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Academic literature on the topic 'Intestinal pleiotropic hormone'
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Journal articles on the topic "Intestinal pleiotropic hormone"
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Stokes, Caroline S., and Frank Lammert. "Vitamin D supplementation: less controversy, more guidance needed." F1000Research 5 (August 17, 2016): 2017. http://dx.doi.org/10.12688/f1000research.8863.1.
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Vitamin D is a secosteroid hormone with multiple functions that extend beyond the regulation of intestinal calcium absorption. In recent years, the publication of research articles investigating associations between vitamin D status and health has reached an all-time high, and an increase in supplementation studies has followed. Given the pleiotropic effects of vitamin D, the scientific focus has gone beyond its known classic benefits on skeletal health to include diabetes and cardiovascular, neurological, respiratory, renal, and liver diseases, yet numerous conflicting findings continue to emerge. This review presents some examples of recent work within the context of controversies surrounding vitamin D and highlights key factors that should be considered when designing vitamin D supplementation regimens.
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Al-Araimi, Amna, Amira Al Kharusi, Asma Bani Oraba, Matar M. Al-Maney, Shadia Al Sinawi, Ibrahim Al-Haddabi, and Fahad Zadjali. "Deletion of SOCS2 Reduces Post-Colitis Fibrosis via Alteration of the TGFβ Pathway." International Journal of Molecular Sciences 21, no. 9 (April 27, 2020): 3073. http://dx.doi.org/10.3390/ijms21093073.
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Inflammatory bowel disease (IBD) is an immunologically mediated chronic intestinal disorder. Growth hormone (GH) administration enhances mucosal repair and decreases intestinal fibrosis in patients with IBD. In the present study, we investigated the effect of cellular sensitivity to GH via suppressor of cytokine signaling 2 (SOCS2) deletion on colitis and recovery. To induce colitis, wild type and SOCS2 knockout (SOCS2−/−) mice were treated with 3% dextran sodium sulphate (DSS), followed by a recovery period. SOCS2−/− mice showed higher disease activity during colitis with increased mRNA expression of the pro-inflammatory cytokines nitric oxide synthase 2 (NOS2) and interleukin 1 β (IL1-β). At recovery time point, SOCS2−/− showed better recovery with less fibrosis measured by levels of α-SMA and collagen deposition. Protein and mRNA expressions of transforming growth factor beta β1 (TGF-β1) receptors were significantly lower in SOCS2−/− mice compared to wild-type littermates. Using an in vivo bromodeoxyuridine (BrdU) proliferation assay, SOCS2−/− mice showed higher intestinal epithelial proliferation compared to wild-type mice. Our results demonstrated that deletion of the SOCS2 protein results in higher growth hormone sensitivity associated with higher pro-inflammatory signaling; however, it resulted in less tissue damage with less fibrotic lesions and higher epithelial proliferation, which are markers of GH-protective effects in IBD. This suggests a pleiotropic effect of SOCS2 and multiple cellular targets. Further study is required to study role of SOCS2 in regulation of TGFβ-mothers against the decapentaplegic homolog (Smad) pathway.
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Kuhre, Rune E., Jens J. Holst, and Camilla Kappe. "The regulation of function, growth and survival of GLP-1-producing L-cells." Clinical Science 130, no. 2 (December 4, 2015): 79–91. http://dx.doi.org/10.1042/cs20150154.
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Glucagon-like peptide-1 (GLP-1) is a peptide hormone, released from intestinal L-cells in response to hormonal, neural and nutrient stimuli. In addition to potentiation of meal-stimulated insulin secretion, GLP-1 signalling exerts numerous pleiotropic effects on various tissues, regulating energy absorption and disposal, as well as cell proliferation and survival. In Type 2 Diabetes (T2D) reduced plasma levels of GLP-1 have been observed, and plasma levels of GLP-1, as well as reduced numbers of GLP-1 producing cells, have been correlated to obesity and insulin resistance. Increasing endogenous secretion of GLP-1 by selective targeting of the molecular mechanisms regulating secretion from the L-cell has been the focus of much recent research. An additional and promising strategy for enhancing endogenous secretion may be to increase the L-cell mass in the intestinal epithelium, but the mechanisms that regulate the growth, survival and function of these cells are largely unknown. We recently showed that prolonged exposure to high concentrations of the fatty acid palmitate induced lipotoxic effects, similar to those operative in insulin-producing cells, in an in vitro model of GLP-1-producing cells. The mechanisms inducing this lipototoxicity involved increased production of reactive oxygen species (ROS). In this review, regulation of GLP-1-secreting cells is discussed, with a focus on the mechanisms underlying GLP-1 secretion, long-term regulation of growth, differentiation and survival under normal as well as diabetic conditions of hypernutrition.
