Vasoactive Intestinal Peptide (VIP)*
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Actions of Vasoactive Intestinal Peptide on the Rat Adrenal Zona Glomerulosa
51 Actions of vasoactive intestinal peptide on the rat adrenal zona glomerulosa J P Hinson, J R Puddefoot and S Kapas1 Molecular and Cellular Biology Section, Division of Biomedical Sciences, St Bartholomew’s and The Royal London School of Medicine and Dentistry, Queen Mary and Westfield College, Mile End Road, London E1 4NS, UK 1Oral Diseases Research Centre, St Bartholomew’s and The Royal London School of Medicine and Dentistry, 2 Newark Street, London E1 2AT, UK (Requests for offprints should be addressed to J P Hinson) Abstract Previous studies, by this group and others, have shown that The response to VIP in adrenals obtained from rats fed vasoactive intestinal peptide (VIP) stimulates aldosterone a low sodium diet was also investigated. Previous studies secretion, and that the actions of VIP on aldosterone have found that adrenals from animals on a low sodium secretion by the rat adrenal cortex are blocked by â diet exhibit increased responsiveness to VIP. Specific VIP adrenergic antagonists, suggesting that VIP may act by binding sites were identified, although the concentration the local release of catecholamines. The present studies or affinity of binding sites in the low sodium group was not were designed to test this hypothesis further, by measur- significantly different from the controls. In the low sodium ing catecholamine release by adrenal capsular tissue in group VIP was found to increase catecholamine release to response to VIP stimulation. the same extent as in the control group, however, in Using intact capsular tissue it was found that VIP caused contrast to the control group, the adrenal response to VIP a dose-dependent increase in aldosterone secretion, with a was not altered by adrenergic antagonists in the low concomitant increase in both adrenaline and noradrenaline sodium group. -
Affect Breast Cancer Risk
HOW HORMONES AFFECT BREAST CANCER RISK Hormones are chemicals made by the body that control how cells and organs work. Estrogen is a female hormone made mainly in the ovaries. It’s important for sexual development and other body functions. From your first monthly period until menopause, estrogen stimulates normal breast cells. A higher lifetime exposure to estrogen may increase breast cancer risk. For example, your risk increases if you start your period at a young age or go through menopause at a later age. Other hormone-related risks are described below. Menopausal hormone therapy Pills Menopausal hormone therapy (MHT) is The U.S. Food and Drug Administration also known as postmenopausal hormone (FDA) recommends women use the lowest therapy and hormone replacement dose that eases symptoms for the shortest therapy. Many women use MHT pills to time needed. relieve hot flashes and other menopausal Any woman currently taking or thinking symptoms. MHT should be used at the Birth control about taking MHT pills should talk with her lowest dose and for the shortest time pills (oral doctor about the risks and benefits. contraceptives) needed to ease menopausal symptoms. Long-term use can increase breast cancer Vaginal creams, suppositories Current or recent use risk and other serious health conditions. and rings of birth control pills There are 2 main types of MHT pills: slightly increases breast Vaginal forms of MHT do not appear to cancer risk. However, estrogen plus progestin and estrogen increase the risk of breast cancer. However, this risk is quite small alone. if you’ve been diagnosed with breast cancer, vaginal estrogen rings and suppositories are because the risk of Estrogen plus progestin MHT breast cancer for most better than vaginal estrogen creams. -
HORMONES and SPORT Insulin, Growth Hormone and Sport
