Preface

The emergence of type 2 diabetes (T2D) as a global pandemic is one of the major challenges to health care in the 21st century. This book is about diabetes type 2 and it covers the newest scientific concepts in the pathogenesis of the disease as well as approaches in the diagnosis and control of diabetes and possible complications.

An important and extensively discussed topic is the progression of prediabetes to type 2 diabetes and possible lifestyle and pharmacological intervention. The role of oxidative stress, DNA damage, and DNA repair in the diabetes' progression is elucidated and the molecular impact of nutritional interventions in patients with T2D is also addressed.

The main focus of this book is glucose monitoring using cutting-edge technologies and the treatment of diabetes, especially in association with obesity. A novel cyber-physical system for management and self-management of cardiometabolic health is presented. Overall, technologies in mobile, computer, email, and internet approaches have shown evidence in enhancing chronic disease management, via supporting clinician decision-making and facilitating patient self-management among diabetic patients.

Updates on glucose lowering therapy are presented, and the new emerging class of SGLT2 inhibitors is discussed in detail. Part of the book is dedicated to the effect of diabetes on mental functions and treatment strategies to prevent cognitive decline. This book aims to contribute to the professional development of physicians, internists, endocrinologists, medical students, and research scientists in diabetes.

**II**

**Chapter 7 113**

**Chapter 8 135**

Cyber-Physical System for Management and Self-Management

Health Information Technologies in Diabetes Management

of Cardiometabolic Health

*byYilin Yoshida and Eduardo J. Simoes*

*by Zsolt Peter Ori*

**Mira Siderova, MD, PhD** Associate Professor, Medical University of Varna, University Hospital St. Marina, Varna, Bulgaria

**1**

Section 1

Pathogenesis of Type 2

Diabetes and Its

Complications

Section 1

Pathogenesis of Type 2 Diabetes and Its Complications

**3**

**Chapter 1**

**Abstract**

Emerging Role of Pancreatic

*Alpana Mukhuty, Chandrani Fouzder, Snehasis Das* 

*and Dipanjan Chattopadhyay*

glucotoxicity, type 2 diabetes

**1. Introduction**

β-Cells during Insulin Resistance

In today's world, type 2 diabetes has become a part of every household and leads

to various complications including high blood sugar level, diabetic retinopathy, diabetic foot, diabetic nephropathy and diabetic neuropathy. Yet people lack awareness about this disease and its detrimental effects. For a better understanding of this disease we must know about the causes and preventive measures since the medications used in treating type 2 diabetes have moderate to severe side effects. Type 2 diabetes is characterized by loss of insulin receptor activity in skeletal muscle and adipocytes, compensatory insulin secretion from pancreatic β-cells, β-cell dysfunction and death. The proper functioning of β-cells is a major criterion for preventing advent of type 2 diabetes. The different natural or physiological insulin secretagogues include glucose, amino acids and fatty acids, which stimulate insulin secretion under the influence of various hormones like incretins, leptin, growth hormone, melatonin and estrogen. However, excess of nutrients lead to β-cell dysfunction and dearth of insulin involving various signal molecules like SIRT1, PPARγ, TLR4, NF-ΚB, Wnt, mTOR, inflammasomes, MCP1, EGFR, and Nrf2. A deeper insight into the functioning of these signaling molecules will also create new avenues for therapeutic interventions of curing β-cell dysfunction and death.

**Keywords:** insulin resistance, pancreatic β-cell dysfunction, lipotoxicity,

Changing food habits, sedentary lifestyle and obesity has made type 2 diabetes (T2D) a global epidemic. T2D has various characteristic features such as insulin resistance caused when peripheral tissues such as liver, muscle and adipocytes have a decreased response to insulin. The progression from normal glucose tolerance to type 2 diabetes involves several transitional stages of impaired fasting glucose and impaired glucose tolerance which is known as prediabetes. The mechanism leading to the development of these glucose metabolic alterations is multifactorial. The most prevalent factor of T2D is insulin resistance that occurs when peripheral tissues such as liver, muscle and adipocytes, the main target organs of Insulin hormone, loses the ability to respond to insulin [1]. Generally in the obese patients without T2D and initially in people who develop insulin resistance, pancreatic β-cells are able to compensate for insulin resistance by increasing insulin secretion by increasing β-cell mass via increased proliferation and hypertrophy [2, 3].
