Watson / Dokken Glucose Intake and Utilization in Pre-Diabetes and Diabetes

Implications for Cardiovascular Disease
1. Auflage 2014
ISBN: 978-0-12-800579-8
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, 442 Seiten

This important reference, edited by Ronald Ross Watson and Betsy Dokken, collects the research needed to make the distinct connection between pre-diabetes, diabetes, and cardiovascular disease. Glucose Intake and Utilization in Pre-Diabetes and Diabetes: Implications for Cardiovascular Disease explains the mechanisms of progression from pre-diabetes to diabetes to cardiovascular disease. Since pre-diabetes and diabetes are important cardiovascular disease risk factors, and impaired glucose metabolism among cardiac patients is extremely prevalent, the importance of reviewing pre-diabetes and its involvement in CVD complications is vital as one applies food and glycemic control to slow progress to diabetes and heart disease. The book further focuses on glucose intake and utilization in diabetes, including coverage of diabetes in the development and pathology of cardiovascular disease, risks and epidemiology of cardiovascular problems promoted by diabetes, macrovascular effects and their safety in therapy of diabetics, beta cell biology and therapy of diabetes, and nutrition to modulate diabetes. - Offers a complete review of cardiac health problems occurring with significant frequency in patients relative to their ability to regulate glucose - Presents coverage of the role of glucose utilization, development of pre-diabetes and the ultimate development of various cardiovascular diseases - Provides thorough dietary, nutrition, complementary and alternative botanical therapies for pre-diabetes and diabetes to halt the progression to cardiovascular disease

Autoren/Hrsg.

