Enhancement by Human Placenta! Lactogen of Mammary Hyperplastic Nodules in Ovariectomized Mice1
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Therapeutic Approaches to Preserve Islet Mass in Type 2 Diabetes
24 Dec 2005 16:24 AR ANRV262-ME57-17.tex XMLPublishSM(2004/02/24) P1: OJO 10.1146/annurev.med.57.110104.115624 Annu. Rev. Med. 2006. 57:265–81 doi: 10.1146/annurev.med.57.110104.115624 Copyright c 2006 by Annual Reviews. All rights reserved THERAPEUTIC APPROACHES TO PRESERVE ISLET MASS IN TYPE 2DIABETES Laurie L. Baggio and Daniel J. Drucker Department of Medicine, Toronto General Hospital, Banting and Best Diabetes Center, University of Toronto, Toronto, Ontario, Canada M5S 2S2; email: [email protected] KeyWords β-cell mass, apoptosis, neogenesis, proliferation ■ Abstract Type 2 diabetes is characterized by hyperglycemia resulting from in- sulin resistance in the setting of inadequate β-cell compensation. Currently available therapeutic agents lower blood glucose through multiple mechanisms but do not directly reverse the decline in β-cell mass. Glucagon-like peptide-1 (GLP-1) receptor agonists, exemplified by Exenatide (exendin-4), not only acutely lower blood glucose but also engage signaling pathways in the islet β-cell that lead to stimulation of β-cell repli- cation and inhibition of β-cell apoptosis. Similarly, glucose-dependent insulinotropic polypeptide (GIP) receptor activation stimulates insulin secretion, enhances β-cell proliferation, and reduces apoptosis. Moreover, potentiation of the endogenous post- prandial levels of GLP-1 and GIP via inhibition of dipeptidyl peptidase-IV (DPP-IV) also expands β-cell mass via related mechanisms. The thiazolidinediones (TZDs) en- hance insulin sensitivity, reduce blood glucose levels, and also preserve β-cell mass, although it remains unclear whether TZDs affect β-cell mass via direct mechanisms. Complementary approaches to regeneration of β-cell mass involve combinations of factors, exemplified by epidermal growth factor and gastrin, which promote islet neo- genesis and ameliorate diabetes in rodent studies. -
Strategies to Increase ß-Cell Mass Expansion
This electronic thesis or dissertation has been downloaded from the King’s Research Portal at https://kclpure.kcl.ac.uk/portal/ Strategies to increase -cell mass expansion Drynda, Robert Lech Awarding institution: King's College London The copyright of this thesis rests with the author and no quotation from it or information derived from it may be published without proper acknowledgement. END USER LICENCE AGREEMENT Unless another licence is stated on the immediately following page this work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International licence. https://creativecommons.org/licenses/by-nc-nd/4.0/ You are free to copy, distribute and transmit the work Under the following conditions: Attribution: You must attribute the work in the manner specified by the author (but not in any way that suggests that they endorse you or your use of the work). Non Commercial: You may not use this work for commercial purposes. No Derivative Works - You may not alter, transform, or build upon this work. Any of these conditions can be waived if you receive permission from the author. Your fair dealings and other rights are in no way affected by the above. Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 Strategies to increase β-cell mass expansion A thesis submitted by Robert Drynda For the degree of Doctor of Philosophy from King’s College London Diabetes Research Group Division of Diabetes & Nutritional Sciences Faculty of Life Sciences & Medicine King’s College London 2017 Table of contents Table of contents ................................................................................................. -
Leptin Stimulates Pituitary Prolactin Release Through an Extracellular Signal-Regulated Kinase-Dependent Pathway
