variability in resting energy expenditure can be explained by differences in SNS activity, and β-blockade can reduce energy expenditure and diet-induced thermogenesis in Caucasians. Excess energy intake leads to SNS activation and increased diet-induced thermogenesis. A relationship has also been demonstrated between spontaneous physical activity and SNS activity. In many animal models the SNS activates brown adipose tissue thermogenesis, hence increasing diet-induced thermogenesis and dissipating excess energy as heat. This effect is mediated via β3-adrenoceptors and activation of an uncoupling protein unique to brown adipose tissue. Homologous proteins have been identified in human tissues and may play a role in human energy expenditure. How the SNS is implicated in this process is unclear at present. β3-Adrenoceptor polymorphism has been associated both with lower resting energy expenditure in some populations and with reduced autonomic nervous system activity. SNS effects on substrate cycling may also play a role. In the development of obesity the effects of the SNS in promoting lipolysis and fat oxidation are likely to be at least as important as its effects on thermogenesis. β-Blockade has relatively small effects on energy expenditure, but more pronounced effects on reducing lipid oxidation, so tending to favour fat storage and weight gain. Low lipid oxidation is a risk factor for weight gain, and there is some evidence that low basal sympathetic nerve activity in muscle is associated with this process. Overall, the relationship between SNS activity and obesity is complex, with evidence of low SNS activity occurring in some, but not all, studies.

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Toescu, Emil C., i Govindan Dayanithi. "Neuroendocrine signalling: Natural variations on a Ca2+ theme". Cell Calcium 51, nr 3-4 (marzec 2012): 207–11. http://dx.doi.org/10.1016/j.ceca.2012.01.010.

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Beyer, Anna-Sophia Liselott, Daniel Kaemmerer, Jörg Sänger i Amelie Lupp. "Co-Expression of Adaptor Protein FAM159B with Different Markers for Neuroendocrine Cells: An Immunocytochemical and Immunohistochemical Study". International Journal of Molecular Sciences 23, nr 21 (4.11.2022): 13503. http://dx.doi.org/10.3390/ijms232113503.

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Little is known about the adaptor protein FAM159B. Recently, FAM159B was shown to be particularly expressed in neuroendocrine cells and tissues, such as pancreatic islets and neuroendocrine cells of the bronchopulmonary and gastrointestinal tracts, as well as in different types of neuroendocrine tumours. To gain insights into possible interactions of FAM159B with other proteins and/or receptors, we analysed the co-expression of FAM159B and various neuroendocrine-specific markers in the cancer cell lines BON-1, PC-3, NCI-h82, OH-1, and A431 and also in human pancreatic tissues and pancreatic neuroendocrine tumours. The markers included prominent markers of neuroendocrine differentiation, such as chromogranin A (CgA), neuron-specific enolase (NSE), synaptophysin (SYP), insulinoma-associated protein 1 (INSM1), neural cell adhesion molecule 1 (NCAM1), serotonin (5-HT), somatostatin-14/28 (SST), and several receptors that are typically expressed by neuroendocrine cells, such as dopamine receptor 2 (D2R), somatostatin receptor (SSTR) 1, 2, 3, 4 and 5, and regulator of G-protein signalling 9 (RGS9). FAM159B was expressed evenly throughout the cytosol in all five cancer cell lines. Immunocytochemical and immunohistochemical analyses revealed co-expression of FAM159B with SYP, INSM1, RGS9, D2R, SSTR2, SSTR3, SSTR4, and SSTR5 and strong overlapping co-localisation with NSE. Double-labelling and co-immunoprecipitation Western blot analyses confirmed a direct association between FAM159B and NSE. These results suggest the involvement of FAM159B in several intracellular signalling pathways and a direct or indirect influence on diverse membrane proteins and receptors.

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Aschbacher, Kirstin, Maria Rodriguez-Fernandez, Herman van Wietmarschen, A. Janet Tomiyama, Shamini Jain, Elissa Epel, Francis J. Doyle i Jan van der Greef. "The hypothalamic–pituitary–adrenal–leptin axis and metabolic health: a systems approach to resilience, robustness and control". Interface Focus 4, nr 5 (6.10.2014): 20140020. http://dx.doi.org/10.1098/rsfs.2014.0020.

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Glucocorticoids contribute to obesity and metabolic syndrome; however, the mechanisms are unclear, and prognostic measures are unavailable. A systems level understanding of the hypothalamic–pituitary–adrenal (HPA)–leptin axis may reveal novel insights. Eighteen obese premenopausal women provided blood samples every 10 min over 24 h, which were assayed for cortisol, adrenocorticotropin releasing hormone (ACTH) and leptin. A published personalized HPA systems model was extended to incorporate leptin, yielding three parameters: (i) cortisol inhibitory feedback signalling, (ii) ACTH–adrenal signalling, and (iii) leptin–cortisol antagonism. We investigated associations between these parameters and metabolic risk profiles: fat and lean body mass (LBM; using dual-energy X-ray absorptiometry), and insulin resistance. Decreased cortisol inhibitory feedback signalling was significantly associated with greater fat (kg; p = 0.01) and insulin resistance ( p = 0.03) but not LBM. Leptin significantly antagonized cortisol dynamics in eight women, who exhibited significantly lower 24 h mean leptin levels, LBM and higher ACTH–adrenal signalling nocturnally (all p < 0.05), compared with women without antagonism. Traditional neuroendocrine measures did not predict metabolic health, whereas a dynamic systems approach revealed that lower central inhibitory cortisol feedback signalling was significantly associated with greater metabolic risk. While exploratory, leptin–cortisol antagonism may reflect a ‘neuroendocrine starvation’ response.

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Gérard, Corinne, Marie Lagarde, Flora Poizat, Sandrine Oziel-Taieb, Vincent Garcia, Catherine Roche, Patricia Niccoli, Anne Barlier i David Romano. "Kinome rewiring during acquired drug resistance in neuroendocrine neoplasms". Endocrine-Related Cancer 28, nr 1 (styczeń 2021): 39–51. http://dx.doi.org/10.1530/erc-19-0142.

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Although there is evidence of a significant rise of neuroendocrine neoplasms (NENs) incidence, current treatments are largely insufficient due to somewhat poor knowledge of these tumours. Despite showing differentiated features, NENs exhibit therapeutic resistance to most common treatments, similar to other cancers in many instances. Molecular mechanisms responsible for this resistance phenomenon are badly understood. We aimed at identifying signalling partners responsible of acquired resistance to treatments in order to develop novel therapeutic strategies. We engineered QGP-1 cells resistant to current leading treatments, the chemotherapeutic agent oxaliplatin and the mTor inhibitor everolimus. Cells were chronically exposed to the drugs and assessed for acquired resistance by viability assay. We used microarray-based kinomics to obtain highthroughput kinase activity profiles from drug sensitive vs resistant cells and identified ‘hit’ kinases hyperactivated in drug-resistant cells, including kinases from FGFR family, cyclin-dependant kinases and PKCs in oxaliplatin-resistant (R-Ox) QGP-1 cells. We then validated these ‘hit’ kinases and observed that ERK signalling is specifically enhanced in QGP-1 R-Ox cells. Finally, we assessed drug-resistant cells sensitivity to pharmacological inhibition of ‘hit’ kinases or their signalling partners. We found that FGFR inhibition markedly decreased ERK signalling and cell viability in QGP-1 R-Ox cells. These results suggest that the FGFR/ERK axis is hyperactivated in response to oxaliplatin-based chemotherapeutic strategy. Thus, this sensitive approach, based on the study of kinome activity, allows identifying potential candidates involved in drug resistance in NENs and may be used to broadly investigate markers of NENs therapeutic response.