Watson, Ronald Ross

Dokken, Betsy

Inhaltsverzeichnis

1;Front Cover;1
2;Glucose Intake and Utilization in Pre-Diabetes and Diabetes;4
3;Copyright Page;5
4;Dedication;6
5;Contents;8
6;List of Contributors;18
7;Preface;22
7.1;Part I: Pre-Diabetes in Health and Disease: Prevention and Treatment;22
7.1.1;Section 1: Modulation of Pre-Diabetes and Altered Glucose Metabolism: Pathophysiology, Drugs, Genetics, Epigenetics, and Nu...;22
7.1.1.1;Section 1A: Background on Pre-Diabetes and Its Management;22
7.1.1.2;Section 1B: Physiological Modulators of Pre-Diabetes and Cardiovascular Disease Development;22
7.1.2;Section 2: Nutrition and Food to Modulate Pre-Diabetes and Resulting Cardiac Disease;22
7.1.2.1;Section 2A: Mechanisms of Pre-Diabetes and Diabetes Modulation of Cardiac Tissues;22
7.1.2.2;Section 2B: Dietary Supplements in Prevention of Pre-Diabetes and Diabetes and Thus Related Cardiac Dysfunction;23
7.2;Part II: Diabetes;23
7.2.1;Section 3: Diabetes in Development and Pathology of Cardiovascular Disease;23
7.2.1.1;Section 3A: Role of Foods in Cardiovascular Problems Promoted by Diabetes;23
7.2.1.2;Section 3B: Exercise Diabetes and Cardiovascular Disease;23
7.2.1.3;Section 3C: Nutrition and Food to Modulate Diabetes: Heart and Vascular Health;23
8;About the Editors;24
9;Acknowledgments;26
10;I. Pre-Diabetes in Health and Disease: Prevention and Treatment;28
10.1;1 Modulation of Pre-Diabetes and Altered Glucose Metabolism: Pathophysiology, Drugs, Genetics, Epigenetics, and Nutrition;30
10.1.1;1A Background on pre-diabetes and its management;32
10.1.1.1;1 Early Origins of Health and Disease;32
10.1.1.1.1;Introduction;32
10.1.1.1.2;Developmental Programming of MS (CVD): Human Data;33
10.1.1.1.2.1;Excess Nutrients During Fetal Growth and Long-Term Consequences;33
10.1.1.1.2.1.1;Mechanisms Underlying Fetal Overgrowth;33
10.1.1.1.2.1.2;Effects of Maternal Gestational Weight Gain;33
10.1.1.1.2.1.3;Consequences of Being Large at Birth;33
10.1.1.1.2.1.4;Consequences of Exposure to Maternal Diabetes or Obesity In Utero;34
10.1.1.1.2.2;Undernutrition During Pregnancy as a Cause of MS and CVD;35
10.1.1.1.2.2.1;The Consequences of Being Small at Birth;35
10.1.1.1.2.2.2;The Thrifty Phenotype Hypothesis;35
10.1.1.1.2.2.3;Maternal Caloric Restriction: the Dutch Famine;35
10.1.1.1.2.2.4;The Consequences of Preterm Birth;35
10.1.1.1.2.3;Effects of Postnatal Nutrition and Catch-Up Growth;36
10.1.1.1.3;Developmental Programming of MS (CVD): Animal Models;37
10.1.1.1.3.1;Nutritional Modifications;37
10.1.1.1.3.1.1;Proteins and Caloric Restriction;37
10.1.1.1.3.1.2;Carbohydrates;38
10.1.1.1.3.1.3;High-Fat Diet;38
10.1.1.1.3.1.4;Neonatal Overnutrition and Catch-Up Growth;38
10.1.1.1.3.2;Animal Models of Human Type 1 and 2 Diabetes;38
10.1.1.1.3.2.1;Animal Models of T1D;38
10.1.1.1.3.2.1.1;Surgical Models;38
10.1.1.1.3.2.1.2;Chemical Model;38
10.1.1.1.3.2.1.3;Spontaneous Animal Models;39
10.1.1.1.3.2.1.3.1;NOD Mouse;39
10.1.1.1.3.2.1.3.2;BB Rat;39
10.1.1.1.3.2.2;Animal Models of T2D;39
10.1.1.1.3.2.2.1;Production of Spontaneous Diabetic Rats;39
10.1.1.1.3.2.2.2;Chemical Model;39
10.1.1.1.3.2.3;Animal Model of Gestational Diabetes;39
10.1.1.1.3.3;Uteroplacental Insufficiency;39
10.1.1.1.3.4;Glucocorticoids Exposure;39
10.1.1.1.4;Mechanisms;40
10.1.1.1.4.1;Oxidative Stress;40
10.1.1.1.4.2;Epigenetic Regulation;40
10.1.1.1.4.2.1;DNA Methylation;40
10.1.1.1.4.2.2;Histone Modifications;41
10.1.1.1.4.2.3;Non-coding RNAs;41
10.1.1.1.5;Conclusion;42
10.1.1.1.6;References;42
10.1.1.2;2 Diabetes and Obesity: The Impact of Their Coincidence on Health and Life;48
10.1.1.2.1;Introduction;48
10.1.1.2.1.1;Epidemiology;48
10.1.1.2.2;Pathophysiology;48
10.1.1.2.2.1;Metabolic Syndrome;50
10.1.1.2.3;Complications of Obesity and DM: Impact on Health and Life;50
10.1.1.2.3.1;Cardiovascular Complications;50
10.1.1.2.3.2;Renal Complications;51
10.1.1.2.3.3;Sexual Dysfunction;51
10.1.1.2.3.4;Osteoporosis;51
10.1.1.2.4;Ways to Prevent/Reduce the Risks;51
10.1.1.2.4.1;Lifestyle Modifications;51
10.1.1.2.4.1.1;Nutrition;51
10.1.1.2.4.1.2;Exercise;52
10.1.1.2.5;Medical Interventions;52
10.1.1.2.5.1;Pharmacotherapy;52
10.1.1.2.5.2;Bariatric Surgery;52
10.1.1.2.6;Summary;53
10.1.1.2.7;References;53
10.1.1.3;3 Diabetes: A New Horizon and Approach to Management;56
10.1.1.3.1;Introduction;56
10.1.1.3.2;Multidisciplinary Approach to Management;57
10.1.1.3.2.1;Glycemic Goals;57
10.1.1.3.2.2;Flexible Glycemic Targets;58
10.1.1.3.3;Non-Pharmacological Interventions for Glycemic Control;58
10.1.1.3.3.1;Diabetes Education;58
10.1.1.3.3.2;Lifestyle Modification;58
10.1.1.3.3.3;Dietary Modification;58
10.1.1.3.3.3.1;Exercise and Weight Reduction;59
10.1.1.3.3.3.2;Bariatric Surgery;59
10.1.1.3.4;Pharmacological Intervention for Diabetes Control;59
10.1.1.3.5;Monotherapy Versus Combination Therapy;59
10.1.1.3.5.1;Monotherapy;59
10.1.1.3.5.2;Combination Therapy;59
10.1.1.3.6;Classification of Pharmacological Agents;60
10.1.1.3.6.1;Insulin Sensitizers;60
10.1.1.3.6.1.1;Biguanides;60
10.1.1.3.6.1.2;Thiazilidinediones;61
10.1.1.3.6.2;Insulin Secretagogues;62
10.1.1.3.6.2.1;Sulfonylureas;62
10.1.1.3.6.2.2;Glinides;62