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Dubé, Philip E., and Patricia L. Brubaker. "Frontiers in glucagon-like peptide-2: multiple actions, multiple mediators." American Journal of Physiology-Endocrinology and Metabolism 293, no. 2 (August 2007): E460—E465. http://dx.doi.org/10.1152/ajpendo.00149.2007.
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Glucagon-like peptide-2 (GLP-2) is a pleiotropic hormone that affects multiple facets of intestinal physiology, including growth, barrier function, digestion, absorption, motility, and blood flow. The mechanisms through which GLP-2 produces these actions are complex, involving unique signaling mechanisms and multiple indirect mediators. As clinical trials have begun for the use of GLP-2 in a variety of intestinal disorders, the elucidation of such mechanisms is vital. The GLP-2 receptor (GLP-2R) is a G protein-coupled receptor, signaling through multiple G proteins to affect the cAMP and mitogen-activated protein kinase pathways, leading to both proliferative and antiapoptotic cellular responses. The GLP-2R also demonstrates unique mechanisms for receptor trafficking. Expression of the GLP-2R in discrete sets of intestinal cells, including endocrine cells, subepithelial myofibroblasts, and enteric neurons, has led to the hypothesis that GLP-2 acts indirectly through multiple mediators to produce its biological effects. Indeed, several studies have now provided important mechanistic data illustrating several of the indirect pathways of GLP-2 action. Thus, insulin-like growth factor I has been demonstrated to be required for GLP-2-induced crypt cell proliferation, likely involving activation of β-catenin signaling. Furthermore, vasoactive intestinal polypeptide modulates the actions of GLP-2 in models of intestinal inflammation, while keratinocyte growth factor is required for GLP-2-induced colonic mucosal growth and mucin expression. Finally, enteric neural GLP-2R signaling affects intestinal blood flow through a nitric oxide-dependent mechanism. Determining how GLP-2 produces its full range of biological effects, which mediators are involved, and how these mediators interact is a continuing area of active research.
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Pereira, Fábio, María Jesús Larriba, and Alberto Muñoz. "Vitamin D and colon cancer." Endocrine-Related Cancer 19, no. 3 (March 1, 2012): R51—R71. http://dx.doi.org/10.1530/erc-11-0388.
Full textAbstract:
The most active vitamin D metabolite, 1α,25-dihydroxyvitamin D3(1,25(OH)2D3), is a pleiotropic hormone with wide regulatory actions. Classically, vitamin D deficiency was known to alter calcium and phosphate metabolism and bone biology. In addition, recent epidemiological and experimental studies support the association of vitamin D deficiency with a large variety of human diseases, and particularly with the high risk of colorectal cancer. By regulating the expression of many genes via several mechanisms, 1,25(OH)2D3induces differentiation, controls the detoxification metabolism and cell phenotype, sensitises cells to apoptosis and inhibits the proliferation of cultured human colon carcinoma cells. Consistently, 1,25(OH)2D3and several of its analogues decrease intestinal tumourigenesis in animal models. Molecular, genetic and clinical data in humans are scarce but they suggest that vitamin D is protective against colon cancer. Clearly, the available evidence warrants new, well-designed, large-scale trials to clarify the role of vitamin D in the prevention and/or therapy of this important neoplasia.
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Krizhanovskii, Camilla, and Anders Franco-Cereceda. "Diabetes, Incretin Therapy and Thoracic Aortic Aneurysm – What Does the Evidence Show?" Current Vascular Pharmacology 17, no. 5 (August 1, 2019): 432–39. http://dx.doi.org/10.2174/1570161116666180828155622.
