Diabetes and Aging-related Complications PDF
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Diabetes and Aging-related Complications Sho-ichi Yamagishi Editor 123 Diabetes and Aging-related Complications Sho-ichi Yamagishi Editor Diabetes and Aging-related Complications Editor Sho-ichi Yamagishi Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications Kurume University School of Medicine Kurume Fukuoka Japan ISBN 978-981-10-4375-8 ISBN 978-981-10-4376-5 (eBook) https://doi.org/10.1007/978-981-10-4376-5 Library of Congress Control Number: 2017955825 © Springer Nature Singapore Pte Ltd. 2018 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. 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The registered company address is: 152 Beach Road, #21-01/04 Gateway East, Singapore 189721, Singapore Preface According to the recent report of Diabetes Atlas in 2015, diabetes affects 415 mil- lion people worldwide, that is, one in every 11 adults is estimated to have diabetes, and half of them are undiagnosed. Further, it is expected that the number of diabetic patients will increase to 642 million by 2040. Diabetes and its associated metabolic derangements are one of the most important risk factors for aging-related and life- threatening disorders, such as atherosclerotic cardiovascular disease, chronic kid- ney disease, cancer, Alzheimer’s disease, and osteoporosis. Indeed, atherosclerotic cardiovascular disease accounts for about 60% of death in diabetic patients, and microvascular complications are leading causes of end-stage renal failure, acquired blindness, and foot amputations. In addition, hazard ratios of death from any cause, non-cardiovascular disease, and several cancers in diabetic patients are 1.8, 1.7, and 1.25, respectively, compared with nondiabetic individuals. Moreover, Alzheimer’s disease and osteoporotic bone fractures are highly prevalent in diabetes, and aver- age life span and healthy life expectancy of diabetic patients are about 10–15 years shorter than those of nondiabetic subjects. These observations suggest that diabetes and its numerous complications are a global health burden and that early detection and treatment of various diabetes-related complications are urgently needed for slowing the aging process and achieving a successful life in diabetic patients. This book entitled Diabetes and Aging-Related Complications deals with why and how aging process is accelerated under diabetes, providing valuable and comprehensive information for management of various types of diabetes- and aging-related disor- ders. I organized a symposium on diabetes and aging in the 58th Annual Meeting of Japan Geriatrics Society in 2016. I selected the contributors of chapters mainly from scientists who presented their updated data in the symposium. I think that the book helps most of the researchers and clinicians in the field of diabetes and its related complications acquire more updated knowledge about a diverse range of topics. Recently, there is accumulating evidence that cumulative hyperglycemic expo- sure has contributed to the development and progression of diabetes- and aging- related disorders. In the Diabetes Control and Complications Trial-Epidemiology of Diabetes Interventions and Complications (DCCT-EDIC) trials, former intensive therapy has been shown to be associated with the reduced risk of all-cause mortality v vi Preface over 27 years’ mean follow-up. The phenomenon is called as metabolic memory, thus suggesting that past hyperglycemic exposure may persistently cause chronic damage in numerous organs and tissues of diabetes that are not easily reversed, even by subsequent, relatively good glycemic control. In other words, the observations suggest that beneficial influence of early glycemic control on the risk of vascular complications and death is sustained in patients with diabetes. The readers of this book will also get information on underlying molecular mechanisms of the meta- bolic memory in diabetes. I hope that the book inspires readers to take various actions on behalf of diabetic patients. Kurume, Japan Sho-ichi Yamagishi, M.D., Ph.D. Contents 1 Diabetic Kidney Disease ..................................... 1 Mai Sugahara, Tetsuhiro Tanaka, Reiko Inagi, and Masaomi Nangaku 2 Diabetic Eye Disease ........................................ 19 Yuichi Kaji 3 Diabetic Neuropathy ........................................ 31 Soroku Yagihashi and Hiroki Mizukami 4 Diabetes and Endothelial Dysfunction ......................... 45 Tatsuya Maruhashi, Yasuki Kihara, and Yukihito Higashi 5 Diabetes and Vascular Calcification ........................... 59 Katsuhito Mori and Masaaki Inaba 6 Diabetes and Adipocyte Dysfunction .......................... 69 Yohko Yoshida, Ippei Shimizu, and Tohru Minamino 7 Diabetes and Liver Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85 Tsuguhito Ota 8 Diabetes and Alzheimer’s Disease ............................. 101 Shuko Takeda and Ryuichi Morishita 9 Diabetes and Cancers ....................................... 