275 Leptin stimulates pituitary prolactin release through an extracellular signal-regulated kinase-dependent pathway Christian K Tipsmark, Christina N Strom, Sean T Bailey and Russell J Borski Department of Zoology, North Carolina State University, Raleigh, North Carolina 27695-7617, USA (Correspondence should be addressed to C K Tipsmark who is now at Institute of Biology, University of Southern Denmark, Campusvej 55, DK-5230 Odense M, Denmark; Email: [email protected]) Abstract Leptin was initially identified as a regulator of appetite and leptin are mediated by the activation of extracellular signal- weight control centers in the hypothalamus, but appears to be regulated kinase (ERK1/2) but nothing is known about the involved in a number of physiological processes. This study cellular mechanisms by which leptin might regulate PRL was carried out to examine the possible role of leptin in secretion in vertebrates. We therefore tested whether regulating prolactin (PRL) release using the teleost pituitary ERK1/2 might be involved in the leptin PRL response and model system. This advantageous system allows isolation of a found that the ERK inhibitor, PD98059, hindered leptin- nearly pure population of lactotropes in their natural, in situ induced PRL release. We further analyzed leptin response by aggregated state. The rostral pars distalis were dissected from quantifying tyrosine and threonine phosphorylation of tilapia pituitaries and exposed to varying concentrations of ERK1/2 using western blots. One hour incubation with leptin (0, 1, 10, 100 nM) for 1 h. Release of PRL was leptin induced a concentration-dependent increase in stimulated by leptin in a potent and concentration-dependent phosphorylated, and thus active, ERK1/2. -
Interleukin 6 Inhibits Mouse Placental Lactogen II but Not Mouse Placental Lactogen I Secretion in Vitro (Trophoblast/Pregnancy/Cytokine) M
Proc. Natl. Acad. Sci. USA Vol. 90, pp. 11905-11909, December 1993 Physiology Interleukin 6 inhibits mouse placental lactogen II but not mouse placental lactogen I secretion in vitro (trophoblast/pregnancy/cytokine) M. YAMAGUCHI*t, L. OGREN*, J. N. SOUTHARD*, H. KURACHI*, A. MIYAKEt, AND F. TALAMANTES*§ *Department of Biology, University of California, Santa Cruz, CA 95064; and tDepartment of Obstetrics and Gynecology, Osaka University Medical School, Osaka, Japan 565 Communicated by George E. Seidel, Jr., September 7, 1993 (receivedfor review June 9, 1993) ABSTRACT The mouse placenta produces several poly- members ofthe PRL-GH gene family. We have used primary peptides belonging to the prolactin-growth hormone gene fam- cultures of placental cells from several days of pregnancy to ily, including mouse placental lactogen (mPL) I and mPL-II. demonstrate that IL-6 regulates the secretion of mPL-II, but The present study was undertaken to determine whether the not mPL-I, and that the sensitivity of mPL-II secretion to secretion of mPL-I and mPL-H is regulated by interleukin 6 IL-6 varies during gestation. (IL-6), which is present in the placenta and has previously been reported to stimulate the secretion ofpituitary members of this gene family. Effects of human and mouse IL-6 on mPL-I and MATERIALS AND METHODS mPL-II secretion were examined in primary cultures of pla- Hormones, Cytokines, and Antisera. mPL-II and recombi- cental cells from days 7, 9, and 12 of pregnancy. IL-6 caused nant mPL-I were purified as described (10, 16). Rabbit a dose-dependent reduction in the mPL-HI concentration in the anti-mPL-I and rabbit anti-mPL-II antisera have been de- medium of cells from days 9 and 12 of pregnancy but did not scribed (11, 16). -
Placental Growth Hormone-Related Proteins and Prolactin-Related Proteins
Placental Growth Hormone-Related Proteins and Prolactin-Related Proteins The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Haig, D. 2008. Placental growth hormone-related proteins and prolactin-related proteins. Placenta 29: 36-41. Published Version doi:10.1016/j.placenta.2007.09.010 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:11148777 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Placental growth hormone-related proteins and prolactin-related proteins. David Haig Department of Organismic and Evolutionary Biology, Harvard University, 26 Oxford Street, Cambridge MA 02138. e-mail: [email protected] phone: 617-496-5125 fax: 617-495-5667 Keywords: GH, PRL, placenta, endometrial glands, placental lactogen The placentas of ruminants and muroid rodents express prolactin (PRL)-related genes whereas the placentas of anthropoid primates express growth hormone (GH)-related genes. The evolution of placental expression is associated with acclerated evolution of the corresponding pituitary hormone and destabilization of conserved endocrine systems. In particular, placental hormones often evolve novel interactions with new receptors. The adaptive functions of some placental hormones may be revealed only under conditions of physiological stress. Introduction Placental hormones are produced by offspring, but act on receptors of mothers. As such, placental hormones and maternal receptors are prime candidates for the expression of parent-offspring conflict [1,2]. -