10.1.1.3.6.3;Alpha-Glucosidase Inhibitors;62
10.1.1.3.6.4;DPP-4 Inhibitors;63
10.1.1.3.6.5;Sodium-Glucose Co-Transporter Inhibitors;63
10.1.1.3.6.6;Injectable Anti-Diabetic Treatment;63
10.1.1.3.6.6.1;Insulin Therapy;63
10.1.1.3.6.6.1.1;Basal Insulins;64
10.1.1.3.6.6.1.2;Bolus Insulins;64
10.1.1.3.6.6.1.3;Premixed Insulins;65
10.1.1.3.6.6.1.4;Basal-Bolus Insulin Regimens;65
10.1.1.3.6.6.2;Side Effects of Insulin Therapy;65
10.1.1.3.6.6.2.1;Hypoglycemia;65
10.1.1.3.6.6.2.2;Weight Gain;65
10.1.1.3.6.6.2.3;Risk of Malignancy;65
10.1.1.3.6.6.3;GLP-1 Analogs;66
10.1.1.3.6.6.3.1;Exenatide;66
10.1.1.3.6.6.3.2;Liraglutide;66
10.1.1.3.6.6.3.3;Side Effects of GLP-1 Receptor Agonists;66
10.1.1.3.6.6.4;Pramlintide;66
10.1.1.3.7;New Therapeutic Modalities in Diabetes Management;67
10.1.1.3.7.1;Inhaled Insulin;67
10.1.1.3.7.2;New Insulin Analogs;67
10.1.1.3.7.3;Artificial Pancreas;67
10.1.1.3.7.3.1;Pancreas Transplantation;67
10.1.1.3.7.3.2;Islet Cell Transplantation;67
10.1.1.3.7.3.3;Islet Cell Regeneration Therapy;67
10.1.1.3.8;Key Recommendations to Achieve Optimum Diabetes Control;68
10.1.1.3.9;Conclusion;68
10.1.1.3.10;References;68
10.1.1.4;4 Psychosocial Factors Associated with Diabetes Self-Management;72
10.1.1.4.1;Psychosocial Factors Associated with Diabetes Self-Management;72
10.1.1.4.2;Self-Management Expectations and Adherence;72
10.1.1.4.3;Psychological Factors Associated with Diabetes Self-Management;73
10.1.1.4.3.1;Memory;73
10.1.1.4.3.2;Self-Efficacy;74
10.1.1.4.3.3;Diabetes-Related Distress, Depression, and Anxiety;74
10.1.1.4.4;Social Factors Associated with Diabetes Self-Management;75
10.1.1.4.4.1;Family and Friends;75
10.1.1.4.4.2;Patient–Provider Relationship;76
10.1.1.4.4.3;Broader Social Influences;77
10.1.1.4.5;Implications for Practice;78
10.1.1.4.6;Conclusion;79
10.1.1.4.7;References;79
10.1.1.5;5 The Relationship Between the Organization of Services for the Treatment of Type 2 Diabetes and the Risk of Long-Term Comp...;84
10.1.1.5.1;Introduction;84
10.1.1.5.1.1;Epidemiological Data;84
10.1.1.5.1.2;Diabetes Mellitus and Chronic Complications;84
10.1.1.5.2;Analysis of Current Organizational Systems;85
10.1.1.5.2.1;Analysis of Clinical Outcomes: Primary Care Physicians versus Diabetologists;85
10.1.1.5.2.2;Analysis of Organizational Models;85
10.1.1.5.3;The Role of the Diabetes Center;86
10.1.1.5.4;Integrated Management with PCPs;88
10.1.1.5.5;Integrated Management with PCPs and the Use of Telemedicine;90
10.1.1.5.6;Future Perspectives;93
10.1.1.5.7;References;94
10.1.1.6;6 Effects of Bariatric Surgery on Comorbid Conditions Associated with Morbid Obesity;98
10.1.1.6.1;Introduction;98
10.1.1.6.2;Current Surgical Therapies for Morbid Obesity;99
10.1.1.6.2.1;Restrictive Procedures;99
10.1.1.6.2.2;Malabsorptive Procedures with Some Restriction;99
10.1.1.6.2.3;Restrictive Procedure with Some Malabsorption;101
10.1.1.6.3;Effect of Bariatric Surgery on Weight Loss and Operative Mortality;101
10.1.1.6.4;Effect of Bariatric Surgery on Obesity-Related Comorbidities;101
10.1.1.6.4.1;Diabetes;101
10.1.1.6.4.1.1;Diabetes: Possible Mechanism(s) of Control After Surgery;102
10.1.1.6.4.2;OSA: The Effect of Bariatric Surgery;103
10.1.1.6.4.3;Dyslipidemia: The Effect of Bariatric Surgery;104
10.1.1.6.4.4;Hypertension: The Effect of Bariatric Surgery on Systolic, Diastolic, and Pulse Pressure;105
10.1.1.6.4.5;Liver Disease: The Effect of Bariatric Surgery on Nonalcoholic Fatty Liver Disease;106
10.1.1.6.5;Summary: Effect of Bariatric Surgery;107
10.1.1.6.6;References;107
10.1.1.7;7 Dietary Management of Pre-Diabetes and Type 2 Diabetes;112
10.1.1.7.1;Introduction;112
10.1.1.7.1.1;What Is “Pre-diabetes”?;112
10.1.1.7.1.2;Carbohydrate;113
10.1.1.7.1.2.1;Glycemic Index and Glycemic Load;113
10.1.1.7.1.2.2;Dietary Fiber and Complex Carbohydrate;113
10.1.1.7.1.2.3;Simple Sugars;113
10.1.1.7.1.3;Fat;113
10.1.1.7.1.3.1;Saturated Fat;114
10.1.1.7.1.3.2;Trans Fats;114
10.1.1.7.1.3.3;Polyunsaturated Fats;114
10.1.1.7.1.3.4;Fish Oils;114
10.1.1.7.1.4;Protein;114
10.1.1.7.1.5;Other Diets;114
10.1.1.7.1.5.1;Mediterranean Diets;114
10.1.1.7.1.6;Nuts;114
10.1.1.7.1.7;Probiotics;115
10.1.1.7.1.8;Vitamin Supplements;115
10.1.1.7.1.8.1;Vitamin D;115
10.1.1.7.1.8.2;Vitamin C;115
10.1.1.7.1.9;Specific Fruit/Vegetables;115
10.1.1.7.1.9.1;Gooseberries;115
10.1.1.7.1.9.2;Fenugreek;116
10.1.1.7.1.9.3;Green Tea;116
10.1.1.7.1.9.4;Bitter Lemon;116
10.1.1.7.1.9.5;Cinnamon;116
10.1.1.7.2;References;116
10.1.2;1B Physiological modulators of pre-diabetes and cardiovascular disease development;122
10.1.2.1;8 Insulin Resistance and Inflammation: Links Between Obesity and Cardiovascular Disease;122
10.1.2.1.1;Introduction;122
10.1.2.1.2;Free Fatty Acids;123
10.1.2.1.2.1;FFA and Insulin Resistance;123
10.1.2.1.2.2;Mechanisms of FFA-Induced Insulin Resistance;123
10.1.2.1.2.3;FFA and Inflammation;123
10.1.2.1.3;ER Stress;124
10.1.2.1.3.1;ER Stress, Insulin Resistance, and Inflammation;124
10.1.2.1.3.2;What Causes ER Stress in Obesity?;124
10.1.2.1.3.3;Mechanisms of ER Stress-Mediated Insulin Resistance/Inflammation;124
10.1.2.1.4;Hyperinsulinemia;124
10.1.2.1.5;Obesity, Insulin Resistance, and CVD;125