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Hrabovszky, E., i Z. Liposits. "Novel Aspects of Glutamatergic Signalling in the Neuroendocrine System". Journal of Neuroendocrinology 20, nr 6 (czerwiec 2008): 743–51. http://dx.doi.org/10.1111/j.1365-2826.2008.01719.x.

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Davis, Tasha R., Mariah R. Pierce, Sadie X. Novak i James L. Hougland. "Ghrelin octanoylation by ghrelin O -acyltransferase: protein acylation impacting metabolic and neuroendocrine signalling". Open Biology 11, nr 7 (lipiec 2021): 210080. http://dx.doi.org/10.1098/rsob.210080.

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The acylated peptide hormone ghrelin impacts a wide range of physiological processes but is most well known for controlling hunger and metabolic regulation. Ghrelin requires a unique posttranslational modification, serine octanoylation, to bind and activate signalling through its cognate GHS-R1a receptor. Ghrelin acylation is catalysed by ghrelin O -acyltransferase (GOAT), a member of the membrane-bound O -acyltransferase (MBOAT) enzyme family. The ghrelin/GOAT/GHS-R1a system is defined by multiple unique aspects within both protein biochemistry and endocrinology. Ghrelin serves as the only substrate for GOAT within the human proteome and, among the multiple hormones involved in energy homeostasis and metabolism such as insulin and leptin, acts as the only known hormone in circulation that directly stimulates appetite and hunger signalling. Advances in GOAT enzymology, structural modelling and inhibitor development have revolutionized our understanding of this enzyme and offered new tools for investigating ghrelin signalling at the molecular and organismal levels. In this review, we briefly summarize the current state of knowledge regarding ghrelin signalling and ghrelin/GOAT enzymology, discuss the GOAT structural model in the context of recently reported MBOAT enzyme superfamily member structures, and highlight the growing complement of GOAT inhibitors that offer options for both ghrelin signalling studies and therapeutic applications.

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Rico, Karen, Suzann Duan, Ritu L. Pandey, Yuliang Chen, Jayati T. Chakrabarti, Julie Starr, Yana Zavros i in. "Genome analysis identifies differences in the transcriptional targets of duodenal versus pancreatic neuroendocrine tumours". BMJ Open Gastroenterology 8, nr 1 (listopad 2021): e000765. http://dx.doi.org/10.1136/bmjgast-2021-000765.

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ObjectiveGastroenteropancreatic neuroendocrine tumours (GEP-NETs) encompass a diverse group of neoplasms that vary in their secretory products and in their location within the gastrointestinal tract. Their prevalence in the USA is increasing among all adult age groups.AimTo identify the possible derivation of GEP-NETs using genome-wide analyses to distinguish small intestinal neuroendocrine tumours, specifically duodenal gastrinomas (DGASTs), from pancreatic neuroendocrine tumours.DesignWhole exome sequencing and RNA-sequencing were performed on surgically resected GEP-NETs (discovery cohort). RNA transcript profiles available in the Gene Expression Omnibus were analysed using R integrated software (validation cohort). Digital spatial profiling (DSP) was used to analyse paraffin-embedded GEP-NETs. Human duodenal organoids were treated with 5 or 10 ng/mL of tumor necrosis factor alpha (TNFα) prior to qPCR and western blot analysis of neuroendocrine cell specification genes.ResultsBoth the discovery and validation cohorts of small intestinal neuroendocrine tumours induced expression of mesenchymal and calcium signalling pathways coincident with a decrease in intestine-specific genes. In particular, calcium-related, smooth muscle and cytoskeletal genes increased in DGASTs, but did not correlate with MEN1 mutation status. Interleukin 17 (IL-17) and tumor necrosis factor alpha (TNFα) signalling pathways were elevated in the DGAST RNA-sequencing. However, DSP analysis confirmed a paucity of immune cells in DGASTs compared with the adjacent tumour-associated Brunner’s glands. Immunofluorescent analysis showed production of these proinflammatory cytokines and phosphorylated signal transducer and activator of transcription 3 (pSTAT3) by the tumours and stroma. Human duodenal organoids treated with TNFα induced neuroendocrine tumour genes, SYP, CHGA and NKX6.3.ConclusionsStromal–epithelial interactions induce proinflammatory cytokines that promote Brunner’s gland reprogramming.

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Mazzoccoli, Gianluigi, Lucia Anna Muscarella, Vito Michele Fazio, Ada Piepoli, Valerio Pazienza, Mariangela Pia Dagostino, Francesco Giuliani, Victoria O. Polyakova i Igor Kvetnoy. "Antiphase signalling in the neuroendocrine-immune system in healthy humans". Biomedicine & Pharmacotherapy 65, nr 4 (lipiec 2011): 275–79. http://dx.doi.org/10.1016/j.biopha.2011.02.002.

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von Arx, Claudia, Monica Capozzi, Elena López-Jiménez, Alessandro Ottaiano, Fabiana Tatangelo, Annabella Di Mauro, Guglielmo Nasti, Maria Lina Tornesello i Salvatore Tafuto. "Updates on the Role of Molecular Alterations and NOTCH Signalling in the Development of Neuroendocrine Neoplasms". Journal of Clinical Medicine 8, nr 9 (22.08.2019): 1277. http://dx.doi.org/10.3390/jcm8091277.

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Neuroendocrine neoplasms (NENs) comprise a heterogeneous group of rare malignancies, mainly originating from hormone-secreting cells, which are widespread in human tissues. The identification of mutations in ATRX/DAXX genes in sporadic NENs, as well as the high burden of mutations scattered throughout the multiple endocrine neoplasia type 1 (MEN-1) gene in both sporadic and inherited syndromes, provided new insights into the molecular biology of tumour development. Other molecular mechanisms, such as the NOTCH signalling pathway, have shown to play an important role in the pathogenesis of NENs. NOTCH receptors are expressed on neuroendocrine cells and generally act as tumour suppressor proteins, but in some contexts can function as oncogenes. The biological heterogeneity of NENs suggests that to fully understand the role and the potential therapeutic implications of gene mutations and NOTCH signalling in NENs, a comprehensive analysis of genetic alterations, NOTCH expression patterns and their potential role across all NEN subtypes is required.

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Furigo, Isadora C., Pryscila D. S. Teixeira, Paula G. F. Quaresma, Naira S. Mansano, Renata Frazão i Jose Donato. "STAT5 ablation in AgRP neurons increases female adiposity and blunts food restriction adaptations". Journal of Molecular Endocrinology 64, nr 1 (styczeń 2020): 13–27. http://dx.doi.org/10.1530/jme-19-0158.