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Epidemiological evidence supports a reduced prevalence of Thoracic Aortic Aneurysm (TAA) and Abdominal Aortic Aneurysm (AAA) in patients with Diabetes (DM). The mechanisms underlying this negative association are unknown. Some studies support that hyperglycemia has effects on the Extracellular Matrix (ECM), resulting in collagen cross-links and altered proteolytic activity, which ultimately counteracts aneurysm formation. However, recent experimental research indicates that incretin- based anti-diabetic therapy and Glucagon-Like Peptide-1 (GLP-1) may reduce the formation of TAA. GLP-1 is a peptide hormone, released from intestinal L-cells in response to hormonal, neural and nutrient stimuli. In addition to potentiation of meal-stimulated insulin secretion, GLP-1 signaling exerts numerous pleiotropic effects on various tissues, including protective effects on the myocardium and vascular endothelium. Recent studies also report protective effects of GLP-1 based therapy on the formation of aneurysms in animal models and direct effects of GLP-1 signaling on the molecular mechanisms suggested to influence TAA formation, including inflammation, proteolytic activity and collagen composition. In this narrative review, we present the available evidence for effects of GLP-1 on experimental aneurysm development and discuss the potential role of GLP-1 in aneurysm formation based on available data from pre-clinical and clinical studies.
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Jantarajit, Walailak, Kornkamon Lertsuwan, Jarinthorn Teerapornpuntakit, Nateetip Krishnamra, and Narattaphol Charoenphandhu. "CFTR-mediated anion secretion across intestinal epithelium-like Caco-2 monolayer under PTH stimulation is dependent on intermediate conductance K+channels." American Journal of Physiology-Cell Physiology 313, no. 1 (July 1, 2017): C118—C129. http://dx.doi.org/10.1152/ajpcell.00010.2017.
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Parathyroid hormone (PTH), a pleiotropic hormone that maintains mineral homeostasis, is also essential for controlling pH balance and ion transport across renal and intestinal epithelia. Optimization of luminal pH is important for absorption of trace elements, e.g., calcium and phosphorus. We have previously demonstrated that PTH rapidly stimulated electrogenic [Formula: see text] secretion in intestinal epithelial-like Caco-2 monolayers, but the underlying cellular mechanism, contributions of other ions, particularly Cl–and K+, and long-lasting responses are not completely understood. Herein, PTH and forskolin were confirmed to induce anion secretion, which peaked within 1–3 min (early phase), followed by an abrupt decay and plateau that lasted for 60 min (late phase). In both early and late phases, apical membrane capacitance was increased with a decrease in basolateral capacitance after PTH or forskolin exposure. PTH also induced a transient increase in apical conductance with a long-lasting decrease in basolateral conductance. Anion secretion in both phases was reduced under [Formula: see text]-free and/or Cl−-free conditions or after exposure to carbonic anhydrase inhibitor (acetazolamide), CFTR inhibitor (CFTRinh-172), Na+/H+exchanger (NHE)-3 inhibitor (tenapanor), or K+channel inhibitors (BaCl2, clotrimazole, and TRAM-34; basolateral side), the latter of which suggested that PTH action was dependent on basolateral K+recycling. Furthermore, early- and late-phase responses to PTH were diminished by inhibitors of PI3K (wortmannin and LY-294002) and PKA (PKI 14–22). In conclusion, PTH requires NHE3 and basolateral K+channels to induce [Formula: see text] and Cl−secretion, thus explaining how PTH regulated luminal pH balance and pH-dependent absorption of trace minerals.
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Agbemafle, Barbara M., Thomas J. Oesterreicher, Chad A. Shaw, and Susan J. Henning. "Immediate early genes of glucocorticoid action on the developing intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 5 (May 2005): G897—G906. http://dx.doi.org/10.1152/ajpgi.00454.2004.
Full textAbstract:
Prior studies have demonstrated that glucocorticoid hormones elicit functional maturation of the small intestine as evidenced by their ability to induce increases in the expression of various digestive hydrolases, such as sucrase-isomaltase and trehalase. However, these increases have a lag time of ∼24 h, suggesting that they are secondary effects of hormone action. To identify candidate primary response genes, we performed microarray analysis on pooled RNA from jejunums of untreated postnatal day 8 mouse pups and from littermates who earlier received dexamethasone 2 h. Fluorescent dye-labeled samples were hybridized in quadruplicate to glass-spotted cDNA microarrays containing 15,000 cDNA clones from the National Institute of Aging cDNA clone set. Analysis of the resulting signals using relatively stringent criteria identified 66 transcripts upregulated and 36 downregulated by 2 h of glucocorticoid treatment. Among the upregulated transcripts, the magnitude of the increase detected by microarray ranged from 1.4- to 16-fold. Selected mRNAs from throughout the range were subsequently analyzed by Northern blot analysis. Of 11 mRNAs chosen all were confirmed, and there was a strong correlation between the magnitude of the increase observed from the microarray analysis and from Northern blot analysis. Additional time points showed that these transcripts peaked between 2 and 6 h and had returned to baseline by 24 h. Gene ontology analysis showed pleiotropic effects of dexamethasone on the developing intestine and pointed to genes in the development category as being likely candidates for mediation of glucocorticoid-induced maturation of intestinal function.
