Challenge of Diabetes Mellitus and Researchers' Contributions to Its
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Type 3 Diabetes and Its Role Implications in Alzheimer's Disease
International Journal of Molecular Sciences Review Type 3 Diabetes and Its Role Implications in Alzheimer’s Disease 1, 2, 3 Thuy Trang Nguyen y, Qui Thanh Hoai Ta y, Thi Kim Oanh Nguyen , Thi Thuy Dung Nguyen 4,* and Vo Van Giau 5,6,* 1 Faculty of Pharmacy, Ho Chi Minh City University of Technology (HUTECH), Ho Chi Minh City 700000, Vietnam; [email protected] 2 Institute of Research and Development, Duy Tan University, Danang 550000, Vietnam; [email protected] 3 Faculty of Food Science and Technology, Ho Chi Minh City University of Food Industry, Ho Chi Minh City 700000, Vietnam; oanhntk@hufi.edu.vn 4 Faculty of Environmental and Food Engineering, Nguyen Tat Thanh University, Ho Chi Minh City 700000, Vietnam 5 Graduate School of Environment Department of Industrial and Environmental Engineering, Gachon University, 1342 Sungnam-daero, Sujung-gu, Seongnam-si, Gyeonggi-do 461-701, Korea 6 Department of Bionano Technology, Gachon Medical Research Institute, Gachon University, 1342 Sungnam-daero, Sujung-gu, Seongnam-si, Gyeonggi-do 461-701, Korea * Correspondence: [email protected] (T.T.D.N.); [email protected] (V.V.G.) These authors contributed equally to this work. y Received: 12 April 2020; Accepted: 28 April 2020; Published: 30 April 2020 Abstract: The exact connection between Alzheimer’s disease (AD) and type 2 diabetes is still in debate. However, poorly controlled blood sugar may increase the risk of developing Alzheimer’s. This relationship is so strong that some have called Alzheimer’s “diabetes of the brain” or “type 3 diabetes (T3D)”. Given more recent studies continue to indicate evidence linking T3D with AD, this review aims to demonstrate the relationship between T3D and AD based on the fact that both the processing of amyloid-β (Aβ) precursor protein toxicity and the clearance of Aβ are attributed to impaired insulin signaling, and that insulin resistance mediates the dysregulation of bioenergetics and progress to AD. -
Diabetes and Dementia Mario Barbagallo* and Ligia J
Barbagallo and Dominguez. Int J Diabetes Clin Res 2015, 2:4 ISSN: 2377-3634 International Journal of Diabetes and Clinical Research Commentary: Open Access Diabetes and Dementia Mario Barbagallo* and Ligia J. Dominguez Geriatric Unit, Department DIBIMIS, University of Palermo, Italy *Corresponding author: Mario Barbagallo, UOC di Geriatria e Lungodegenza, AOUP Azienda Universitaria Policlinico, University of Palermo, Italy, Tel: +390916552885, Fax: +390916552952, E-mail: [email protected] speed and executive functions [13,14]. Not only frank dementia, Abstract but also mild cognitive impairment (MCI) is associated with DM2, Persons with type 2 diabetes mellitus (DM2) have an increased as well as an accelerated progression from MCI to dementia [15]. incidence of cognitive decline and dementia. An increased cortical Dementia is the most common comorbidity in persons with diabetes and subcortical atrophy has been found after controlling for in nursing homes [16]. vascular disease and inadequate cerebral circulation. A possible role of insulin resistance and hyperinsulinemia has been suggested Several studies on the cerebral structure of patients with diabetes to mediate the link between DM2 and Alzheimer’s Disease (AD). have evidenced increased cortical and subcortical atrophy (besides Altered insulin signaling may contribute to AD biochemical and increased leukoaraiosis and cerebrovascular disease), which were histopathological lesions. Both hyperglycemia and hypoglycemia associated with impaired cognitive performance [17,18]. Insulin may contribute to cognitive decline in DM2. Recurrent symptomatic and asymptomatic hypoglycemic episodes have been suggested itself and insulin resistance have been suggested as mediators of to cause subclinical brain damage, and permanent cognitive AD-type neurodegeneration. It has been proposed that AD may be impairment. -