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AgRP neurons are important players in the control of energy homeostasis and are responsive to several hormones. In addition, STAT5 signalling in the brain, which is activated by metabolic hormones and growth factors, modulates food intake, body fat and glucose homeostasis. Given that, and the absence of studies that describe STAT5 function in AgRP cells, the present study investigated the metabolic effects of Stat5a/b gene ablation in these neurons. We observed that STAT5 signalling in AgRP neurons regulates body fat in female mice. However, male and female STAT5-knockout mice did not exhibit altered food intake, energy expenditure or glucose homeostasis compared to control mice. The counter-regulatory response or glucoprivic hyperphagia induced by 2-deoxy-d-glucose treatment were also not affected by AgRP-specific STAT5 ablation. However, under 60% food restriction, AgRP STAT5-knockout mice had a blunted upregulation of hypothalamic Agrp mRNA expression and corticosterone serum levels compared to control mice, suggesting a possible role for STAT5 in AgRP neurons for neuroendocrine adaptations to food restriction. Interestingly, ad libitum fed knockout male mice had reduced Pomc and Ucp-1 mRNA expression compared to control group. Taken together, these results suggest that STAT5 signalling in AgRP neurons regulates body adiposity in female mice, as well as some neuroendocrine adaptations to food restriction.

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Robinson, Hugh P. C., i Leanne Li. "Autocrine, paracrine and necrotic NMDA receptor signalling in mouse pancreatic neuroendocrine tumour cells". Open Biology 7, nr 12 (grudzień 2017): 170221. http://dx.doi.org/10.1098/rsob.170221.

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N -Methyl- d -aspartate receptor (NMDAR) activation is implicated in the malignant progression of many cancer types, as previously shown by the growth-inhibitory effects of NMDAR antagonists. NMDAR-mediated calcium influx and its downstream signalling depend critically, however, on the dynamics of membrane potential and ambient glutamate concentration, which are poorly characterized in cancer cells. Here, we have used low-noise whole-cell patch-clamp recording to investigate the electrophysiology of glutamate signalling in pancreatic neuroendocrine tumour (PanNET) cells derived from a genetically-engineered mouse model (GEMM) of PanNET, in which NMDAR signalling is known to promote cancer progression. Activating NMDARs caused excitation and intracellular calcium elevation, and intracellular perfusion with physiological levels of glutamate led to VGLUT-dependent autocrine NMDAR activation. Necrotic cells, which are often present in rapidly-growing tumours, were shown to release endogenous cytoplasmic glutamate, and necrosis induced by mechanical rupture of the plasma membrane produced intense NMDAR activation in nearby cells. Computational modelling, based on these results, predicts that NMDARs in cancer cells can be strongly activated in the tumour microenvironment by both autocrine glutamate release and necrosis.

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Chang, John P., Hamid R. Habibi, Yi Yu, Mina Moussavi, Caleb L. Grey i Joshua G. Pemberton. "Calcium and other signalling pathways in neuroendocrine regulation of somatotroph functions". Cell Calcium 51, nr 3-4 (marzec 2012): 240–52. http://dx.doi.org/10.1016/j.ceca.2011.11.001.

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Aristizabal Prada, E. T., i C. J. Auernhammer. "Targeted therapy of gastroenteropancreatic neuroendocrine tumours: preclinical strategies and future targets". Endocrine Connections 7, nr 1 (styczeń 2018): R1—R25. http://dx.doi.org/10.1530/ec-17-0286.

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Molecular targeted therapy of advanced neuroendocrine tumours (NETs) of the gastroenteropancreatic (GEP) system currently encompasses approved therapy with the mammalian target of rapamycin (mTOR) inhibitor everolimus and the multi-tyrosinkinase inhibitor sunitinib. However, clinical efficacy of these treatment strategies is limited by low objective response rates and limited progression-free survival due to tumour resistance. Further novel strategies for molecular targeted therapy of NETs of the GEP system are needed. This paper reviews preclinical research models and signalling pathways in NETs of the GEP system. Preclinical and early clinical data on putative novel targets for molecular targeted therapy of NETs of the GEP system are discussed, including PI3K, Akt, mTORC1/mTORC2, GSK3, c-Met, Ras–Raf–MEK–ERK, embryogenic pathways (Hedgehog, Notch, Wnt/beta-catenin, TGF-beta signalling and SMAD proteins), tumour suppressors and cell cycle regulators (p53, cyclin-dependent kinases (CDKs) CDK4/6, CDK inhibitor p27, retinoblastoma protein (Rb)), heat shock protein HSP90, Aurora kinase, Src kinase family, focal adhesion kinase and epigenetic modulation by histone deacetylase inhibitors.

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Hörsch, D., S. Tielke i J. Schrader. "Expression and activation of mTOR in neuroendocrine tumors. Effects of mTOR inhibition by RAD001 upon growth, cell cycle regulation and signalling in neuroendocrine cell lines". Journal of Clinical Oncology 25, nr 18_suppl (20.06.2007): 10570. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.10570.

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10570 Background: Molecular pathogenesis of neuroendocrine tumors of the digestive tract is largely unknown. We examined paraffin sections of different types of neuroendocrine tumors for expression of activated kinases involved in regulation of growth and protection against apoptosis. In addition, we studied effects of a newly developed inhibitor of mTOR (RAD001) upon growth, cell cycle regulation and signaling in two different neuroendocrine cell lines. Methods: Immunohistochemistry with antibodies for native and activated signaling kinases was performed on paraffin sections. MTT assays were used to determine growth rates of neuroendocrine cell lines and FACS analysis was performed for cell cycle analysis. Immunoblotting revealed activation of kinases. Results: Extracellular activated kinase 1/2 (ERK1/2), cAMP regulated element binding protein (CREB), protein kinase B (PKB) and mTOR were expressed in the majority of insulinomas (n = 40) and serotonin-producing neuroendocrine tumors (carcinoids, n = 49). Phosphorylated forms of these kinases corresponding to their activated state were also detected in these tumors. Most neuroendocrine tumors expressed high levels of activated CREB, PKB and mTOR whereas phosphorylated ERK1/2 was present only a minority of dNETs. Inhibition of mTOR kinase by different concentrations of RAD001 induced growth arrest in insulinoma (INS-1) and human neuroendocrine serotonin-producing cells (BON) in concentrations between 10 and 100 nM. Interestingly, we observed pronounced synergism between octrotide and RAD001 upon growth inhibition in these cell lines. Growth inhibition by RAD001 corresponded to decreased S-phase and increased G0/G1 peak in cell cycle analysis. RAD001 inhibited effectively phosphorylation of mTOR with an IC50 of 10 nM. However, we observed only minor inhibition of PKB and CREB by RAD001 and partial inhibition of ERK signaling by RAD in concentrations between 100 nM and 1 μM. Conclusions: mTOR is expressed and activated in different neuroendocrine tumors and inhibition of mTOR by RAD001 induces growth inhibition, cell cycle arrest and decreased signaling by mTOR and ERK1/2 in neuroendcrine cell lines INS-1 and BON. No significant financial relationships to disclose.