10.1.2.1.5.1;Insulin Resistance, Hyperinsulinemia, and CVD;125
10.1.2.1.5.2;Selective Insulin Resistance and Hyperinsulinemia;125
10.1.2.1.5.3;Hyperinsulinemia and Activation of Matrix Metalloproteinases;125
10.1.2.1.5.4;Hyperinsulinemia and Blood Coagulation;125
10.1.2.1.6;References;126
10.1.2.2;9 Cardiovascular Risk Assessment in Pre-Diabetes: A Hypothesis;130
10.1.2.2.1;Introduction;130
10.1.2.2.2;Background to Hypothesis;131
10.1.2.2.2.1;Dysglycemias in Diabetes and Pre-diabetes Are Apparently the Same;131
10.1.2.2.2.1.1;Hyperglycemic Toxicity;131
10.1.2.2.2.1.2;Diabetic Dyslipidemia;132
10.1.2.2.2.1.3;Metabolic Syndrome;132
10.1.2.2.2.2;Hyperglycemia-Induced OS Is Primary to Development of Hypertension in Diabetes;132
10.1.2.2.2.3;The VT Are Indices of Oxidative Damage Associated with Diabetic Macrovascular Progression;133
10.1.2.2.2.4;There Is up to 25% Prevalence of Pre-diabetes Concomitant with Dyslipidemia in the General Population;133
10.1.2.2.3;The Problems;134
10.1.2.2.3.1;Programs for Identification of Pre-diabetes and UDM Are Limited;134
10.1.2.2.3.2;Current Cardiovascular Risk Screening Programs Have Yet to Provide for Pre-diabetes and UDM;135
10.1.2.2.4;The Hypotheses: Alternative Model of Cardiovascular Risk Assessment in Pre-diabetes and UDM Plus Strategy for Early/Improve...;135
10.1.2.2.4.1;Strategy for Early and Improved Identification of Pre-diabetes;135
10.1.2.2.4.2;Alternative Model for Improved Cardiovascular Risk Assessment in Pre-diabetes;135
10.1.2.2.5;Discussion: Significance of Hypothesis;137
10.1.2.2.5.1;Issue Being Discriminated;137
10.1.2.2.5.2;Addition to Knowledge;137
10.1.2.2.5.3;Adoptability: Agenda for Corrections of Omission-in-Practice;138
10.1.2.2.5.4;Relevance: Potential Implications;140
10.1.2.2.6;Conclusion;141
10.1.2.2.7;Acknowledgment;142
10.1.2.2.8;References;142
10.1.2.3;10 Pre-Diabetes, Cardiovascular Risk Factors, Arterial Stiffness—ADMA;146
10.1.2.3.1;Introduction;146
10.1.2.3.2;Hyperglycemia and Atherosclerosis;148
10.1.2.3.3;Atherosclerosis and Arterial Stiffness;149
10.1.2.3.4;Molecular Mechanisms of Arterial Stiffness;149
10.1.2.3.5;Cellular Component of Arterial Stiffening;150
10.1.2.3.6;ADMA, Pre-Diabetes, and CVD;151
10.1.2.3.7;Conclusion;151
10.1.2.3.8;References;151
10.2;2 Nutrition and Food to Modulate Pre-Diabetes and Resulting Cardiac Disease;158
10.2.1;2A Mechanisms of pre-diabetes and diabetes modulation of cardiac tissues;160
10.2.1.1;11 Effect of Fiber and Low Glycemic Load Diet on Blood Glucose Profile and Cardiovascular Risk Factors in Diabetes and Poor...;160
10.2.1.1.1;Introduction;160
10.2.1.1.1.1;Glycated Hemoglobin;161
10.2.1.1.1.2;GI and GL of Carbohydrates;162
10.2.1.1.2;Effect of Fiber on Postprandial Blood Glucose and Diabetes;162
10.2.1.1.2.1;Effect of DF on Insulin Sensitivity;164
10.2.1.1.2.2;Effect of DF on Colonic Fermentation and Gut Bacteria;164
10.2.1.1.3;Effect of Low GI, GL, and Fiber in Diet on Glucose Control in GDM;165
10.2.1.1.4;Effect of Low GL Diet on HbA1c in Poorly Controlled Diabetes Patients;166
10.2.1.1.5;Effect of Low GL Diet on Changes in Cardiovascular Risk Factors in Poorly Controlled Diabetic Patients;167
10.2.1.1.6;References;169
10.2.1.2;12 Glucose Uptake and Its Consequence on Cardiomyocyte Function;174
10.2.1.2.1;Introduction;174
10.2.1.2.2;Cardiac Metabolism Under Physiological Conditions;174
10.2.1.2.3;Modification of Metabolism in the Diabetic Heart;176
10.2.1.2.4;Modification of Cardiac Function in the Diabetic Heart;177
10.2.1.2.5;Targeting Glucose Utilization and Insulin Response in the Diabetic Cardiomyocyte;177
10.2.1.2.6;Glucotoxicity: The Dark Side of Glucose;178
10.2.1.2.7;Conclusion;179
10.2.1.2.8;Funding;179
10.2.1.2.9;References;179
10.2.1.3;13 Hypertension and Dyslipidemia in Patients with Pre-Diabetes: Dietary and Other Therapies;184
10.2.1.3.1;Introduction;184
10.2.1.3.2;Dyslipidemia in Pre-Diabetes: Mechanisms and Clinical Characteristics;185
10.2.1.3.3;Clinical Significance of Dyslipidemia in Pre-Diabetes;186
10.2.1.3.4;Targets of Lipid-Lowering Interventions in Pre-Diabetic Subjects;187
10.2.1.3.5;Therapeutic Options;188
10.2.1.3.5.1;Lifestyle Modification;188
10.2.1.3.5.2;Antidiabetic Agents;189
10.2.1.3.5.3;Lipid-Lowering Agents;189
10.2.1.3.5.3.1;Statins;189
10.2.1.3.5.3.2;Fibrates;190
10.2.1.3.5.3.3;Drugs Inhibiting Intestinal Cholesterol Absorption;190
10.2.1.3.5.3.4;Omega-3 Fatty Acids;191
10.2.1.3.6;The Role of RAAS in BP and Glucose Metabolism;191
10.2.1.3.7;Angiotensin II;191
10.2.1.3.7.1;Oxidative Stress;191
10.2.1.3.7.2;Insulin Signaling;192
10.2.1.3.7.3;Inflammation;192
10.2.1.3.7.4;Fibrinolytic Balance;192
10.2.1.3.8;Aldosterone;192
10.2.1.3.8.1;Hypokalemia;193
10.2.1.3.8.2;Effects of Aldosterone in Adipose Tissue and Skeletal Muscle;193
10.2.1.3.8.3;Effects of Insulin on Aldosterone Production;193
10.2.1.3.9;Effects of Antihypertensive Drugs Other Than Those Acting on RAAS on Glucose Metabolism;193
10.2.1.3.9.1;Thiazide Diuretics;193
10.2.1.3.9.2;ß-Blockers;193
10.2.1.3.9.3;Calcium Channel Blockers;194
10.2.1.3.9.4;Other Antihypertensive Drugs;194
10.2.1.3.10;Development of New-Onset T2DM with Different Antihypertensive Drug Classes;194