Pathophysiology of Gestational Diabetes Mellitus: the Past, the Present and the Future
6 Pathophysiology of Gestational Diabetes Mellitus: The Past, the Present and the Future Mohammed Chyad Al-Noaemi1 and Mohammed Helmy Faris Shalayel2 1Al-Yarmouk College, Khartoum, 2National College for Medical and Technical Studies, Khartoum, Sudan 1. Introduction It is just to remember that “Pathophysiology” refers to the study of alterations in normal body function (physiology and biochemistry) which result in disease. E.g. changes in the normal thyroid hormone level causes either hyper or hypothyroidism. Changes in insulin level as a decrease in its blood level or a decrease in its action will cause hyperglycemia and finally diabetes mellitus. Scientists agreed that gestational diabetes mellitus (GDM) is a condition in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy. From our experience most women with GDM in the developing countries are not aware of the symptoms (i.e., the disease will be symptomless). While some of the women will have few symptoms and their GDM is most commonly diagnosed by routine blood examinations during pregnancy which detect inappropriate high level of glucose in their blood samples. GDM should be confirmed by doing fasting blood glucose and oral glucose tolerance test (OGTT), according to the WHO diagnostic criteria for diabetes. A decrease in insulin sensitivity (i.e. an increase in insulin resistance) is normally seen during pregnancy to spare the glucose for the fetus. This is attributed to the effects of placental hormones. In a few women the physiological changes during pregnancy result in impaired glucose tolerance which might develop diabetes mellitus (GDM). The prevalence of GDM ranges from 1% to 14% of all pregnancies depending on the population studied and the diagnostic tests used. -
The Importance of Determining Human
JMB 2009; 28 (2) DOI: 10.2478/v10011-009-0003-1 UDK 577.1 : 61 ISSN 1452-8258 JMB 28: 97–100, 2009 Original paper Originalni nau~ni rad THE IMPORTANCE OF DETERMINING HUMAN PLACENTAL LACTOGEN IN THE THIRD TRIMESTER OF PREGNANCY ZNA^AJ ODRE\IVANJA HUMANOG PLACENTALNOG LAKTOGENA U TRE]EM TRIMESTRU TRUDNO]E Jasmina Durkovi}1, Bojana Mandi}2 1Department of Genetics , Town Hospital, Subotica, Serbia 2Mega Lab, Biochemical Laboratory, Subotica, Serbia Summary: Human placental lactogen (HPL) is a hormone Kratak sadr`aj: Humani placentalni laktogen (HPL) jeste produced by the placenta with a role in the re gu lation of hormon koji izlu~uje placenta i regulator je fetoplacen- fetoplacental growth. In this paper, the results of HPL de- talnog rasta. U radu su prikazani rezultati odre|ivanja HPL- termination in the third trimester of pregnancy are pre- a u tre}em trimestru trudno}e, sa ciljem da se ispita senzi - sented with the aim of testing the sensitivity of this bio - tivnost tog biohemijskog markera za otkrivanje poreme}aja chemical marker for detecting placental dysfunction, fetal funkcije placente, vitaliteta fetusa i rizika za lo{ ishod. vitality and risk of bad outcome. The tests were performed Ispitivanje je obavljeno na uzorku od 370 rizi~nih trudno}a on 370 women with high-risk pregnancy, between the 20th izme|u 20 i 36 nedelje trudno}e. HPL je odre|en ELISA and 36th week of pregnancy. HPL was determined by an metodom, testovima »Bioserv Diagnostics«, a rezultati su ELISA method using Bioserv Diagnostics tests and the o~itani na rideru »STAT–FAX 303+«. -
Fetal Growth Signals