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Vitali, Eleonora, Valeria Cambiaghi, Alessandro Zerbi, Carlo Carnaghi, Piergiuseppe Colombo, Erika Peverelli, Anna Spada, Giovanna Mantovani i Andrea G. Lania. "Filamin-A is required to mediate SST2 effects in pancreatic neuroendocrine tumours". Endocrine-Related Cancer 23, nr 3 (5.01.2016): 181–90. http://dx.doi.org/10.1530/erc-15-0358.

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Somatostatin receptor type 2 (SST2) is the main pharmacological target of somatostatin (SS) analogues widely used in patients with pancreatic neuroendocrine tumours (P-NETs), this treatment being ineffective in a subset of patients. Since it has been demonstrated that Filamin A (FLNA) is involved in mediating GPCR expression, membrane anchoring and signalling, we investigated the role of this cytoskeleton protein in SST2 expression and signalling, angiogenesis, cell adhesion and cell migration in human P-NETs and in QGP1 cell line. We demonstrated that FLNA silencing was not able to affect SST2 expression in P-NET cells in basal conditions. Conversely, a significant reduction in SST2 expression (−43±21%, P<0.05 vs untreated cells) was observed in FLNA silenced QGP1 cells after long term SST2 activation with BIM23120. Moreover, the inhibitory effect of BIM23120 on cyclin D1 expression (−46±18%, P<0.05 vs untreated cells), P-ERK1/2 levels (−42±14%; P<0.05 vs untreated cells), cAMP accumulation (−24±3%, P<0.05 vs untreated cells), VEGF expression (−31±5%, P<0.01 vs untreated cells) and in vitro release (−40±24%, P<0.05 vs untreated cells) was completely lost after FLNA silencing. Interestingly, BIM23120 promoted cell adhesion (+86±45%, P<0.05 vs untreated cells) and inhibited cell migration (−24±2%, P<0.00001 vs untreated cells) in P-NETs cells and these effects were abolished in FLNA silenced cells. In conclusion, we demonstrated that FLNA plays a crucial role in SST2 expression and signalling, angiogenesis, cell adhesion and cell migration in P-NETs and in QGP1 cell line, suggesting a possible role of FLNA in determining the different responsiveness to SS analogues observed in P-NET patients.

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Mendez, Pablo, Iñigo Azcoitia i Luis Miguel Garcia-Segura. "Interdependence of oestrogen and insulin-like growth factor-I in the brain: potential for analysing neuroprotective mechanisms". Journal of Endocrinology 185, nr 1 (kwiecień 2005): 11–17. http://dx.doi.org/10.1677/joe.1.06058.

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The actions of oestradiol in the brain involve interaction with growth factors, such as insulin-like growth factor-I (IGF-I). Many cells in the brain co-express receptors for oestradiol and IGF-I and both factors interact to regulate neural function. The relationship of oestrogen receptor α with IGF-I receptor through the mitogen-activated protein kinase and the phosphoinositide 3-kinase signalling pathways may represent the point of convergence used by these two factors to cooperatively modulate neuritic growth, synaptic plasticity, neuroendocrine events, reproductive behaviour and neuronal survival. In addition, Akt and glycogen synthase kinase 3β are key molecular targets to explain the interaction of oestrogen and IGF-I receptor signalling in the promotion of neuroprotection.

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Kolasińska-Ćwikła, Agnieszka. "The mTOR signalling pathways in the pathogenesis and treatment of neuroendocrine tumours". OncoReview 6, nr 1 (31.03.2016): 37–42. http://dx.doi.org/10.5604/20828691.1198520.

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Rauschenbach, I. Y., E. K. Karpova, N. V. Adonyeva, O. V. Andreenkova, N. V. Faddeeva, E. V. Burdina, A. A. Alekseev, P. N. Menshanov i N. E. Gruntenko. "Disruption of insulin signalling affects the neuroendocrine stress reaction in Drosophila females". Journal of Experimental Biology 217, nr 20 (11.09.2014): 3733–41. http://dx.doi.org/10.1242/jeb.106815.

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Meza-Herrera, CA, A. Gonzalez-Bulnes, RT Kridli, M. Mellado, CF Arechiga-Flores, H. Salinas i JM Luginbuhl. "Neuroendocrine, Metabolic and Genomic Cues Signalling the Onset of Puberty in Females". Reproduction in Domestic Animals 45, nr 6 (8.04.2009): e495-e502. http://dx.doi.org/10.1111/j.1439-0531.2009.01355.x.

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Zanini, Sara, Francesco Giovinazzo, Daniele Alaimo, Ben Lawrence, Roswitha Pfragner, Claudio Bassi, Irvin Modlin i Mark Kidd. "GNA15 expression in small intestinal neuroendocrine neoplasia: Functional and signalling pathway analyses". Cellular Signalling 27, nr 5 (maj 2015): 899–907. http://dx.doi.org/10.1016/j.cellsig.2015.02.001.

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Trumble, Benjamin C., Eric A. Smith, Kathleen A. O'Connor, Hillard S. Kaplan i Michael D. Gurven. "Successful hunting increases testosterone and cortisol in a subsistence population". Proceedings of the Royal Society B: Biological Sciences 281, nr 1776 (7.02.2014): 20132876. http://dx.doi.org/10.1098/rspb.2013.2876.

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Controversy over the adaptive significance of male hunting in subsistence societies hinges on the relative importance of familial provisioning and mate-quality signalling. This paper examines the proximate and ultimate motivations of hunting behaviour from a neuroendocrine perspective, using salivary testosterone and cortisol data collected before, during and after hunting focal follows from 31 Tsimane hunters aged 18–82 years. Despite circadian declines in hormone levels, testosterone and cortisol of Tsimane hunters increased at the time of a kill, and remained high as successful hunters returned home. Previous studies of hormonal changes during competitions find that high-stakes and success in the presence of relevant audiences result in increased neuroendocrine arousal. If men hunt primarily to provision their families, then an additional audience would not be expected to impact testosterone or cortisol, nor would the size of the animal killed. However, if signalling male quality by ‘showing off’ was a larger relative driver of men's hunting behaviour, one would expect greater hormonal response in cases where men returned with large sharable kills, especially in the presence of community members. Consistent with provisioning models of male hunting motivation, neither kill size nor encountering an audience of villagers while returning from hunting was associated with hormonal changes for successful hunters.

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Simbolo, Michele, Giovanni Centonze, Luca Giudice, Federica Grillo, Patrick Maisonneuve, Anastasios Gkountakos, Chiara Ciaparrone i in. "Combined Large Cell Neuroendocrine Carcinomas of the Lung: Integrative Molecular Analysis Identifies Subtypes with Potential Therapeutic Implications". Cancers 14, nr 19 (24.09.2022): 4653. http://dx.doi.org/10.3390/cancers14194653.