10.2.1.3.10.1;Diuretics and/or ß-Blockers Versus Placebo;194
10.2.1.3.10.2;Thiazide Diuretics Versus ß-Blockers;194
10.2.1.3.10.3;RAAS Inhibitors Versus Placebo;194
10.2.1.3.10.4;CCBs Versus Diuretics and/or ß-Blockers;195
10.2.1.3.10.5;CCB/HCTZ Versus HCTZ;195
10.2.1.3.10.6;RAAS Inhibitors Versus Diuretics and/or ß-Blockers;195
10.2.1.3.10.7;Studies Assessing DM Incidence with RAAS Inhibitors, CCBs, Diuretics, and/or ß-Blockers or Other Drugs (in Various Combinat...;196
10.2.1.3.11;New-Onset T2DM and Cardiovascular Outcomes;197
10.2.1.3.12;Antihypertensive Treatment in Patients with Pre-Diabetes;198
10.2.1.3.12.1;Lifestyle Modification;198
10.2.1.3.12.2;Pharmacotherapy;198
10.2.1.3.13;ARBs with Peroxisome Proliferator-Activated Receptor-. Properties;199
10.2.1.3.14;Conclusions;200
10.2.1.3.15;References;200
10.2.1.4;14 Animal Models of Diabetic Cardiomyopathy;208
10.2.1.4.1;Introduction;208
10.2.1.4.1.1;Diabetic Cardiomyopathy and Its Pathogenesis;208
10.2.1.4.2;Models of Diabetic Cardiomyopathy;209
10.2.1.4.2.1;Minimal Criteria for Models of Diabetic Cardiomyopathy;209
10.2.1.4.2.2;Validation Criteria for Models of Diabetic Cardiomyopathy;209
10.2.1.4.3;The Streptozotocin Model;210
10.2.1.4.4;OVE26 Mouse Model;211
10.2.1.4.5;Zucker Fatty Rat and Zucker Diabetic Fatty Rat Models;211
10.2.1.4.6;Models of Lipotoxicity;211
10.2.1.4.7;Model of Fibrosis;212
10.2.1.4.8;Models of Insulin Resistance and Obesity;212
10.2.1.4.8.1;ob/ob Mouse Model;212
10.2.1.4.8.2;db/db Mouse Model;212
10.2.1.4.9;Some Additional Genetic Models with Defective Insulin Signaling;213
10.2.1.4.9.1;Dominant Negative PI3K;213
10.2.1.4.9.2;Heart and Skeletal Muscle PDK1 KO;213
10.2.1.4.10;Cardiomyocyte GLUT4-KO;213
10.2.1.4.11;UCP-DTA Mouse;213
10.2.1.4.12;Goto-Kakizaki Rat;213
10.2.1.4.13;Additional Models of Diabetic Cardiomyopathy;213
10.2.1.4.14;Conclusion;213
10.2.1.4.15;References;214
10.2.1.5;15 4-Hydroxyisoleucine: A Potential Antidiabetic Agent from Trigonella foenum-graecum;218
10.2.1.5.1;Introduction;218
10.2.1.5.2;4-Hydroxyisoleucine;219
10.2.1.5.2.1;Extraction and Isolation of 4-Hydroxyisoleucine;219
10.2.1.5.2.2;Standardization of 4-Hydroxyisoleucine;220
10.2.1.5.3;Antidiabetic Activity of 4-OH-Ile;220
10.2.1.5.4;Mechanism of Action at the Molecular Level;222
10.2.1.5.5;Metabolism of 4-OH-Ile;222
10.2.1.5.5.1;Other Activities;223
10.2.1.5.6;Conclusion;223
10.2.1.5.7;References;224
10.2.1.6;16 mHealth Technologies in Pre-Diabetes and Diabetes Care;226
10.2.1.6.1;Introduction;226
10.2.1.6.1.1;The Diabetes Epidemic;226
10.2.1.6.1.2;The Shifting Focus of Healthcare;226
10.2.1.6.1.3;Convergence of Mobile Technology and Healthcare;227
10.2.1.6.1.4;mHealth for Pre-Diabetes and Diabetes;228
10.2.1.6.2;Types of Diabetes-Related Technologies;228
10.2.1.6.2.1;Traditional Diagnostics and Therapeutics;229
10.2.1.6.2.1.1;Handheld Blood Glucose Meters;229
10.2.1.6.2.1.2;Continuous Glucose Monitoring;229
10.2.1.6.2.1.3;Insulin Pumps and Artificial Pancreas Systems;231
10.2.1.6.2.2;Modern Innovations Using mHealth;232
10.2.1.6.2.2.1;Diet and Exercise Tracking;232
10.2.1.6.2.2.2;Messaging Systems for Patient Education and Coaching;233
10.2.1.6.2.2.3;Adaptations to the Blood Glucose Meter;233
10.2.1.6.2.2.4;Modern DMSs;234
10.2.1.6.2.2.5;Future Approaches for Diabetes Care;235
10.2.1.6.3;Challenges Associated with Adoption of mHealth Diabetes Care Solutions;236
10.2.1.6.3.1;Limited Data to Support Effectiveness;236
10.2.1.6.3.2;Cost-Effectiveness, Affordability, and Reimbursement;236
10.2.1.6.3.3;FDA Regulation;237
10.2.1.6.3.4;Integration into Diabetes Care Environments;238
10.2.1.6.4;Conclusion;238
10.2.1.6.5;References;238
10.2.1.7;17 Fruit and Glycemic Control in Type 2 Diabetes;242
10.2.1.7.1;Fruit and Glycemic Control;243
10.2.1.7.2;Acute Studies: Postprandial Blood Glucose;243
10.2.1.7.3;Potential Problems Using GI Studies;243
10.2.1.7.4;Long-Term Studies: HbA1c;244
10.2.1.7.5;How Many Pieces of Fruit at a Time?;246
10.2.1.7.6;How Much Fruit a Day?;246
10.2.1.7.7;Mechanisms Involved in the Effects of Fruit on Glycemic Control;246
10.2.1.7.8;Potential Negative Effects of Fruit and Fructose;246
10.2.1.7.9;Beneficial Effects of Fruit on Diseases;247
10.2.1.7.10;Conclusions;247
10.2.1.7.11;References;247
10.2.1.8;18 Antihyperglycemic Activity of Bioactive Compounds from Soybeans;252
10.2.1.8.1;Introduction;252
10.2.1.8.2;Botanical Description;252
10.2.1.8.3;Antihyperglycemic Bioactive Compounds from Soya;252
10.2.1.8.4;Summary Points;253
10.2.1.8.5;References;254
10.2.1.9;19 Myoinositol Supplementation on Insulin Resistance in Gestational Diabetes;256
10.2.1.9.1;Myoinositol;256
10.2.1.9.2;Insulin Resistance and Gestational Diabetes Mellitus;257
10.2.1.9.3;Myoinositol in Clinical Practice;258
10.2.1.9.4;References;259
10.2.1.10;20 The Tibetan Herbal Preparation Padma 28 (Padma Basic) in the Treatment and Prevention of Diabetic Complications and Athe...;262
10.2.1.10.1;Network Etiology of Complex Diseases: The Example of Diabetes-Associated Diseases;262
10.2.1.10.2;Padma 28 in Atherogenesis as an Example of the Multi-target Mode of Action;262