13 HORMONES AND SPORT Insulin, growth hormone and sport P H Sonksen Guy’s, King’s and St Thomas’ School of Medicine, St Thomas’ Hospital, London SE1 7EH, UK; Email: [email protected] Abstract This review examines some interesting ‘new’ histories of blood rather than urine samples. The first method has a insulin and reviews our current understanding of its window of opportunity lasting about 24 h after an injec- physiological actions and synergy with GH in the regu- tion and is most suitable for ‘out of competition’ testing. lation of metabolism and body composition. It reviews the The second method has reasonable sensitivity for as long as history of GH abuse that antedates by many years the 2 weeks after the last injection of GH and is uninfluenced awareness of endocrinologists to its potent anabolic actions. by extreme exercise and suitable for post-competition Promising methods for detection of GH abuse have been samples. This method has a greater sensitivity in men than developed but have yet to be sufficiently well validated to in women. The specificity of both methods seems accept- be ready for introduction into competitive sport. So far, ably high but lawyers need to decide what level of there are two promising avenues for detecting GH abuse. scientific probability is needed to obtain a conviction. Both The first uses immunoassays that can distinguish the methods need further validation before implementation. isomers of pituitary-derived GH from the monomer of Research work carried out as part of the fight against recombinant human GH. The second works through doping in sport has opened up a new and exciting area of demonstrating circulating concentrations of one or more endocrinology. -
Thyroid Hormones in Fetal Growth and Prepartum Maturation
A J FORHEAD and A L FOWDEN Thyroid hormones and fetal 221:3 R87–R103 Review development Thyroid hormones in fetal growth and prepartum maturation A J Forhead1,2 and A L Fowden1 Correspondence should be addressed 1Department of Physiology, Development and Neuroscience, University of Cambridge, Physiology Building, to A L Fowden Downing Street, Cambridge CB2 3EG, UK Email 2Department of Biological and Medical Sciences, Oxford Brookes University, Oxford OX3 0BP, UK [email protected] Abstract The thyroid hormones, thyroxine (T4) and triiodothyronine (T3), are essential for normal Key Words growth and development of the fetus. Their bioavailability in utero depends on " thyroid hormones development of the fetal hypothalamic–pituitary–thyroid gland axis and the abundance " intrauterine growth of thyroid hormone transporters and deiodinases that influence tissue levels of bioactive " maturation hormone. Fetal T4 and T3 concentrations are also affected by gestational age, nutritional and " neonatal adaptation endocrine conditions in utero, and placental permeability to maternal thyroid hormones, which varies among species with placental morphology. Thyroid hormones are required for the general accretion of fetal mass and to trigger discrete developmental events in the fetal brain and somatic tissues from early in gestation. They also promote terminal differentiation of fetal tissues closer to term and are important in mediating the prepartum maturational effects of the glucocorticoids that ensure neonatal viability. Thyroid hormones act directly through anabolic effects on fetal metabolism and the stimulation of fetal oxygen Journal of Endocrinology consumption. They also act indirectly by controlling the bioavailability and effectiveness of other hormones and growth factors that influence fetal development such as the catecholamines and insulin-like growth factors (IGFs). -
Recent Advances in Vasoactive Intestinal Peptide Physiology And
F1000Research 2019, 8(F1000 Faculty Rev):1629 Last updated: 28 NOV 2019 REVIEW Recent advances in vasoactive intestinal peptide physiology and pathophysiology: focus on the gastrointestinal system [version 1; peer review: 4 approved] Mari Iwasaki1, Yasutada Akiba 1,2, Jonathan D Kaunitz 1,3 1Greater Los Angeles Veterans Affairs Healthcare System, Los Angeles, CA, USA 2Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA 3Departments of Medicine and Surgery, UCLA School of Medicine, Los Angeles, CA, USA First published: 12 Sep 2019, 8(F1000 Faculty Rev):1629 ( Open Peer Review v1 https://doi.org/10.12688/f1000research.18039.1) Latest published: 12 Sep 2019, 8(F1000 Faculty Rev):1629 ( https://doi.org/10.12688/f1000research.18039.1) Reviewer Status Abstract Invited Reviewers Vasoactive intestinal peptide (VIP), a gut peptide hormone originally 1 2 3 4 reported as a vasodilator in 1970, has multiple physiological and pathological effects on development, growth, and the control of neuronal, version 1 epithelial, and endocrine cell