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Background: Combined large cell neuroendocrine carcinoma (CoLCNEC) is given by the association of LCNEC with adeno or squamous or any non-neuroendocrine carcinoma. Molecular bases of CoLCNEC pathogenesis are scant and no standardized therapies are defined. Methods: 44 CoLCNECs: 26 with adenocarcinoma (CoADC), 7 with squamous cell carcinoma (CoSQC), 3 with small cell carcinoma (CoSCLC), 4 with atypical carcinoid (CoAC) and 4 napsin-A positive LCNEC (NapA+), were assessed for alterations in 409 genes and transcriptomic profiling of 20,815 genes. Results: Genes altered included TP53 (n = 30), RB1 (n = 14) and KRAS (n = 13). Targetable alterations included six KRAS G12C mutations and ALK-EML4 fusion gene. Comparison of CoLCNEC transcriptomes with 86 lung cancers of pure histology (8 AC, 19 ADC, 19 LCNEC, 11 SCLC and 29 SQC) identified CoLCNEC as a separate entity of neuroendocrine tumours with three different molecular profiles, two of which showed a non-neuroendocrine lineage. Hypomethylation, activation of MAPK signalling and association to immunotherapy signature specifically characterized each of three CoLCNEC molecular clusters. Prognostic stratification was also provided. Conclusions: CoLCNECs are an independent histologic category. Our findings support the extension of routine evaluation of KRAS mutations, fusion genes and immune-related markers to offer new perspectives in the therapeutic management of CoLCNEC.

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Beyer, Anna-Sophia Lieselott, Daniel Kaemmerer, Jörg Sänger, Katja Evert i Amelie Lupp. "Immunohistochemical Evaluation of Adaptor Protein FAM159B Expression in Normal and Neoplastic Human Tissues". International Journal of Molecular Sciences 22, nr 22 (12.11.2021): 12250. http://dx.doi.org/10.3390/ijms222212250.

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FAM159B is a so-called adaptor protein. These proteins are essential components in numerous cell signalling pathways. However, little is known regarding FAM159B expression in normal and neoplastic human tissues. The commercially available rabbit polyclonal anti-human FAM159B antibody HPA011778 was initially characterised for its specificity using Western blot analyses and immunocytochemistry and then applied to a large series of formalin-fixed, paraffin-embedded normal and neoplastic human tissue samples. Confirmation of FAM159B’s predicted size and antibody specificity was achieved in BON-1 cells, a neuroendocrine tumour cell line endogenously expressing FAM159B, using targeted siRNA. Immunocytochemical experiments additionally revealed cytoplasmic expression of the adaptor protein. Immunohistochemical staining detected FAM159B expression in neuronal and neuroendocrine tissues such as the cortex, the trigeminal ganglia, dorsal root and intestinal ganglia, the pancreatic islets and the neuroendocrine cells of the bronchopulmonary and gastrointestinal tract, but also in the syncytiotrophoblasts of the placenta. FAM159B was also expressed in many of the 28 tumour entities investigated, with high levels in medullary and anaplastic thyroid carcinomas, parathyroid adenomas, lung and ovarian carcinomas, lymphomas and neuroendocrine tumours of different origins. The antibody HPA011778 can act as a useful tool for basic research and identifying FAM159B expression in tissue samples.

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Grozinsky-Glasberg, Simona, Kate E. Lines, Shani Avniel-Polak, Chas Bountra i Rajesh V. Thakker. "Preclinical drug studies in MEN1-related neuroendocrine neoplasms (MEN1-NENs)". Endocrine-Related Cancer 27, nr 9 (wrzesień 2020): R345—R355. http://dx.doi.org/10.1530/erc-20-0127.

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Neuroendocrine neoplasms (NENs) occur usually as sporadic tumours; however, rarely, they may arise in the context of a hereditary syndrome, such as multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant disorder characterised by the combined development of pancreatic NENs (pNENs) together with parathyroid and anterior pituitary tumours. The therapeutic decision for sporadic pNENs patients is multi-disciplinary and complex: based on the grade and stage of the tumor, various options (and their combinations) are considered, such as surgical excision (either curative or for debulking aims), biological drugs (somatostatin analogues), targeted therapies (mTOR inhibitors or tyrosine kinases (TK)/receptors inhibitors), peptide receptor radioligand therapy (PRRT), chemotherapy, and liver-directed therapies. However, treatment of MEN1-related NENs’ patients is even more challenging, as these tumours are usually multifocal with co-existing foci of heterogeneous biology and malignant potential, rendering them more resistant to the conventional therapies used in their sporadic counterparts, and therefore associated with a poorer prognosis. Moreover, clinical data using standard therapeutic options in MEN1-related NENs are scarce. Recent preclinical studies have identified potentially new targeted therapeutic options for treating MEN1-associated NENs, such as epigenetic modulators, Wnt pathway-targeting β-catenin antagonists, Ras signalling modulators, Akt/mTOR signalling modulators, novel somatostatin receptors analogues, anti-angiogenic drugs, as well as MEN1 gene replacement therapy. The present review aims to summarize these novel therapeutic opportunities for NENs developing in the context of MEN1 syndrome, with an emphasis on pancreatic NENs, as they are the most frequent ones studied in MEN1-NENs models to date; moreover, due to the recent shifting nomenclature of ‘pituitary adenomas’ to ‘pituitary neuroendocrine neoplasms’, relevant data on MEN1-pituitary tumours, when appropriate, are briefly described.

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Blažević, Anela, Johannes Hofland, Leo J. Hofland, Richard A. Feelders i Wouter W. de Herder. "Small intestinal neuroendocrine tumours and fibrosis: an entangled conundrum". Endocrine-Related Cancer 25, nr 3 (marzec 2018): R115—R130. http://dx.doi.org/10.1530/erc-17-0380.

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Small intestinal neuroendocrine tumours (SI-NETs) are neoplasms characterized by their ability to secrete biogenic amines and peptides. These cause distinct clinical pathology including carcinoid syndrome, marked by diarrhoea and flushing, as well as fibrosis, notably mesenteric fibrosis. Mesenteric fibrosis often results in significant morbidity by causing intestinal obstruction, oedema and ischaemia. Although advancements have been made to alleviate symptoms of carcinoid syndrome and prolong the survival of patients with SI-NETs, therapeutic options for patients with mesenteric fibrosis are still limited. As improved insight in the complex pathogenesis of mesenteric fibrosis is key to the development of new therapies, we evaluated the literature for known and putative mediators of fibrosis in SI-NETs. In this review, we discuss the tumour microenvironment, growth factors and signalling pathways involved in the complex process of fibrosis development and tumour progression in SI-NETs, in order to elucidate potential new avenues for scientific research and therapies to improve the management of patients suffering from the complications of mesenteric fibrosis.

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Bastos, Diogo Assed, Brenda Gumz i Frederico Costa. "Antitumour Effects of Somatostatin Analogues in the Treatment of Neuroendocrine Tumours". European Endocrinology 8, nr 2 (2010): 94. http://dx.doi.org/10.17925/ee.2012.08.02.94.

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Neuroendocrine tumours (NETs) are rare and heterogeneous neoplasms that can present with functional syndromes due to the hypersecretion of peptides. Somatostatin analogues (SSAs) have been used since the 1980s for the treatment of neuroendocrine tumours, with the aim of controlling the symptoms of functioning tumours and improving patients’ quality of life. Data from preclinical studies offer evidence of both direct and indirect mechanisms by which SSAs can exert antitumour effects. The activation of somatostatin receptors by SSAs leads to the activation of phosphotyrosine phosphatases, which control downstream apoptotic and antiproliferation signalling pathways. Also, the suppression of secretion of several growth factors and inhibition of antiangiogenic activity by SSAs indirectly inhibits tumour cell proliferationin vitro. Previous uncontrolled studies had shown tumour shrinkage and disappearance in response to the SSA octreotide. Recent results from the randomised and placebo-controlled PROMID trial have demonstrated that octreotide has antitumour activity in patients with metastatic mid-gut NETs. This article examines recent data providing evidence of the antitumour activity of somatostatin analogues.