Ruthenium-Catalyzed CH Functionalization Of(Hetero)
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Science and Technology 1465 Ruthenium-catalyzed C-H Functionalization of (Hetero)arenes KARTHIK DEVARAJ ACTA UNIVERSITATIS UPSALIENSIS ISSN 1651-6214 ISBN 978-91-554-9783-5 UPPSALA urn:nbn:se:uu:diva-310998 2017 Dissertation presented at Uppsala University to be publicly examined in B22, BMC, Husargatan 3, Uppsala, Uppsala, Friday, 24 February 2017 at 09:30 for the degree of Doctor of Philosophy. The examination will be conducted in English. Faculty examiner: Professor Victor A. Snieckus (Department of Chemistry, Queen's University, Canada). Abstract Devaraj, K. 2017. Ruthenium-catalyzed C-H Functionalization of (Hetero)arenes. Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Science and Technology 1465. 59 pp. Uppsala: Acta Universitatis Upsaliensis. ISBN 978-91-554-9783-5. This thesis concerned about the Ru-catalyzed C-H functionalizations on the synthesis of 2- arylindole unit, silylation of heteroarenes and preparation of aryne precursor. In the first project, we developed the Ru-catalyzed C2-H arylation of N-(2-pyrimidyl) indoles and pyrroles with nucleophilic arylboronic acids under oxidative conditions. Wide variety of arylboronic acids afforded the desired product in excellent yield regardless of the substituents or functional group electronic nature. Electron-rich heteroarenes are well suited for this method than electron-poor heteroarenes. Halides such as bromide and iodide also survived, further derivatisation of the halide is shown by Heck alkenylation. In order to find catalytic on-cycle intermediate extensive mechanistic experiments have been carried out by preparing presumed ruthenacyclic complexes and C-H/D exchange reactions. -
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wjpls, 2020, Vol. 6, Issue 8, 61-75 Review Article ISSN 2454-2229 Mitali et al. World Journal of Pharmaceutical and Life Science World Journal of Pharmaceutical and Life Sciences WJPLS www.wjpls.org SJIF Impact Factor: 6.129 INSULIN THERAPY AND IT’S NEW APPROACHES Tejaswini S. Kawanpure and Dr. Mitali M. Bodhankar* Gurunanak College of Pharmacy, Near Dixit Nagar, Nari Road, Nagpur- 440026. Corresponding Author: Dr. Mitali M. Bodhankar Gurunanak College of Pharmacy, Near Dixit Nagar, Nari Road, Nagpur- 440026. Article Received on 01/06/2020 Article Revised on 22/06/2020 Article Accepted on 12/07/2020 ABSTRACT Diabetes mellitus is a serious pathologic condition which is responsible for major healthcare problems worldwide Insulin replacement therapy has been used in the clinical Management of diabetes mellitus for more than 84 years. Insulin has remained indispensable in dispensable in management of diabetes mellitus since its discovery in 1921. Comparatively, a large percentage of world population is affected by diabetes mellitus, out of which approximately 5-10% with type 1 diabetes while the remaining 90% with type 2. The present mode of insulin administration is by the subcutaneous route through which insulin introduced into the body in a non-physiological manner having many challenges. Hence novel approaches for insulin delivery are being explored. Challenges that have adverse effect on oral route of insulin administration mainly includes rapid enzymatic degradation in the stomach, inactivation and digestion by proteolytic enzymes in the intestinal lumen and poor permeability across intestinal epithelium because of its high molecular weight and its lipophilicity. Approaches such as liposomes, micro emulsions, nano cubicle, insulin chewing gum and so forth have been prepared to ensure the oral delivery of insulin. -
Clinical Practice Guideline for Diagnosis, Treatment and Follow-Up of Diabetes Mellitus and Its Complications - 2019