10.2.1.10.3;Pathogenesis of Diabetes-Associated Diseases;263
10.2.1.10.4;Oxidative Stress and Antioxidative Mechanisms of Padma 28;264
10.2.1.10.5;Advanced Glycation End-products;265
10.2.1.10.6;Chronic Low-Level Inflammation and Anti-inflammatory Mechanisms of Padma 28;266
10.2.1.10.7;Outlook and Conclusions;267
10.2.1.10.8;References;267
11;II. Diabetes;268
11.1;3 Diabetes in Development and Pathology of Cardiovascular Disease;270
11.1.1;3A Role of foods in cardiovascular problems promoted by diabetes;272
11.1.1.1;21 Cardiovascular Biomarker Assessment Across Glycemic Status;272
11.1.1.1.1;A Review of Macrovascular Results in Past Major Clinical Trials Involving Glucose Control;273
11.1.1.1.1.1;University Group Diabetes Program;273
11.1.1.1.1.2;DCCT, EDIC, and UKPDS;273
11.1.1.1.1.3;ACCORD and ADVANCE;273
11.1.1.1.1.4;Veterans Affairs Diabetes Trial;275
11.1.1.1.1.5;Summary: Insufficient Understanding of Macrovascular Risk;275
11.1.1.1.2;Overview of Current Clinical Biomarkers for Cardiovascular Risk;276
11.1.1.1.2.1;C-Reactive Protein;276
11.1.1.1.2.1.1;CRP and Diabetes;278
11.1.1.1.2.1.2;Current Clinical Considerations of CRP;279
11.1.1.1.3;Myeloperoxidase;279
11.1.1.1.4;Cardiac Troponins;281
11.1.1.1.4.1;cTns as a Prognostic Tool;282
11.1.1.1.4.2;Diabetes and cTns;283
11.1.1.1.5;B-Type Natriuretic Peptide;283
11.1.1.1.5.1;BNP in the Prevention of Subclinical CVD;284
11.1.1.1.6;Albuminuria;285
11.1.1.1.7;Perspectives on Biomarkers for Cardiovascular Risk;286
11.1.1.1.7.1;Multi-Biomarker Profiles for Prognostics;286
11.1.1.1.8;Conclusion;287
11.1.1.1.9;References;288
11.1.1.2;22 The Transcultural Diabetes Nutrition Algorithm: From Concept to Implementation;296
11.1.1.2.1;Nutritional Medicine and Comprehensive Diabetes Care;296
11.1.1.2.2;White Papers on Nutrition and T2D;297
11.1.1.2.3;Clinical Algorithms as Practice Management Tools;297
11.1.1.2.4;The Transculturalization Process;298
11.1.1.2.5;The Transcultural Diabetes Nutrition Algorithm Concept and Development;300
11.1.1.2.6;Translating the tDNA Development Process into Results;300
11.1.1.2.7;tDNA Content Validation;303
11.1.1.2.8;tDNA Clinical Validation Plans;305
11.1.1.2.9;Conclusions;305
11.1.1.2.10;References;306
11.1.1.3;23 Microcirculation: A Key Effector in Insulin Resistance;308
11.1.1.3.1;Introduction;308
11.1.1.3.2;Background;308
11.1.1.3.3;How to Measure Microcirculation;309
11.1.1.3.4;Microcirculation: Structural and Functional Specificities;309
11.1.1.3.4.1;Structures;309
11.1.1.3.4.2;Glycocalyx;310
11.1.1.3.4.3;Arteriolar Vasomotion;310
11.1.1.3.5;Insulin as a Vasoactive Hormone;311
11.1.1.3.5.1;Insulin and Microflow;311
11.1.1.3.5.2;Physiology Versus Pharmacology;313
11.1.1.3.5.3;Insulin Transendothelial Transport;313
11.1.1.3.5.4;Blood Flow and Glucose Metabolism;314
11.1.1.3.6;Limitations and Technical Biases;314
11.1.1.3.6.1;Regional Physiological Differences;314
11.1.1.3.6.2;Species, Gender, Age, and Ethnicity;314
11.1.1.3.6.3;Protocol/Techniques;314
11.1.1.3.6.4;Animals/Humans;315
11.1.1.3.7;Microcirculation in Pre-Diabetes;315
11.1.1.3.8;Conclusion;318
11.1.1.3.9;References;318
11.1.1.4;24 Glucose Intake and Utilization in Pre-Diabetes and Diabetes: Tomato and Diabetes;328
11.1.1.4.1;Introduction;328
11.1.1.4.1.1;Diabetes;328
11.1.1.4.1.1.1;Incidence and Prevalence;328
11.1.1.4.1.1.2;Categories of Diabetes and Glucose Regulation;328
11.1.1.4.1.1.2.1;Type 1 Diabetes;328
11.1.1.4.1.1.2.1.1;Symptoms of Type 1 Diabetes;329
11.1.1.4.1.1.2.1.1.1;High Blood Sugar;329
11.1.1.4.1.1.2.1.1.2;Low Blood Sugar;329
11.1.1.4.1.1.2.2;Type 2 Diabetes;329
11.1.1.4.1.1.2.2.1;Symptoms of Type 2 Diabetes;329
11.1.1.4.1.1.3;Categories of Increased Risk for Diabetes;329
11.1.1.4.1.1.4;Criteria for the Diagnosis of Diabetes;329
11.1.1.4.1.2;Tomato;330
11.1.1.4.1.2.1;Carotenoids;330
11.1.1.4.1.2.1.1;Chemistry and Dietary Sources;331
11.1.1.4.1.2.2;Lycopene;331
11.1.1.4.1.2.2.1;Dietary Sources of Lycopene;331
11.1.1.4.1.2.2.2;The Role of Lycopene in Human Health;331
11.1.1.4.1.2.3;Tomato and Diabetes;331
11.1.1.4.1.2.3.1;Tomato and Antioxidant Property;331
11.1.1.4.1.2.3.2;Tomato and Lipid Profiles;332
11.1.1.4.1.2.3.3;Tomato and Hypertension;333
11.1.1.4.2;Conclusion;336
11.1.1.4.3;References;337
11.1.1.5;25 Optimal Carbohydrate and Nutrient Intake for Japanese Elderly Patients with Type 2 Diabetes;342
11.1.1.5.1;Introduction;342
11.1.1.5.2;Diabetes in Older Adults;342
11.1.1.5.3;Characteristics of Asian Diabetic Patients;343
11.1.1.5.4;MNT in Diabetes Management;343
11.1.1.5.5;Dietary Intake in Japanese Elderly Diabetic Patients;344
11.1.1.5.6;Obesity and Dietary Intake in Japanese Elderly Diabetic Patients;347
11.1.1.5.7;Optimal Carbohydrate Intake in Japanese Elderly Diabetic Patients;347
11.1.1.5.8;The Relationship Between Vegetable Intake and Diabetes Control;349
11.1.1.5.9;References;350
11.1.1.6;26 Mediterranean Diet for Prevention of Cardiovascular Disease and Type 2 Diabetes;354
11.1.1.6.1;Introduction;354
11.1.1.6.2;The Med Diet;355
11.1.1.6.3;Measuring Adherence to a Med Diet: the Med Diet Score;355
11.1.1.6.4;Epidemiologic Studies;357
11.1.1.6.4.1;Epidemiologic Evidence Linking Adherence to a Med Diet and CVD Risk;357