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Bastos, Diogo Assed, Brenda Gumz i Frederico Costa. "Antitumour Effects of Somatostatin Analogues in the Treatment of Neuroendocrine Tumours". European Oncology & Haematology 08, nr 03 (2012): 156. http://dx.doi.org/10.17925/eoh.2012.08.3.156.

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Neuroendocrine tumours (NETs) are rare and heterogeneous neoplasms that can present with functional syndromes due to the hypersecretion of peptides. Somatostatin analogues (SSAs) have been used since the 1980s for the treatment of neuroendocrine tumours, with the aim of controlling the symptoms of functioning tumours and improving patients’ quality of life. Data from preclinical studies offer evidence of both direct and indirect mechanisms by which SSAs can exert antitumour effects. The activation of somatostatin receptors by SSAs leads to the activation of phosphotyrosine phosphatases, which control downstream apoptotic and antiproliferation signalling pathways. Also, the suppression of secretion of several growth factors and inhibition of antiangiogenic activity by SSAs indirectly inhibits tumour cell proliferationin vitro. Previous uncontrolled studies had shown tumour shrinkage and disappearance in response to the SSA octreotide. Recent results from the randomised and placebo-controlled PROMID trial have demonstrated that octreotide has antitumour activity in patients with metastatic mid-gut NETs. This article examines recent data providing evidence of the antitumour activity of somatostatin analogues.

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Soengas, José Luis, José Miguel Cerdá-Reverter i María Jesús Delgado. "Central regulation of food intake in fish: an evolutionary perspective". Journal of Molecular Endocrinology 60, nr 4 (maj 2018): R171—R199. http://dx.doi.org/10.1530/jme-17-0320.

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Evidence indicates that central regulation of food intake is well conserved along the vertebrate lineage, at least between teleost fish and mammals. However, several differences arise in the comparison between both groups. In this review, we describe similarities and differences between teleost fish and mammals on an evolutionary perspective. We focussed on the existing knowledge of specific fish features conditioning food intake, anatomical homologies and analogies between both groups as well as the main signalling pathways of neuroendocrine and metabolic nature involved in the homeostatic and hedonic central regulation of food intake.

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Spampatti, M. P., G. Vlotides, G. Spoettl, J. Maurer, B. Goeke, D. Conte i C. J. Auernhammer. "OC.09.2 ASPIRIN REDUCED CELL VIABILITY AND MTOR SIGNALLING IN NEUROENDOCRINE TUMOR CELL LINES". Digestive and Liver Disease 46 (marzec 2014): S22. http://dx.doi.org/10.1016/s1590-8658(14)60059-1.

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Atkinson, T. J. "Central and peripheral neuroendocrine peptides and signalling in appetite regulation: considerations for obesity pharmacotherapy". Obesity Reviews 9, nr 2 (marzec 2008): 108–20. http://dx.doi.org/10.1111/j.1467-789x.2007.00412.x.

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Clift, Ashley K., i Andrea Frilling. "Using genetics to inform the pharmacological targeting of neuroendocrine neoplasms". Endocrine-Related Cancer 27, nr 9 (wrzesień 2020): R293—R305. http://dx.doi.org/10.1530/erc-20-0074.

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Neuroendocrine neoplasms (NEN) are a class of tumours heterogeneous in terms of their anatomical sites of origin and clinical behaviour. Outdated perspectives of indolence have been superseded by appreciation for their myriad clinical challenges, such as the high rates of regional and distant metastases at initial diagnosis, lack of clarity on optimal treatment strategies/sequencing, and incompletely elucidated genetic/other pathophysiological drivers. The first randomised controlled trials in this arena were published approximately a decade ago – since then, increased understanding of the genetic drivers and signalling pathway perturbations in these tumours have suggested promise for precision therapy influenced by an individual tumour’s molecular sub-type, but this is yet to be realised for manifold reasons. In this article, the authors review the genetic landscapes as currently understood for selected forms of NEN and discuss the current and developing evidence to support the use of genetic information to influence therapy. They provide a critical assessment of the potential limitations of using such approaches and also posit avenues for future developments in this arena.

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Reubi, Jean Claude, Daniel Fourmy, Arnau Cordomi, Irina G. Tikhonova i Véronique Gigoux. "GIP receptor: Expression in neuroendocrine tumours, internalization, signalling from endosomes and structure-function relationship studies". Peptides 125 (marzec 2020): 170229. http://dx.doi.org/10.1016/j.peptides.2019.170229.

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Cella, Chiara Alessandra, Saverio Minucci, Francesca Spada, Salvatore Galdy, Mohamed Elgendy, Paola Simona Ravenda, Maria Giulia Zampino, Sabina Murgioni i Nicola Fazio. "Dual inhibition of mTOR pathway and VEGF signalling in neuroendocrine neoplasms: From bench to bedside". Cancer Treatment Reviews 41, nr 9 (listopad 2015): 754–60. http://dx.doi.org/10.1016/j.ctrv.2015.06.008.

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Stern, Javier E. "Nitric oxide and homeostatic control: an intercellular signalling molecule contributing to autonomic and neuroendocrine integration?" Progress in Biophysics and Molecular Biology 84, nr 2-3 (luty 2004): 197–215. http://dx.doi.org/10.1016/j.pbiomolbio.2003.11.015.

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Avila, Matías A. "Long distance calling for liver regeneration: Identification of neuroendocrine signalling pathways activated after partial hepatectomy". Journal of Hepatology 54, nr 3 (marzec 2011): 403–5. http://dx.doi.org/10.1016/j.jhep.2010.08.009.

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Johnson, James D., i John P. Chang. "Function- and agonist-specific Ca2+signalling: The requirement for and mechanism of spatial and temporal complexity in Ca2+signals". Biochemistry and Cell Biology 78, nr 3 (2.04.2000): 217–40. http://dx.doi.org/10.1139/o00-012.

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Calcium signals have been implicated in the regulation of many diverse cellular processes. The problem of how information from extracellular signals is delivered with specificity and fidelity using fluctuations in cytosolic Ca2+concentration remains unresolved. The capacity of cells to generate Ca2+signals of sufficient spatial and temporal complexity is the primary constraint on their ability to effectively encode information through Ca2+. Over the past decade, a large body of literature has dealt with some basic features of Ca2+-handling in cells, as well as the multiplicity and functional diversity of intracellular Ca2+stores and extracellular Ca2+influx pathways. In principle, physiologists now have the necessary information to attack the problem of function- and agonist-specificity in Ca2+signal transduction. This review explores the data indicating that Ca2+release from diverse sources, including many types of intracellular stores, generates Ca2+signals with sufficient complexity to regulate the vast number of cellular functions that have been reported as Ca2+-dependent. Some examples where such complexity may relate to neuroendocrine regulation of hormone secretion/synthesis are discussed. We show that the functional and spatial heterogeneity of Ca2+stores generates Ca2+signals with sufficient spatiotemporal complexity to simultaneously control multiple Ca2+-dependent cellular functions in neuroendocrine systems.Key words: signal coding, IP3receptor, ryanodine receptor, endoplasmic reticulum, Golgi, secretory granules, mitochondria, exocytosis.