113 Hiroshi Noto 10 Diabetes and Osteoporosis ................................... 127 Ippei Kanazawa and Toshitsugu Sugimoto 11 Diabetes and Sarcopenia .................................... 141 Masaki Mogi and Masatsugu Horiuchi 12 Diabetes and Frailty ........................................ 153 Mitsutaka Yakabe and Sumito Ogawa vii viii Contents 13 Diabetes and LOH Syndrome ................................ 167 Hisamitsu Ide, Mayuko Kanayama, and Shigeo Horie 14 Diabetes and Female Sterility/Infertility. . . . . . . . . . . . . . . . . . . . . . . . 177 Kuniaki Ota, Hiroaki Ohta, and Sho-ichi Yamagishi 15 Diabetes and Periodontitis ................................... 185 Takanori Shinjo and Fusanori Nishimura 16 Diabetes and Advanced Glycation End Products ................ 201 Sho-ichi Yamagishi Chapter 1 Diabetic Kidney Disease Mai Sugahara, Tetsuhiro Tanaka, Reiko Inagi, and Masaomi Nangaku Abstract Renal senescence is accompanied by a gradual decrease in its function. Although it rarely causes clinical problems per se, superimposition of various dis- eases, such as diabetes, may accelerate this functional decline. Recent research has revealed some of the complex mechanisms of how diabetes promotes the aging process in the kidney, including the pathogenic roles of hemodynamic changes, tubulointerstitial hypoxia, oxidative stress, advanced glycation end-products, and impaired autophagy. Diabetes also modulates aging-related signaling pathways, such as sirtuins and mammalian target of rapamycin. Current therapeutic strategy for diabetic kidney disease consists of glycemic control and antihypertensive treat- ment with renin-angiotensin system inhibitors. However, they fail to fully prevent the progression of diabetic kidney disease, raising an urgent need for novel thera- peutic methods. Some pharmacological agents are being developed based on the knowledge of hemodynamic and molecular basis of diabetes- and aging-related kid- ney function decline. Keywords Diabetic kidney disease • Hypoxia • Oxidative stress • Advanced glyca- tion end-products • Autophagy 1.1 Introduction Aging is a universal process that affects all organs including the kidney. Even in healthy individuals, glomerular filtration rate (GFR) starts to decline at 30 years of age and proceeds at the rate of approximately 8 ml/min/1.73 m2 per decade [1]. This loss in renal function is largely attributed to hemodynamic changes within the kid- ney and age-related vulnerability to physiological stress, such as hypoxia and oxida- tive stress. M. Sugahara • T. Tanaka (*) • R. Inagi • M. Nangaku Division of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan e-mail: [email protected] © Springer Nature Singapore Pte Ltd. 2018 1 S.-i. Yamagishi (ed.), Diabetes and Aging-related Complications, https://doi.org/10.1007/978-981-10-4376-5_1 2 M. Sugahara et al. The rate of kidney function decline may increase with superimposition of vari- ous diseases. Diabetes is one of the strong drivers of this decline, and it accelerates the process of aging through several different mechanisms, such as hemodynamic changes, endothelial dysfunction, tubulointerstitial hypoxia, oxidative stress, accu- mulation of advanced glycation end-p roducts (AGEs), and impaired autophagy. Diabetes also modulates some aging-related signaling pathways including sirtuins and mammalian target of rapamycin (mTOR). This chapter discusses the pathogen- esis of diabetic kidney disease (DKD) in relation to aging process and introduces some potential therapeutic methods to cope with diabetes-related kidney function decline. 1.2 Hemodynamic Changes and Chronic Hypoxia at the Center of Aging Kidney and DKD 1.2.1 Vasculature of the Kidney (Fig. 1.1) [2] The kidney has a unique spatial arrangement of vasculature; it has two capillary networks that run in series. The renal artery bifurcates into interlobar arteries, arcu- ate arteries, interlobular arteries, and afferent arterioles. The afferent arterioles give Efferent Glomerular arteriole Interlobular artery capsule and vein Proximal convoluted tubule Arcuate artery Renal artery and vein Afferent arteriole Collecting duct Renal artery Distal tubule Renal vein Cortex Renal vein Ureter Medulla Loop of Henle Peritubular capillary network Fig. 1.1 Vasculature of the kidney. The renal artery bifurcates into interlobar arteries, arcuate arteries, interlobular arteries, and afferent arterioles. The afferent arterioles give rise to the first capillary network, the glomerulus, and they merge again at the vascular pole to form efferent arte- rioles. The efferent arterioles enter the second capillary network, the peritubular capillaries, which surround tubules and offer oxygen and nutrients to tubular and interstitial cells. The enlargement shows the architecture of a nephron with arrows indicating the direction of blood flow. Reprinted by permission from Macmillan Publishers Ltd.: Nat Rev. Nephrol 6: 667–78, © 2010
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