11.1.1.6.4.2;Epidemiologic Evidence Linking Adherence to a Med Diet with T2DM Risk;358
11.1.1.6.4.3;Summary of Epidemiologic Evidence Linking Adherence to a Med Diet with Development of CVD or T2DM;358
11.1.1.6.5;Intervention Studies;358
11.1.1.6.5.1;Effect of a Med Diet on CVD Risk;358
11.1.1.6.5.2;Effect of a Med Diet on T2DM Risk;359
11.1.1.6.5.3;Effect of a Med Diet on Intermediate End-Points for CVD and T2DM: Potential Mechanisms of Action;359
11.1.1.6.5.3.1;Effect of a Med Diet on Blood Lipid Levels and Blood Pressure;359
11.1.1.6.5.3.2;Effect of a Med Diet on Inflammatory Markers;360
11.1.1.6.5.3.3;Effect of a Med Diet on Metabolic Syndrome, Endothelial Function, and IR;360
11.1.1.6.5.3.4;Effect of a Med Diet on Body Weight;360
11.1.1.6.5.4;Summary of Intervention Study Evidence Examining a Med Diet for Prevention of CVD and T2DM;361
11.1.1.6.6;The Protective Effect of Individual Med Diet Food Components;361
11.1.1.6.6.1;Olive Oil;361
11.1.1.6.6.2;Whole Grains;361
11.1.1.6.6.3;Fruit and Vegetables;362
11.1.1.6.6.4;Nuts;362
11.1.1.6.6.5;Oily Fish;362
11.1.1.6.6.6;Alcohol;362
11.1.1.6.7;Conclusion;363
11.1.1.6.8;References;363
11.1.1.7;27 The Role of Nutrition and Supplementation in Dialysis Patient Health;368
11.1.1.7.1;Chronic Kidney Disease and Dialysis Treatment;368
11.1.1.7.2;Dietary Recommendations for Dialysis Patients;369
11.1.1.7.2.1;Carbohydrates;369
11.1.1.7.2.2;Lipids;369
11.1.1.7.2.3;Protein;369
11.1.1.7.2.4;Phosphorus;370
11.1.1.7.2.5;Potassium;370
11.1.1.7.2.6;Sodium;370
11.1.1.7.3;Supplements in Dialysis Patients;370
11.1.1.7.3.1;Omega-3;370
11.1.1.7.3.2;Conjugated Linoleic Acid;371
11.1.1.7.3.3;Vitamin E (Alpha-Tocopherol);371
11.1.1.7.3.4;Vitamin D;371
11.1.1.7.3.5;Polyphenols;371
11.1.1.7.3.6;Creatine;372
11.1.1.7.3.7;L-Carnitine;372
11.1.1.7.3.8;Probiotics and Prebiotics;372
11.1.1.7.4;References;373
11.1.1.8;28 Bioactive Compounds Increase Incretins with Beneficial Effects on Diabetes;376
11.1.1.8.1;Introduction;376
11.1.1.8.2;Mode of Action;376
11.1.1.8.3;Incretin Mimetic and Incretin Enhancer;376
11.1.1.8.3.1;GLP-1 Receptor Agonists;377
11.1.1.8.3.2;DPP-4 Inhibitors;377
11.1.1.8.4;Sitagliptin;378
11.1.1.8.5;Vildagliptin;378
11.1.1.8.6;Berberine;379
11.1.1.8.7;Lupeol;379
11.1.1.8.8;Conclusion;380
11.1.1.8.9;References;380
11.1.2;3B Exercise diabetes and cardiovascular disease;382
11.1.2.1;29 Exercise and Diet Improve Cardiometabolic Risk in Overweight and Obese Individuals Without Weight Loss;382
11.1.2.1.1;Introduction;382
11.1.2.1.2;Reduction in T2D Risk;383
11.1.2.1.3;Glucose Metabolism and Insulin Action;384
11.1.2.1.4;Blood Pressure;385
11.1.2.1.5;Lipids and Lipoproteins;386
11.1.2.1.6;Endothelial Function;387
11.1.2.1.7;Inflammation;388
11.1.2.1.8;Skeletal Muscle Adaptations with Exercise Training;389
11.1.2.1.9;Summary and Conclusions;389
11.1.2.1.10;References;390
11.1.3;3C Nutrition and food to modulate diabetes: Heart and vascular health;396
11.1.3.1;30 Protein in the Treatment of Type 2 Diabetes Mellitus;396
11.1.3.1.1;Introduction;396
11.1.3.1.2;HP Diets and Weight Loss;396
11.1.3.1.3;HP Diets and Blood Lipids;397
11.1.3.1.4;HP Diets and Glycemic Control in T2DM;397
11.1.3.1.5;HP Diets and Blood Pressure;397
11.1.3.1.6;Protein and Satiety;398
11.1.3.1.6.1;Studies Using VAS;398
11.1.3.1.6.2;Studies Using Preloads or Meals;398
11.1.3.1.6.3;Studies Using Measures of Hormonal Change;398
11.1.3.1.7;Protein and Energy Expenditure;399
11.1.3.1.8;Effect of Protein on Glycemic Response;399
11.1.3.1.9;Potential Risks of HP Diet;399
11.1.3.1.9.1;Renal Function;400
11.1.3.1.9.2;Bone Loss;400
11.1.3.1.9.3;Cancer;400
11.1.3.1.10;Summary;400
11.1.3.1.11;References;401
11.1.3.2;31 Nutritional Support in Hospitalized Patients with Diabetes Mellitus;404
11.1.3.2.1;List of Abbreviations;404
11.1.3.2.2;Introduction;404
11.1.3.2.3;General Nutrition in Diabetes;405
11.1.3.2.4;Nutrition in Hospitalized Patients;405
11.1.3.2.5;EN in Diabetic Patients;406
11.1.3.2.6;Diabetes Medication Administration with EN;407
11.1.3.2.7;PN in Diabetes;408
11.1.3.2.8;PN Macronutrient Effect on Hyperglycemia;409
11.1.3.2.9;Micronutrient Adjunct Therapy in PN;409
11.1.3.2.10;Conclusion;410
11.1.3.2.11;References;410
11.1.3.3;32 Amino Acids Supplementation as Nutritional Therapy Strategy in Diabetes Mellitus;414
11.1.3.3.1;Amino Acids Supplementation as a Rational Approach to Treatment of Pre-Diabetes and Diabetes;414
11.1.3.3.2;ß-Cell Nutrient Metabolism Is Central to the Insulin Secretion;415
11.1.3.3.2.1;Amino Acids as Secretagogues;415
11.1.3.3.2.2;Arginine;416
11.1.3.3.2.3;Glutamine;416
11.1.3.3.2.4;Branched Chain Amino Acids;417
11.1.3.3.2.5;Other Amino Acids;418
11.1.3.3.3;Concluding Remarks on Secretagogue Effects of Amino Acids;418
11.1.3.3.4;Amino Acids Supplementation to Maintain Muscle Mass in T2DM;419
11.1.3.3.5;Exercise-Induced Improvement of the Positive Effects of Amino Acids in Pre-Diabetes and T2DM: An Open Issue;421
11.1.3.3.6;Clusters of Amino Acids and Risk of Diabetes: An Intriguing Issue;421
11.1.3.3.7;Amino Acids and Mitochondrial Biogenesis in Diabetes;422
11.1.3.3.8;Concluding Remarks;422
11.1.3.3.9;References;422
12;Index;430