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Tobiansky, Daniel J., George V. Kachkovski, Reilly T. Enos, Kim L. Schmidt, E. Angela Murphy i Kiran K. Soma. "Sucrose consumption alters steroid and dopamine signalling in the female rat brain". Journal of Endocrinology 245, nr 2 (maj 2020): 231–46. http://dx.doi.org/10.1530/joe-19-0386.

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Sucrose consumption is associated with type 2 diabetes, cardiovascular disease, and cognitive deficits. Sucrose intake during pregnancy might have particularly prominent effects on metabolic, endocrine, and neural physiology. It remains unclear how consumption of sucrose affects parous females, especially in brain circuits that mediate food consumption and reward processing. Here, we examine whether a human-relevant level of sucrose before, during, and after pregnancy (17–18 weeks total) influences metabolic and neuroendocrine physiology in female rats. Females were fed either a control diet or a macronutrient-matched, isocaloric sucrose diet (25% of kcal from sucrose). Metabolically, sucrose impairs glucose tolerance, increases liver lipids, and increases a marker of adipose inflammation, but has no effect on body weight or overall visceral adiposity. Sucrose also decreases corticosterone levels in serum but not in the brain. Sucrose increases progesterone levels in serum and in the brain and increases the brain:serum ratio of progesterone in the mesocorticolimbic system and hypothalamus. These data suggest a dysregulation of systemic and local steroid signalling. Moreover, sucrose decreases tyrosine hydroxylase (TH), a catecholamine-synthetic enzyme, in the medial prefrontal cortex. Finally, sucrose consumption alters the expression pattern of FOSB, a marker of phasic dopamine signalling, in the nucleus accumbens. Overall, chronic consumption of sucrose at a human-relevant level alters metabolism, steroid levels, and brain dopamine signalling in a female rat model.

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Kenny, David A., i Kate Keogh. "409 Early life nutrition on the molecular control of sexual development in the bull". Journal of Animal Science 98, Supplement_4 (3.11.2020): 187–88. http://dx.doi.org/10.1093/jas/skaa278.346.

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Abstract Duration of the generation interval and intensity of selection in cattle are heavily influenced by the timing of availability of semen from genetically elite young. Enhancing early life nutrition stimulates the functionality of the hypothalamic-pituitary-testicular axis, mediated through complex biochemical interplay between metabolic and neuroendocrine signals and culminating in enhanced testicular growth, steroidogenesis, spermatogenesis, and ultimately, earlier onset of sexual maturation. Indeed, recent evidence indicates Current efforts employing high throughput nucleic acid sequencing and global proteomic approaches have reported clear effects of enhanced early-life nutrition on testicular tissue development, particularly in relation to steroidogenic biochemical pathways. However, the precise effect of enhanced nutrition in early life on the molecular control of the hypothalamus and pituitary gland maturation and functionality remains to be fully understood, with recent evidence suggesting roles, for example, for the complement and coagulation signalling cascade and MAPK signalling pathways in the hypothalamus and anterior pituitary glands, respectively. Although early-life nutrition clearly affects the sexual maturation process, there is little evidence for latent effects on postpubertal semen characteristics. Equally, postpubertal fertility, assessed through in vitro fertilization and early embryogenesis, is apparently not influenced by nutritional status during early life. Notwithstanding this, recent studies have highlighted potential latent effects of calfhood dietary management on sperm methylation patterns of early post pubertal bulls, and such epigenetic influence warrants further investigation. Certainly, the integration and interrogation of molecular “omics” data within a systems biology framework holds promise in deciphering the influence of nutritional management on the complex regulation of neuroendocrine and testicular cellular processes. Such information can be harnessed to identify potential genomic targets as part of genomically assisted breeding programs, as well as facilitating development of strategic nutritional regimens to optimize sexual maturation and subsequent semen availability from genetically elite young bulls.

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Villanueva, José, Yolanda Gimenez-Molina, Bazbek Davletov i Luis M. Gutiérrez. "Vesicle Fusion as a Target Process for the Action of Sphingosine and Its Derived Drugs". International Journal of Molecular Sciences 23, nr 3 (19.01.2022): 1086. http://dx.doi.org/10.3390/ijms23031086.

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The fusion of membranes is a central part of the physiological processes involving the intracellular transport and maturation of vesicles and the final release of their contents, such as neurotransmitters and hormones, by exocytosis. Traditionally, in this process, proteins, such SNAREs have been considered the essential components of the fusion molecular machinery, while lipids have been seen as merely structural elements. Nevertheless, sphingosine, an intracellular signalling lipid, greatly increases the release of neurotransmitters in neuronal and neuroendocrine cells, affecting the exocytotic fusion mode through the direct interaction with SNAREs. Moreover, recent studies suggest that FTY-720 (Fingolimod), a sphingosine structural analogue used in the treatment of multiple sclerosis, simulates sphingosine in the promotion of exocytosis. Furthermore, this drug also induces the intracellular fusion of organelles such as dense vesicles and mitochondria causing cell death in neuroendocrine cells. Therefore, the effect of sphingosine and synthetic derivatives on the heterologous and homologous fusion of organelles can be considered as a new mechanism of action of sphingolipids influencing important physiological processes, which could underlie therapeutic uses of sphingosine derived lipids in the treatment of neurodegenerative disorders and cancers of neuronal origin such neuroblastoma.

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Khan, Rao Saad Ali. "Endoscopic Sleeve Gastroplasty: Best Obesity Treatment". Pakistan Armed Forces Medical Journal 73, nr 1 (22.02.2023): 1–2. http://dx.doi.org/10.51253/pafmj.v73i1.9966.

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Obesity and its related health problems like diabetes mellitus, stroke and heart disease are an epidemic not restricted to industrialized countries. However, around 115 million people in developing countries suffer from obesity-related problems.1 Regarding treating obesity, GI weight loss surgery (GIWLS) has shown remarkable results.2,3 However, a very small percentage of individuals requiring GIWLS undergo this treatment.4,5 That is mainly due to the high risks associated with surgical procedures. The GIWLS has evolved from mechanical restriction resulting in malabsorption to manipulation of gut anatomy, causing changes in the gut neuroendocrine signalling to the associated organs for regulation of food intake by enhancing satiety & improving glucose homeostasis.6,7

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Simpson, Sian J. S., Lorna I. F. Smith, Peter M. Jones i James E. Bowe. "UCN2: a new candidate influencing pancreatic β-cell adaptations in pregnancy". Journal of Endocrinology 245, nr 2 (maj 2020): 247–57. http://dx.doi.org/10.1530/joe-19-0568.