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Kundu, Parag, Hae Ung Lee, Isabel Garcia-Perez, Emmy Xue Yun Tay, Hyejin Kim, Llanto Elma Faylon, Katherine A. Martin, et al. "Neurogenesis and prolongevity signaling in young germ-free mice transplanted with the gut microbiota of old mice." Science Translational Medicine 11, no. 518 (November 13, 2019): eaau4760. http://dx.doi.org/10.1126/scitranslmed.aau4760.
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The gut microbiota evolves as the host ages, yet the effects of these microbial changes on host physiology and energy homeostasis are poorly understood. To investigate these potential effects, we transplanted the gut microbiota of old or young mice into young germ-free recipient mice. Both groups showed similar weight gain and skeletal muscle mass, but germ-free mice receiving a gut microbiota transplant from old donor mice unexpectedly showed increased neurogenesis in the hippocampus of the brain and increased intestinal growth. Metagenomic analysis revealed age-sensitive enrichment in butyrate-producing microbes in young germ-free mice transplanted with the gut microbiota of old donor mice. The higher concentration of gut microbiota–derived butyrate in these young transplanted mice was associated with an increase in the pleiotropic and prolongevity hormone fibroblast growth factor 21 (FGF21). An increase in FGF21 correlated with increased AMPK and SIRT-1 activation and reduced mTOR signaling. Young germ-free mice treated with exogenous sodium butyrate recapitulated the prolongevity phenotype observed in young germ-free mice receiving a gut microbiota transplant from old donor mice. These results suggest that gut microbiota transplants from aged hosts conferred beneficial effects in responsive young recipients.
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Thomas, Linto, Jessica A. Dominguez Rieg, and Timo Rieg. "Npt2a as a target for treating hyperphosphatemia." Biochemical Society Transactions 50, no. 1 (January 7, 2022): 439–46. http://dx.doi.org/10.1042/bst20211005.
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Hyperphosphatemia results from an imbalance in phosphate (Pi) homeostasis. In patients with and without reduced kidney function, hyperphosphatemia is associated with cardiovascular complications. The current mainstays in the management of hyperphosphatemia are oral Pi binder and dietary Pi restriction. Although these options are employed in patients with chronic kidney disease (CKD), they seem inadequate to correct elevated plasma Pi levels. In addition, a paradoxical increase in expression of intestinal Pi transporter and uptake may occur. Recently, studies in rodents targeting the renal Na+/Pi cotransporter 2a (Npt2a), responsible for ∼70% of Pi reabsorption, have been proposed as a potential treatment option. Two compounds (PF-06869206 and BAY-767) have been developed which are selective for Npt2a. These Npt2a inhibitors significantly increased urinary Pi excretion consequently lowering plasma Pi and PTH levels. Additionally, increases in urinary excretions of Na+, Cl− and Ca2+ have been observed. Some of these results are also seen in models of reduced kidney function. Responses of FGF23, a phosphaturic hormone that has been linked to the development of left ventricular hypertrophy in CKD, are ambiguous. In this review, we discuss the recent advances on the role of Npt2a inhibition on Pi homeostasis as well as other pleiotropic effects observed with Npt2a inhibition.
Dissertations / Theses on the topic "Intestinal pleiotropic hormone"
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NARDINI, PATRIZIA. "The study of the enteric nervous system in the distal colon: the GLP-2 protective effects against cisplatin-induced neuropathy and the neo-neurogenesis in colon-rectal cancer." Doctoral thesis, 2019. http://hdl.handle.net/2158/1152066.
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Studio della co-somministrazione di un ormone endogeno GLP-2 e Cisplatino come terapia adiuvante in grado di alleviare i noti e frequenti effetti collaterali associati al tratto gastrointestinale durante il trattamento chemioterapico a lungo termine.
Study of the co-administration between the endogenous hormone GLP-2 and Cisplatin as adjuvant therapy able to alleviate the frequent and well known gastrointestinal side effects during long-term chemotherapy treatment.