Arch Dis Child: first published as 10.1136/adc.64.1_Spec_No.53 on 1 January 1989. Downloaded from Archives of Disease in Childhood, 1989, 64, 53-57 Current topic Fetal growth signals R D G MILNER AND D J HILL Department of Paediatrics, Children's Hospital, Sheffield Human fetal growth is not uniform. Tissue patterns growth factor fi like peptide is found in the vegetal and organ primordia are established during embryo- pole ectoderm of the early Xenopus embryo and is genesis, then from the end of the first trimester and transcribed by a maternally derived gene designated throughout the second the fetus undergoes massive Vgl. An ectodermal cell line, XTC, from the meta- hyperplasia. In the third trimester further organ morphosing tadpole releases a transforming growth modelling and functional maturation occur in pre- factor I8 like peptide in vitro.5 In the 11-18 day fetal paration for extrauterine life. Each aspect ofdevelop- mouse transforming growth factor 3 can be detected ment requires orchestrated intercellular signalling at in bone and connective tissue, particularly that two levels. The release of peptide growth factors derived from neural crest such as palate, larynx, and the modulation of an extracellular matrix are facial mesenchyme, and teeth.6 Staining was most paracrine actions that occur within cell populations intense at sites of tissue morphogenesis affecting and between adjacent germ layers. In contrast, mesodermal and epithelial interaction such as hair endocrine hormones may stimulate growth non- follicles, teeth, and secondary palate. copyright. specifically or promote specific maturational events. Recently both fibroblast growth factor and trans- The interactions between paracrinology, endocrino- forming growth factor i have been shown to exert logy, and environmental constraints to growth remarkable effects on embryonal morphology. -
The Endocrine Function of the Placenta: Interactions Between Trophic Peptides and Hormones
Placenlal Function and Fetal Nutrition, edited by Frederick C. Battaglia, Nestle Nutrition Workshop Series. Vol. 39. Nestec Ltd.. Vevey/Lippincott-Raven Publishers. Philadelphia. © 1997. The Endocrine Function of the Placenta: Interactions Between Trophic Peptides and Hormones Lise Cedard U. 361 INSERM, Maternite Baudelocque, 121 Boulevard de Port-Royal Paris, France The placenta is classically considered to be a source of hormones that play an important role in the establishment and maintenance of pregnancy. Because of its hemochorial structure, the human placenta produces hormones and easily secretes them into the maternal circulation. They include steroid hormones, such as estrogens and progesterone, and protein hormones, the most important of which are the chori- onic gonadotrophins (hCG), discovered in 1927. During the period from 1960 to 1980, the concept of a fetoplacental unit (1) with a complementary role for the fetus in steroid production offered a new approach to steroid metabolism, and since then new proteins and neuropeptides have been discovered (2,3). However, the lack of innervation of placental tissue highlights the importance of understanding neuroen- docrine regulation of placental physiology. Sophisticated culture methods enabling the study of biologic phenomena occurring during transformation of cytotrophoblast cells into a syncytiotrophoblast (4) have been combined with electron microscopy and histochemistry. Possibilities offered by molecular biology, including in situ hybridization and molecular cloning studies, -
Regulation of Glucokinase As Lslets Adapt to Pregnancy
Matschinsky FM, Magnuson MA (eds): Glucokinase and Glycemic Disease: From Basics to Novel Therapeutics. Front Diabetes. Basel, Karger, 2004, vol 16, pp 222-239 Regulationof Glucokinaseas lsletsAdapt to Pregnancy RobertL. Sorenson,Anthony J. Weinhaus,T. Clark Brelje Department of Genetics Cell Biology and Development, University of Minnesota Medical School, Minneapolis,Minn., USA Pregnancyis an occasionin the life history of the B-cell where there is an increasedneed for insulinthat'occurs over a relativelyshort period of time. This amountsto daysin rodentsand monthsin humans.The needfor enhanced islet function emergesas a consequenceof an increasein peripheralinsulin resistanceat the sametime as the placenta,a major targetorgan for insulin, develops.To accommodatethis increasein insulin demand,the islet must undergochanges that lead to increasedinsulin secretionunder normal glucose conditions. The primary short-termregulation of insulin secretionis