functions that in turn regulate ion secretion, published nutrient absorption, gut motility, glycemic control, carcinogenesis, immune 12 Sep 2019 responses, and circadian rhythms. Genetic ablation of this peptide and its receptors in mice also provides new insights into the contribution of VIP towards physiological signaling and the pathogenesis of related diseases. F1000 Faculty Reviews are written by members of Here, we discuss the impact of VIP on gastrointestinal function and the prestigious F1000 Faculty. They are diseases based on recent findings, also providing insight into its possible commissioned and are peer reviewed before therapeutic application to diabetes, autoimmune diseases and cancer. -
Diabetes Is a Disease in Which the Body's Ability to Produce Or Respond
Early Signs and Symptoms of diabetes: Early symptoms of diabetes, especially type 2 diabetes, can be subtle or seemingly harmless. Over time, however, you may Diabetes is a disease in which the develop diabetes complications, even if you body’s ability to produce or respond to haven't had diabetes symptoms. In the the hormone insulin is impaired, United States alone, more than 8 million resulting in abnormal metabolism of people have undiagnosed diabetes, Treatments: carbohydrates and elevated levels of according to the American Diabetes Association. Understanding possible glucose (sugar) in the blood. • Insulin therapy diabetes symptoms can lead to early • Oral medications diagnosis and treatment and a lifetime of Diabetes can be broken down into • better health. If you're experiencing any of Diet changes two types, Type 1 and Type 2. Type 1 • Exercise diabetes involves the the following diabetes signs and symptoms, see your doctor. body attacking itself by The medications you take vary by mistake, this then the type of diabetes and how well the causes the body to stop making insulin. With medicine controls you blood glucose levels. Type 2 diabetes the Type 1 diabetics must have insulin. Type 2 body does not respond may or may not include insulin and may just like it should to the be controlled with diet and exercise alone. insulin the pancreas is If you notice any of these changes notify making. Your body tells the pancreas that it needs to make more insulin since the your health care provider. The earlier • insulin that is already there is not working. -
PROGESTERONE? PO Box12004 Like Estrogen, Which Gets Much More Public Attention, Progesterone Is a Female Sex Hormone
FOLD FOLD FOLD DO NOT PRINT DO NOT PRINT DO NOT PRINT Overland Park,KS66282 WHAT IS PROGESTERONE? PO Box12004 Like estrogen, which gets much more public attention, progesterone is a female sex hormone. Women produce it in the ovaries and adrenal glands, and during pregnancy in the placenta. With all the talk about estrogen, progesterone is sometimes left behind as the forgotten female hormone. UNDERSTANDING WHAT ARE HORMONES AND HOW DO THEY WORK? IS PROGESTIN THE SAME THING AS PROGESTERONE? Hormones are our bodies’ chemical messengers. PROGESTERONE They travel through the bloodstream to trigger certain No. Although these terms are often used interchangeably, activities or changes in the body. Hormones work by they do not mean the same thing. Progesterone refers binding to specialized areas of cells known as receptor to the hormone produced in the body, or produced sites. There they initiate a chain of events in specific from a plant source but still chemically identical to cells or organs. For example, progesterone has been human progesterone. In contrast, progestin is a known to initiate a calming effect in the brain, hormone that is synthetically produced and may differ reducing anxiety. in structure to progesterone. You may also have heard of progestogens. This is a general term that applies WHAT DOES PROGESTERONE DO? to the category of both natural and synthetic hormones that act like progesterone in the uterus. See the During the reproductive years, progesterone prepares difference in the molecular structure depicted below. the uterine lining (or womb) for pregnancy. Each month, progesterone levels rise following ovulation. -
Secretin and Autism: a Clue but Not a Cure