THE SOCIETY of ENDOCRINOLOGY and METABOLISM of TURKEY (SEMT) Clinical Practice Guideline for Diagnosis, Treatment and Follow-up of Diabetes Mellitus and Its Complications - 2019 English Version of the 12th Edition SEMT Diabetes Mellitus Working Group ISBN: 978-605-4011-39-1 CLINICAL PRACTICE GUIDELINE FOR DIAGNOSIS, TREATMENT, AND FOLLOW-UP OF DIABETES MELLITUS AND ITS COMPLICATIONS-2019 © SEMT -2019 This material has been published and distributed by The Society of Endocrinology and Metabolism of Turkey (SEMT). Whole or part of this guideline cannot be reproduced or used for commercial purposes without permission. THE SOCIETY of ENDOCRINOLOGY and METABOLISM of TURKEY (SEMT) Meşrutiyet Cad., Ali Bey Apt. 29/12, Kızılay 06420, Ankara, Turkey Phone. +90 312 425 2072 http://www.temd.org.tr ISBN: 978-605-4011-39-1 English Version of the 12th Edition Publishing Services BAYT Bilimsel Araştırmalar Basın Yayın ve Tanıtım Ltd. Şti. Ziya Gökalp Cad. 30/31 Kızılay 06420, Ankara, Turkey Phone. +90 312 431 3062 Fax +90 312 431 3602 www.bayt.com.tr Printing Miki Matbaacılık San. ve Tic. Ltd. Şti. Matbaacılar Sanayi Sitesi 1516/1 Sk. No. 27 İvedik, Yenimahalle / Ankara, Turkey Phone. +90 312 395 2128 Print Date: October 23, 2019 “Major achievements and important undertakings are only possible through collaborations” “Büyük işler, mühim teşebbüsler; ancak, müşterek mesai ile kabil-i temindir.” MUSTAFA KEMAL ATATÜRK, 1925 PREFACE Dear colleagues, The prevalence of diabetes has been increasing tremendously in the last few decades. As a result , medical professionals/ specialists from different fields encounter many diabetics in their daily practice. At this point, updated guidelines on diabetes management, which take regional specification into consideration is needed. -
Diabetes and Health
Diabetes and Health Diabetes Prevention and Control Program Population and Community Health Bureau Public Health Division NM Department of Health Jill Joseph, Nurse Consultant May 21, 2021 1190 S. St. Francis Drive • Santa Fe, NM 87505 • Phone: 505-827-2613 • Fax: 505-827-2530 • nmhealth.org • Jill Joseph BSN • Nurse Consultant, Diabetes Prevention and Control Program • [email protected] • (505) 476-7618 • There are no conflicts of interest to disclose 1190 S. St. Francis Drive • Santa Fe, NM 87505 • Phone: 505-827-2613 • Fax: 505-827-2530 • nmhealth.org Today’s Discussion • Introduction • Diabetes Basics • Diabetes defined • Common forms • Uncommon forms • Risk Factors/Complications • Management • Prevention • Questions 1190 S. St. Francis Drive • Santa Fe, NM 87505 • Phone: 505-827-2613 • Fax: 505-827-2530 • nmhealth.org New Mexico Department of Health Diabetes Prevention and Control Program • Prevent or delay diabetes • Prevent complications, disabilities, and burden associated with diabetes and related chronic conditions • Advance health equity to improve health outcomes and quality of life among all New Mexicans. 1190 S. St. Francis Drive • Santa Fe, NM 87505 • Phone: 505-827-2613 • Fax: 505-827-2530 • nmhealth.org JJ1 Diabetes and Prediabetes Why talk about these? • Because of the numbers • Because diabetes has profound effects on our bodies 1190 S. St. Francis Drive • Santa Fe, NM 87505 • Phone: 505-827-2613 • Fax: 505-827-2530 • nmhealth.org Slide 5 JJ1 Jill Joseph, 5/17/2021 Diabetes is: • A disorder of the body’s ability to process food for energy use. The food we eat is turned into glucose, or sugar, for our bodies to use for energy. -
(12) Patent Application Publication (10) Pub. No.: US 2016/0220631 A1 Mezey Et Al
US 2016O220631A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2016/0220631 A1 Mezey et al. (43) Pub. Date: Aug. 4, 2016 (54) METHODS OF MODULATING Publication Classification ERYTHROPOESS WITH ARGINNE VASOPRESSIN RECEPTOR 1B MOLECULES (51) Int. Cl. A638/II (2006.01) (71) Applicant: THE USA, AS REPRESENTED BY A613 L/404 (2006.01) THE SECRETARY DEPARTMENT A613 L/46.5 (2006.01) OF HEALTH AND HUMAN A638/8 (2006.01) SERVICES, Bethesda, MD (US) A6II 45/06 (2006.01) (52) U.S. Cl. (72) Inventors: Eva M. Mezey, Rockville, MD (US); CPC ............. A61K 38/11 (2013.01); A61 K38/1816 Balazs Mayer, Budakeszi (HU); (2013.01); A61K 45/06 (2013.01); A61 K Krisztian Nemeth, Budapest (HU); 3 1/465 (2013.01); A61 K31/404 (2013.01) Miklos Krepuska, Rockville, MD (US) (73) Assignee: The USA, as represented by the (57) ABSTRACT Secretary, Departm-ent of Health and Disclosed are methods of modulating erythropoiesis with Human Service, Bethesda, MD (US) arginine vasopressin receptor 1B (AVPR1B) molecules, such Appl. No.: as AVPR1B agonists or antagonists. In one example, a (21) 15/022,531 method of stimulating erythropoiesis is disclosed including (22) PCT Fled: Oct. 1, 2014 administering an effective amount of an AVPR1B stimulatory molecule to a subject in need thereof, thereby stimulating (86) PCT NO.: PCT/US2O14/058613 erythropoiesis. Also disclosed is a method of stimulating hematopoetic stem cell (HSC) proliferation which includes S371 (c)(1), administering an effective amount of an AVPR1B stimulatory (2) Date: Mar. 16, 2016 molecule to a subject in need thereof, thereby stimulating HSC proliferation. -
Constitutive Endocytic Cycle of the CB1 Cannabinoid Receptor. Christophe Leterrier, Damien Bonnard, Damien Carrel, Jean Rossier, Zsolt Lenkei
Constitutive endocytic cycle of the CB1 cannabinoid receptor. Christophe Leterrier, Damien Bonnard, Damien Carrel, Jean Rossier, Zsolt Lenkei To cite this version: Christophe Leterrier, Damien Bonnard, Damien Carrel, Jean Rossier, Zsolt Lenkei. Constitutive endocytic cycle of the CB1 cannabinoid receptor.. Journal of Biological Chemistry, American Society for Biochemistry and Molecular Biology, 2004, 279 (34), pp.36013-36021. 10.1074/jbc.M403990200. hal-00250336 HAL Id: hal-00250336 https://hal.archives-ouvertes.fr/hal-00250336 Submitted on 6 Feb 2018 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Supplemental Material can be found at: http://www.jbc.org/cgi/content/full/M403990200/DC1 THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 279, No. 34, Issue of August 20, pp. 36013–36021, 2004 © 2004 by The American Society for Biochemistry and Molecular Biology, Inc. Printed in U.S.A. Constitutive Endocytic Cycle of the CB1 Cannabinoid Receptor*□S Received for publication, April 9, 2004, and in revised form, June 9, 2004 Published, JBC Papers in Press, June -
Pancreatic Diabetes
CHAPTER Pancreatic Diabetes 163 Sidhartha Das, SK Tripathy, BP Panda INTRODUCTION and is now called Pancreatic Diabetes or Type 3c Diabetes. Pancreatic or pancreatogenic diabetes is a form of There was a time when the cyanide containing cassava secondary diabetes where pancreatic diseases with was thought to be the cause of chronic pancreatitis and exocrine deficiency leads to endocrine dysfunction diabetes. Epidemiological studies had shown that this resulting in defective glucose homeostasis. Though it type of diabetes was common in the countries of tropics was felt over last few decades that patient’s suffering where cassava consumption was high in the diet of from diabetes mellitus who have pancreatic diseases like countries like Brazil, Africa and South India particularly chronic pancreatitis, cystic fibrosis, post pancreatectomy Kerala. Now a days various causes of chronic pancreatitis states, pancreatic carcinoma etc. behave in a different are incrimated in Pancreatic Diabetes.3 1 manner from that of Type 1 & Type 2 diabetic patients , Later pancreatic diabetes due to other causes like chronic only over last few years it was proved to be a distinct pancreatitis, pancreatic carcinoma etc. was given separate entity needing specific tailored approach. DM due to recognition by ADA & WHO as Type 3C diabetes, in the cystic fibrosis was recognized as a distinct clinical state current classification & criteria for its diagnosis was laid because the patients have poor nutritional status, severe down. (Table 1) respiratory inflammatory symptoms, increased mortality rate from respiratory failure.2 They needed special care in EPIDEMIOLOGY evaluation and treatment. This type of secondary diabetes In the general population prevalence of Type 2 DM is was called CFRD (cystic fibrosis related diabetes) where around 8%.5 As awareness regarding the pancreatic exocrine defect altered the pancreatic endocrine system. -
Can Alzheimer Disease Be a Form of Type 3 Diabetes?