achievedby ele- vating the glucoseconcentration. However, if this were the primary adaptive mechanismsduring pregnancy,there would be a need for persistenthyper- glycemia- a conditiondeleterious to the developingembryo, fetus and mother. Thus, in the face of this increaseddemand for insulin, islets must undergo structuraland functional changes.The outcomeof this long term upregulation of isletsmust be enhancedinsulin secretion at normalglucose levels. Failure of this long-termadaptive process can lead to gestationaldiabetes. Evidence for functional changes in islets during pregnancy first appearedin the 1960sshortly after the developmentof a sensitiveradioimm- unoassayfor insulin. Spellacyand coworkers[1 3] reportedthat there was a progressiveincrease in both fasting and glucose-stimulatedinsulin secretion throughoutthe courseof pregnancy.These and subsequentstudies led to the charucterizationof pregnancyas a condition of elevatedserum insulin levels, slightly lower blood glucose levels and peripheralinsulin resistance(see reviews[4, 5]). -
Rfamide Peptides: Structure, Function, Mechanisms and Pharmaceutical Potential
Pharmaceuticals 2011, 4, 1248-1280; doi:10.3390/ph4091248 OPEN ACCESS Pharmaceuticals ISSN 1424-8247 www.mdpi.com/journal/pharmaceuticals Review RFamide Peptides: Structure, Function, Mechanisms and Pharmaceutical Potential Maria Findeisen †, Daniel Rathmann † and Annette G. Beck-Sickinger * Institute of Biochemistry, Leipzig University, Brüderstraße 34, 04103 Leipzig, Germany; E-Mails: [email protected] (M.F.); [email protected] (D.R.) † These authors contributed equally to this work. * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +49-341-9736900; Fax: +49-341-9736909. Received: 29 August 2011; in revised form: 9 September 2011 / Accepted: 15 September 2011 / Published: 21 September 2011 Abstract: Different neuropeptides, all containing a common carboxy-terminal RFamide sequence, have been characterized as ligands of the RFamide peptide receptor family. Currently, five subgroups have been characterized with respect to their N-terminal sequence and hence cover a wide pattern of biological functions, like important neuroendocrine, behavioral, sensory and automatic functions. The RFamide peptide receptor family represents a multiligand/multireceptor system, as many ligands are recognized by several GPCR subtypes within one family. Multireceptor systems are often susceptible to cross-reactions, as their numerous ligands are frequently closely related. In this review we focus on recent results in the field of structure-activity studies as well as mutational exploration of crucial positions within this GPCR system. The review summarizes the reported peptide analogs and recently developed small molecule ligands (agonists and antagonists) to highlight the current understanding of the pharmacophoric elements, required for affinity and activity at the receptor family. -
Co-Regulation of Hormone Receptors, Neuropeptides, and Steroidogenic Enzymes 2 Across the Vertebrate Social Behavior Network 3 4 Brent M
bioRxiv preprint doi: https://doi.org/10.1101/435024; this version posted October 4, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Co-regulation of hormone receptors, neuropeptides, and steroidogenic enzymes 2 across the vertebrate social behavior network 3 4 Brent M. Horton1, T. Brandt Ryder2, Ignacio T. Moore3, Christopher N. 5 Balakrishnan4,* 6 1Millersville University, Department of Biology 7 2Smithsonian Conservation Biology Institute, Migratory Bird Center 8 3Virginia Tech, Department of Biological Sciences 9 4East Carolina University, Department of Biology 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 1 bioRxiv preprint doi: https://doi.org/10.1101/435024; this version posted October 4, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Running Title: Gene expression in the social behavior network 2 Keywords: dominance, systems biology, songbird, territoriality, genome 3 Corresponding Author: 4 Christopher Balakrishnan 5 East Carolina University 6 Department of Biology 7 Howell Science Complex 8 Greenville, NC, USA 27858 9 [email protected] 10 2 bioRxiv preprint doi: https://doi.org/10.1101/435024; this version posted October 4, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.