SCIENCE & MEDICINE Secretin and Autism: A Clue But Not a Cure by Clarence E. Schutt, Ph.D. he world of autism has been shaken by NBC’s broadcast connections could not be found. on Dateline of a film segment documenting the effect of Tsecretin on restoring speech and sociability to autistic chil- The answer was provided nearly one hundred years ago by dren. At first blush, it seems unlikely that an intestinal hormone Bayless and Starling, who discovered that it is not nerve signals, regulating bicarbonate levels in the stomach in response to a but rather a novel substance that stimulates secretion from the good meal might influence the language centers of the brain so cells forming the intestinal mucosa. They called this substance profoundly. However, recent discoveries in neurobiology sug- “secretin.” They suggested that there could be many such cir- gest several ways of thinking about the secretin-autism connec- culating substances, or molecules, and they named them “hor- tion that could lead to the breakthroughs we dream about. mones” based on the Greek verb meaning “to excite”. As a parent with more than a decade of experience in consider- A simple analogy might help. If the body is regarded as a commu- ing a steady stream of claims of successful treatments, and as a nity of mutual service providers—the heart and muscles are the pri- scientist who believes that autism is a neurobiological disorder, I mary engines of movement, the stomach breaks down foods for have learned to temper my hopes about specific treatments by distribution, the liver detoxifies, and so on—then the need for a sys- seeing if I could construct plausible neurobiological mechanisms tem of messages conveyed by the blood becomes clear. -
Potential for Gut Peptide-Based Therapy in Postprandial Hypotension
nutrients Review Potential for Gut Peptide-Based Therapy in Postprandial Hypotension Malcolm J. Borg 1, Cong Xie 1 , Christopher K. Rayner 1, Michael Horowitz 1,2, Karen L. Jones 1,2 and Tongzhi Wu 1,2,* 1 Adelaide Medical School and Centre of Research Excellence in Translating Nutritional Science to Good Health, The University of Adelaide, Adelaide 5000, Australia; [email protected] (M.J.B.); [email protected] (C.X.); [email protected] (C.K.R.); [email protected] (M.H.); [email protected] (K.L.J.) 2 Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide 5000, Australia * Correspondence: [email protected]; Tel.: +61-8-8313-6535 Abstract: Postprandial hypotension (PPH) is an important and under-recognised disorder resulting from inadequate compensatory cardiovascular responses to meal-induced splanchnic blood pool- ing. Current approaches to management are suboptimal. Recent studies have established that the cardiovascular response to a meal is modulated profoundly by gastrointestinal factors, including the type and caloric content of ingested meals, rate of gastric emptying, and small intestinal transit and absorption of nutrients. The small intestine represents the major site of nutrient-gut interactions and associated neurohormonal responses, including secretion of glucagon-like peptide-1, glucose- dependent insulinotropic peptide and somatostatin, which exert pleotropic actions relevant to the postprandial haemodynamic profile. This review summarises knowledge relating to the role of these gut peptides in the cardiovascular response to a meal and their potential application to the management of PPH. Keywords: postprandial hypotension; glucagon-like peptide-1; glucose-dependent insulinotropic Citation: Borg, M.J.; Xie, C.; Rayner, polypeptide; somatostatin; diabetes mellitus; autonomic failure C.K.; Horowitz, M.; Jones, K.L.; Wu, T. -
Effect of the Natural Sweetener Xylitol on Gut Hormone Secretion and Gastric Emptying in Humans: a Pilot Dose-Ranging Study
nutrients Article Effect of the Natural Sweetener Xylitol on Gut Hormone Secretion and Gastric Emptying in Humans: A Pilot Dose-Ranging Study Anne Christin Meyer-Gerspach 1,2,* , Jürgen Drewe 3, Wout Verbeure 4 , Carel W. le Roux 5, Ludmilla Dellatorre-Teixeira 5, Jens F. Rehfeld 6, Jens J. Holst 7 , Bolette Hartmann 7, Jan Tack 4, Ralph Peterli 8, Christoph Beglinger 1,2 and Bettina K. Wölnerhanssen 1,2,* 1 St. Clara Research Ltd. at St. Claraspital, 4002 Basel, Switzerland; [email protected] 2 Faculty of Medicine, University of Basel, 4001 Basel, Switzerland 3 Department of Clinical Pharmacology and Toxicology, University Hospital of Basel, 4001 Basel, Switzerland; [email protected] 4 Translational Research Center for Gastrointestinal Disorders, Catholic University of Leuven, 3000 Leuven, Belgium; [email protected] (W.V.); [email protected] (J.T.) 5 Diabetes Complications Research Centre, Conway Institute University College Dublin, 3444 Dublin, Ireland; [email protected] (C.W.l.R.); [email protected] (L.D.