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The corticotropin-releasing hormone (CRH) family of peptides, including urocortin (UCN) 1, 2 and 3, are established hypothalamic neuroendocrine peptides, regulating the physiological and behaviour responses to stress indirectly, via the hypothalamic-pituitary-adrenal (HPA) axis. More recently, these peptides have been implicated in diverse roles in peripheral organs through direct signalling, including in placental and pancreatic islet physiology. CRH has been shown to stimulate insulin release through activation of its cognate receptors, CRH receptor 1 (CRHR1) and 2. However, the physiological significance of this is unknown. We have previously reported that during mouse pregnancy, expression of CRH peptides increase in mouse placenta suggesting that these peptides may play a role in various biological functions associated with pregnancy, particularly the pancreatic islet adaptations that occur in the pregnant state to compensate for the physiological increase in maternal insulin resistance. In the current study, we show that mouse pregnancy is associated with increased circulating levels of UCN2 and that when we pharmacologically block endogenous CRHR signalling in pregnant mice, impairment of glucose tolerance is observed. This effect on glucose tolerance was comparable to that displayed with specific CRHR2 blockade and not with specific CRHR1 blockade. No effects on insulin sensitivity or the proliferative capacity of β-cells were detected. Thus, CRHR2 signalling appears to be involved in β-cell adaptive responses to pregnancy in the mouse, with endogenous placental UCN2 being the likely signal mediating this.

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Capodanno, Y., F. O. Buishand, L. Y. Pang, J. Kirpensteijn, J. A. Mol i D. J. Argyle. "Notch pathway inhibition targets chemoresistant insulinoma cancer stem cells". Endocrine-Related Cancer 25, nr 2 (luty 2018): 131–44. http://dx.doi.org/10.1530/erc-17-0415.

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Insulinomas (INS) are the most common neuroendocrine pancreatic tumours in humans and dogs. The long-term prognosis for malignant INS is still poor due to a low success rate of the current treatment modalities, particularly chemotherapy. A better understanding of the molecular processes underlying the development and progression of INS is required to develop novel targeted therapies. Cancer stem cells (CSCs) are thought to be critical for the engraftment and chemoresistance of many tumours, including INS. This study was aimed to characterise and target INS CSCs in order to develop novel targeted therapies. Highly invasive and tumourigenic human and canine INS CSC-like cells were successfully isolated. These cells expressed stem cell markers (OCT4,SOX9, SOX2, CD133 and CD34), exhibited greater resistance to 5-fluorouracil (5-FU) and demonstrated a more invasive and tumourigenic phenotypein vivocompared to bulk INS cells. Here, we demonstrated that Notch-signalling-related genes (NOTCH2andHES1)were overexpressed in INS CSC-like cells. Protein analysis showed an active NOTCH2-HES1 signalling in INS cell lines, especially in cells resistant to 5-FU. Inhibition of the Notch pathway, using a gamma secretase inhibitor (GSI), enhanced the sensitivity of INS CSC-like cells to 5-FU. When used in combination GSI and 5-FU, the clonogenicityin vitroand the tumourigenicityin vivoof INS CSC-like cells were significantly reduced. These findings suggested that the combined strategy of Notch signalling inhibition and 5-FU synergistically attenuated enriched INS CSC populations, providing a rationale for future therapeutic exploitation.

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Kidd, M., B. Svejda, R. Pfragner i I. M. Modlin. "Serotonin is a critical signalling molecule in the local and metastatic small intestinal neuroendocrine tumour microenvironment". Regulatory Peptides 164, nr 1 (wrzesień 2010): 38. http://dx.doi.org/10.1016/j.regpep.2010.07.094.

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Garcia, Nicholas W., Timothy J. Greives, Devin A. Zysling, Susannah S. French, Emily M. Chester i Gregory E. Demas. "Exogenous insulin enhances humoural immune responses in short-day, but not long-day, Siberian hamsters ( Phodopus sungorus )". Proceedings of the Royal Society B: Biological Sciences 277, nr 1691 (17.03.2010): 2211–18. http://dx.doi.org/10.1098/rspb.2009.2230.

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Many animals experience marked seasonal fluctuations in environmental conditions. In response, animals display adaptive alterations in physiology and behaviour, including seasonal changes in immune function. During winter, animals must reallocate finite energy stores from relatively costly, less exigent systems (e.g. reproduction and immunity) to systems critical for immediate survival (e.g. thermoregulation). Seasonal changes in immunity are probably mediated by neuroendocrine factors signalling current energetic state. One potential hormonal candidate is insulin, a metabolic hormone released in response to elevated blood glucose levels. The aim of the present study was to explore the potential role of insulin in signalling energy status to the immune system in a seasonally breeding animal, the Siberian hamster ( Phodopus sungorus ). Specifically, exogenous insulin was administered to male hamsters housed in either long ‘summer-like’ or short ‘winter-like’ days. Animals were then challenged with an innocuous antigen and immune responses were measured. Insulin treatment significantly enhanced humoural immune responses in short, but not long days. In addition, insulin treatment increased food intake and decreased blood glucose levels across photoperiodic treatments. Collectively, these data support the hypothesis that insulin acts as an endocrine signal integrating seasonal energetic changes and immune responses in seasonally breeding rodents.

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Jiménez, Beatriz, Mei Ran Abellona U, Panagiotis Drymousis, Michael Kyriakides, Ashley K. Clift, Daniel S. K. Liu, Eleanor Rees i in. "Neuroendocrine Neoplasms: Identification of Novel Metabolic Circuits of Potential Diagnostic Utility". Cancers 13, nr 3 (20.01.2021): 374. http://dx.doi.org/10.3390/cancers13030374.

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The incidence of neuroendocrine neoplasms (NEN) is increasing, but established biomarkers have poor diagnostic and prognostic accuracy. Here, we aim to define the systemic metabolic consequences of NEN and to establish the diagnostic utility of proton nuclear magnetic resonance spectroscopy (1H-NMR) for NEN in a prospective cohort of patients through a single-centre, prospective controlled observational study. Urine samples of 34 treatment-naïve NEN patients (median age: 59.3 years, range: 36–85): 18 had pancreatic (Pan) NEN, of which seven were functioning; 16 had small bowel (SB) NEN; 20 age- and sex-matched healthy control individuals were analysed using a 600 MHz Bruker 1H-NMR spectrometer. Orthogonal partial-least-squares-discriminant analysis models were able to discriminate both PanNEN and SBNEN patients from healthy control (Healthy vs. PanNEN: AUC = 0.90, Healthy vs. SBNEN: AUC = 0.90). Secondary metabolites of tryptophan, such as trigonelline and a niacin-related metabolite were also identified to be universally decreased in NEN patients, while upstream metabolites, such as kynurenine, were elevated in SBNEN. Hippurate, a gut-derived metabolite, was reduced in all patients, whereas other gut microbial co-metabolites, trimethylamine-N-oxide, 4-hydroxyphenylacetate and phenylacetylglutamine, were elevated in those with SBNEN. These findings suggest the existence of a new systems-based neuroendocrine circuit, regulated in part by cancer metabolism, neuroendocrine signalling molecules and gut microbial co-metabolism. Metabonomic profiling of NEN has diagnostic potential and could be used for discovering biomarkers for these tumours. These preliminary data require confirmation in a larger cohort.

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