Leseproben

List of Contributors

John M. Abbamonte, MA,     Department of Psychology, Rutgers University, Camden, NJ, USA

Ahmad Afaghi, PhD, MS, MSPH,     Qazvin University of Medical Science, School of Medicine, Qazvin, Iran

Olubukola Ajala, MD, MRCP,     Department of Diabetes and Endocrinology, Western Sussex Hospitals NHS Trust, Worthing, United Kingdom

Renata Moneda Alberto dos Santos, BSc,     Clinical Hospital of Ribeirão Preto Medical School and Ribeirão Preto Medical School, University of São Paulo, Brazil

Siddhartha S. Angadi, PhD,     Healthy Lifestyles Research Center, School of Nutrition and Health Promotion, Arizona State University, Phoenix, AZ, USA

Gol-Naz Arjomand, MSc,     Department of Nutrition and Diet Therapy, School of Nutrition and Dietary, Tehran University of Medical Sciences, Tehran, Iran

Kristin J. August, PhD,     Department of Psychology, Rutgers University, Camden, NJ, USA

Sachin L. Badole, PhD,     Department of Pharmacology, PES’s Modern College of Pharmacy, Sector 21, Yamuna Nagar, Nigadi, Pune, India

Christophe Beauloye, MD, PhD,     Université Catholique de Louvain, Institut de Recherche Expérimentale et Clinique, Pôle de Recherche Cardiovasculaire, Brussels, Belgium

Luc Bertrand, PhD,     Université Catholique de Louvain, Institut de Recherche Expérimentale et Clinique, Pôle de Recherche Cardiovasculaire, Brussels, Belgium

Guenther Boden, MD,     Division of Endocrinology, Diabetes, Metabolism and the Clinical Research Center, Temple University School of Medicine, Philadelphia, PA, USA

F. Boubred, MD-PhD,     Department of Neonatology, University Hospital, Marseille, France

M. Jason Brooke, MSE, JD,     Vasoptic Medical Inc., Columbia, MD, USA

José Abrão Cardeal da Costa, MD, PhD,     Clinical Hospital of Ribeirão Preto Medical School and Ribeirão Preto Medical School, University of São Paulo, Brazil

Zijian Chen, MD,     Beth Israel Medical Center, Division of Endocrinology, Diabetes and Bone Disease, Icahn School of Medicine, Mt. Sinai, Israel

Allan Stubbe Christensen, MHSc, RD,     Department of Nutrition, Regional Hospital West Jutland, Denmark

Christian Loepfe, MSc,     Regulatory and Medical Scientific Affairs, Padma Inc., Hinwil, Switzerland

Francesco Corrado, PhD, MD,     Department of Obstetrics and Gynecology, University of Messina, Italy

Giuseppe D’Antona, MD, PhD,     Department of Molecular Medicine and Laboratory for Motor Activities in Rare Diseases (Lusammr), University of Pavia, Pavia, Italy

Amy A. Devitt, PhD,     Abbott Nutrition Research and Development, Columbus, OH, USA

Patrick English, MD, FRCP,     Department of Diabetes and Endocrinology, Plymouth Hospitals NHS Trust, Crownhill, Plymouth, United Kingdom

M. Florentin, MD,     Department of Internal Medicine, Medical School, University of Ioannina, Ioannina, Greece

Glenn A. Gaesser, PhD,     Healthy Lifestyles Research Center, School of Nutrition and Health Promotion, Arizona State University, Phoenix, AZ, USA

Søren Gregersen, MD, PhD,     Department of Endocrinology and Metabolism, Aarhus University Hospital, Denmark

Refaat A. Hegazi, MD,     Abbott Nutrition Research and Development, Columbus, OH, USA

Sandrine Horman, PhD,     Université Catholique de Louvain, Institut de Recherche Expérimentale et Clinique, Pôle de Recherche Cardiovasculaire, Brussels, Belgium

Syed Khalid Imam, FCPS,     Al-Mouwasat Hospital, Jubail Industrial City, KSA

Ganesh B. Jangam, Mpharm,     Department of Pharmacology, PES’s Modern College of Pharmacy, Sector 21, Yamuna Nagar, Nigadi, Pune, India

Catherine Jarrett, MS, RD,     Healthy Lifestyles Research Center, School of Nutrition and Health Promotion, Arizona State University, Phoenix, AZ, USA

Chiemi Kamada, MS,     Training Department of Administrative Dietitians, Faculty of Human Life Science, Shikoku University, Furakawa, Ojin-cho, Tokushima-shi, Japan

Caitlin S. Kelly, MA,     Department of Psychology, Rutgers University, Camden, NJ, USA

Arash Kordi, MD,     Azad Islamic University, School of Medicine, Tehran, Iran

Jeremy Krebs, MD,     Centre for Endocrine, Diabetes and Research, Capital and Coast District Health Board, Wellington South, New Zealand

Daniel Y. Li, BSc,     Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, Cleveland, OH, USA

Fabíola Pansani Maniglia, MSc,     Clinical Hospital of Ribeirão Preto Medical School and Ribeirão Preto Medical School, University of São Paulo, Brazil

Maria Lisa Marcon, PgDip,     Metabolic and Nutrition Unit, Department of Medicine, Local Health Authority (ULSS 9), Treviso, Veneto, Italy

Claire T. McEvoy, RD, PhD,     Centre for Public Health, Queen’s University Belfast, Belfast, Northern Ireland

Jeffrey I. Mechanick, MD,     Division of Endocrinology, Diabetes, and Bone Disease, Icahn School of Medicine at Mount Sinai, New York, NY, USA

Dean J. Mikami, MD,     Department of Surgery, Division of General and Gastrointestinal Surgery, The Ohio State University, Wexner Medical Center, Columbus, OH, USA

D. Mitanchez, MD-PhD,     Division of Neonatology, Department of Perinatology, Armand Trousseau Hospital, 75012 Paris & Sorbonne Universités UPMC University Paris 06, Paris, France

Bradley J. Needleman, MD,     Department of Surgery, Division of General and Gastrointestinal Surgery, The Ohio State University, Wexner Medical Center, Columbus, OH, USA

Laura Nollino, MD,     Metabolic and Nutrition Unit, Department of Medicine, Local Health Authority (ULSS 9), Treviso, Veneto, Italy

Sabrena F. Noria, MD, PhD,     Department of Surgery, Division of General and Gastrointestinal Surgery, The Ohio State University, Wexner Medical Center, Columbus, OH, USA

Ezekiel Uba Nwose, BSc, MSc, PhD

School of Community Health, Charles Sturt University, Orange, NSW, Australia

School of Public & Community Health, Novena University, Ogume DTS, Nigeria

Agostino Paccagnella, MD,     Metabolic and Nutrition Unit, Department of Medicine, Local Health Authority (ULSS 9), Treviso, Veneto, Italy

Athanasia K. Papazafiropoulou, MD, MSc, PhD,     Diabetes Center, Tzaneio General Hospital of Piraeus, Piraeus, Greece

Amber Parry-Strong, PhD,     Centre for Endocrine, Diabetes and Research, Capital and Coast District Health Board, Wellington South, New Zealand

Kalyani Y. Patil, MTech,     Department of Cosmetic Technology, Nikalas Mahila Mahavidhyalaya, Khamla, Nagpur, India

Roberta Pirolo, PharmD,     Local Pharmacy Service, Local Health Authority (ULSS 9), Treviso, Veneto, Italy

Jahan Porhomayon, MD, FCCP, FCCM,     Department of Anesthesiology, University at Buffalo, Buffalo, NY,...