CORE Metadata, citation and similar papers at core.ac.uk Provided by Archivio istituzionale della ricerca - Università di Palermo REJUVENATION RESEARCH Volume 15, Number 2, 2012 ª Mary Ann Liebert, Inc. DOI: 10.1089/rej.2011.1289 Can Alzheimer Disease Be a Form of Type 3 Diabetes? Giulia Accardi,1 Calogero Caruso,1 Giuseppina Colonna-Romano,1 Cecilia Camarda,2 Roberto Monastero,2 and Giuseppina Candore1 Abstract Alzheimer disease (AD) and metabolic syndrome are two highly prevalent pathological conditions of Western society due to incorrect diet, lifestyle, and vascular risk factors. Recent data have suggested metabolic syndrome as an independent risk factor for AD and pre-AD syndrome. Furthermore, biological plausibility for this rela- tionship has been framed within the ‘‘metabolic cognitive syndrome’’ concept. Due to the increasing aging of populations, prevalence of AD in Western industrialized countries will rise in the near future. Thus, new knowledge in the area of molecular biology and epigenetics will probably help to make an early molecular diagnosis of dementia. An association between metabolic syndrome and specific single-nucleotide poly- lmorphisms (SNPs) in the gene INPPL1, encoding for SHIP2, a SH2 domain-containing inositol 5-phosphatase involved in insulin signaling, has been described. According to recent data suggesting that Type 2 diabetes represents an independent risk factor for AD and pre-AD, preliminary results of a case–control study performed to test the putative association between three SNPs in the SHIP2 gene and AD show a trend toward association of these SNPs with AD. Introduction However, today some different pathophysiological theo- ries regarding AD exist, suggesting that the disease could be lzheimer disease (AD) is the most common form of driven by inflammation, vascular changes, and metabolic Adementia, accounting for more than 50% of all cases disorders. -
Engagement of Β-Arrestin by Transactivated Insulin-Like Growth Factor Receptor Is Needed for V2 Vasopressin Receptor-Stimulated ERK1/2 Activation
Engagement of β-arrestin by transactivated insulin-like growth factor receptor is needed for V2 vasopressin receptor-stimulated ERK1/2 activation Geneviève Oligny-Longpréa, Maithé Corbanib, Joris Zhoua, Mireille Hoguea, Gilles Guillonb, and Michel Bouviera,1 aInstitut de Recherche en Immunologie et Cancérologie, Département de Biochimie and Groupe de Recherche Universitaire sur le Médicament, Universitéde Montréal, Montréal, QC, Canada H3C 3J7; and bInstitut de Génomique Fonctionnelle, Département d’Endocrinologie, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5203, Institut National de la Santé et de la Recherche Médicale Unité 661, Universités Montpellier I et II, 34094 Montpellier Cedex 05, France Edited* by Jean-Pierre Changeux, Institut Pasteur, Paris, France, and approved March 9, 2012 (received for review August 12, 2011) G protein-coupled receptors (GPCRs) have been shown to activate ceptor (EGFR) and has only been described for EGFR ligands the mitogen-activated protein kinases, ERK1/2, through both G thus far (5, 6). Although GPCR-mediated transactivation of protein-dependent and -independent mechanisms. Here, we de- several other RTKs [including the PDGF (7), FGF (8), VEGF scribe a G protein-independent mechanism that unravels an un- (9), and tropomyosin-receptor kinase A (TrkA) (10) receptors] anticipated role for β-arrestins. Stimulation of the V2 vasopressin leading to MAPK activation has been documented, the specific receptor (V2R) in cultured cells or in vivo in rat kidney medullar mechanism responsible for the RTK engagement remains poorly collecting ducts led to the activation of ERK1/2 through the metal- characterized. Intracellular scaffolding that promotes the forma- loproteinase-mediated shedding of a factor activating the insulin- tion of protein complexes with nonreceptor tyrosine kinases, such – like growth factor receptor (IGFR). -
Insulin in the Nervous System and the Mind: Functions in Metabolism, Memory, and Mood
Insulin in the nervous system and the mind: Functions in metabolism, memory, and mood The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Lee, Seung-Hwan, Janice M. Zabolotny, Hu Huang, Hyon Lee, and Young-Bum Kim. 2016. “Insulin in the nervous system and the mind: Functions in metabolism, memory, and mood.” Molecular Metabolism 5 (8): 589-601. doi:10.1016/j.molmet.2016.06.011. http:// dx.doi.org/10.1016/j.molmet.2016.06.011. Published Version doi:10.1016/j.molmet.2016.06.011 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:29407539 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 Review Insulin in the nervous system and the mind: Functions in metabolism, memory, and mood Seung-Hwan Lee 1,2,5, Janice M. Zabolotny 1,5, Hu Huang 1,3, Hyon Lee 4, Young-Bum Kim 1,* ABSTRACT Background: Insulin, a pleotrophic hormone, has diverse effects in the body. Recent work has highlighted the important role of insulin’s action in the nervous system on glucose and energy homeostasis, memory, and mood. Scope of review: Here we review experimental and clinical work that has broadened the understanding of insulin’s diverse functions in the central and peripheral nervous systems, including glucose and body weight homeostasis, memory and mood, with particular emphasis on intranasal insulin.