-T.) 6 Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, Denmark; [email protected] 7 Department of Biomedical Sciences and Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark; [email protected] (J.J.H.); [email protected] (B.H.) 8 Department of Surgery, Clarunis, St. Claraspital, 4002 Basel, Switzerland; [email protected] * Correspondence: [email protected] (A.C.M.-G.); [email protected] (B.K.W.); Tel.: +41-61-685-85-85 (A.C.M.-G. -
Growth Hormone-Releasing Hormone in Lung Physiology and Pulmonary Disease
cells Review Growth Hormone-Releasing Hormone in Lung Physiology and Pulmonary Disease Chongxu Zhang 1, Tengjiao Cui 1, Renzhi Cai 1, Medhi Wangpaichitr 1, Mehdi Mirsaeidi 1,2 , Andrew V. Schally 1,2,3 and Robert M. Jackson 1,2,* 1 Research Service, Miami VAHS, Miami, FL 33125, USA; [email protected] (C.Z.); [email protected] (T.C.); [email protected] (R.C.); [email protected] (M.W.); [email protected] (M.M.); [email protected] (A.V.S.) 2 Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33101, USA 3 Department of Pathology and Sylvester Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33101, USA * Correspondence: [email protected]; Tel.: +305-575-3548 or +305-632-2687 Received: 25 August 2020; Accepted: 17 October 2020; Published: 21 October 2020 Abstract: Growth hormone-releasing hormone (GHRH) is secreted primarily from the hypothalamus, but other tissues, including the lungs, produce it locally. GHRH stimulates the release and secretion of growth hormone (GH) by the pituitary and regulates the production of GH and hepatic insulin-like growth factor-1 (IGF-1). Pituitary-type GHRH-receptors (GHRH-R) are expressed in human lungs, indicating that GHRH or GH could participate in lung development, growth, and repair. GHRH-R antagonists (i.e., synthetic peptides), which we have tested in various models, exert growth-inhibitory effects in lung cancer cells in vitro and in vivo in addition to having anti-inflammatory, anti-oxidative, and pro-apoptotic effects. One antagonist of the GHRH-R used in recent studies reviewed here, MIA-602, lessens both inflammation and fibrosis in a mouse model of bleomycin lung injury. -
Plasma Hormones Facilitated the Hypermotility of the Colon in a Chronic Stress Rat Model
Plasma Hormones Facilitated the Hypermotility of the Colon in a Chronic Stress Rat Model Chengbai Liang, Hesheng Luo*, Ying Liu, Jiwang Cao, Hong Xia Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China Abstract Objective: To study the relationship between brain-gut peptides, gastrointestinal hormones and altered motility in a rat model of repetitive water avoidance stress (WAS), which mimics the irritable bowel syndrome (IBS). Methods: Male Wistar rats were submitted daily to 1-h of water avoidance stress (WAS) or sham WAS (SWAS) for 10 consecutive days. Plasma hormones were determined using Enzyme Immunoassay Kits. Proximal colonic smooth muscle (PCSM) contractions were studied in an organ bath system. PCSM cells were isolated by enzymatic digestion and IKv and IBKca were recorded by the patch-clamp technique. Results: The number of fecal pellets during 1 h of acute restraint stress and the plasma hormones levels of substance P (SP), thyrotropin-releasing hormone (TRH), motilin (MTL), and cholecystokinin (CCK) in WAS rats were significantly increased compared with SWAS rats, whereas vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP) and corticotropin releasing hormone (CRH) in WAS rats were not significantly changed and peptide YY (PYY) in WAS rats was significantly decreased. Likewise, the amplitudes of spontaneous contractions of PCSM in WAS rats were significantly increased comparing with SWAS rats. The plasma of WAS rats (100 ml) decreased the amplitude of spontaneous contractions of controls. The IKv and IBKCa of PCSMs were significantly decreased in WAS rats compared with SWAS rats and the plasma of WAS rats (100 ml) increased the amplitude of IKv and IBKCa in normal rats.