Rev Diabet Stud, 2010, 7(1):6-14 DOI 10.1900/RDS.2010.7.6

Functional Alterations of Proinflammatory Monocytes by T Regulatory Cells: Implications for the Prevention and Reversal of Type 1 Diabetes

Charles Sia1, Arno Hänninen2

1Vaccine Center, National Health Research Institutes, Zhunan Township, Miaoli County, Taiwan 350
2Department of Medical Microbiology & Immunology, Turku University, Finland
Address correspondence to: Charles Sia, e-mail:


The onset and development of type 1 diabetes (T1D) occurs in genetically predisposed individuals, and is attributed to autoimmune destruction of pancreatic β-cells involving a multitude of immune mechanisms. Defects in immune regulation may play a central role in T1D, involving impaired function and communication of both myeloid and lymphoid cells of the innate and adaptive immune compartments. Dendritic cells and regulatory T (Treg) cells are part of this network, which seem to be hampered in their quest to control and regulate tissue-destructive autoimmunity. Recent studies have shown that in vivo activated CD16- blood monocytes exhibiting proinflammatory features are present in diabetic subjects. These monocytes may govern T cell-mediated immune responses towards the development of tissue-destructive Th1 and Th17 subtypes, and give rise to inflammatory macrophages in tissues. Differential effects of cytokines IFN-γ and IL-4 in the development of inflammatory macrophages, and the distinct developmental pathways of proinflammatory or tissue-repair-associated monocytes suggest that controlling the activity of these monocytes could be part of an immune intervention strategy to prevent T1D. Similarly, strategies to target autoantigens to immature, steady-state dendritic cells could guide the immune response away from Th1 and Th17 immune effectors. This review examines potential approaches to this goal by manipulation of myeloid and lymphoid cell regulatory networks in T1D.

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Rev Diabet Stud, 2010, 7(1):15-25 DOI 10.1900/RDS.2010.7.15

Oxidative Stress, Nitric Oxide, and Diabetes

Dario Pitocco1,2, Francesco Zaccardi1,2, Enrico Di Stasio3, Federica Romitelli3, Stefano A. Santini3, Cecilia Zuppi3, Giovanni Ghirlanda1

1Institute of Internal Medicine, Catholic University of Rome, Largo Agostino Gemelli 8, 00168 Rome, Italy
2Contributed equally to the article
3Department of Biochemistry, Catholic University of Rome, 00168 Rome, Italy
Address correspondence to: Dario Pitocco, e-mail:


In the recent decades, oxidative stress has become focus of interest in most biomedical disciplines and many types of clinical research. Increasing evidence from research on several diseases show that oxidative stress is associated with the pathogenesis of diabetes, obesity, cancer, ageing, inflammation, neurodegenerative disorders, hypertension, apoptosis, cardiovascular diseases, and heart failure. Based on this research, the emerging concept is that oxidative stress is the “final common pathway”, through which risk factors of several diseases exert their deleterious effects. Oxidative stress causes a complex dysregulation of cell metabolism and cell-cell homeostasis. In this review, we discuss the role of oxidative stress in the pathogenesis of insulin resistance and beta-cell dysfunction. These are the two most relevant mechanisms in the pathophysiology of type 2 diabetes, and in the pathogenesis of diabetic vascular complications, the leading cause of death in diabetic patients.

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Rev Diabet Stud, 2010, 7(1):26-35 DOI 10.1900/RDS.2010.7.26

The Role of Diet and Lifestyle in Primary, Secondary, and Tertiary Diabetes Prevention: A Review of Meta-Analyses

Theodora Psaltopoulou1, Ioannis Ilias2, Maria Alevizaki3

1Department of Hygiene, Epidemiology and Medical Statistics, School of Medicine, University of Athens, Greece
2Department of Endocrinology, Diabetes and Metabolism, Elena Venizelou Hospital, Athens, Greece
3Endocrine Unit, Department of Clinical Therapeutics, Athens University School of Medicine, Alexandra Hospital, Athens, Greece
Address correspondence to: Theodora Psaltopoulou, e-mail:


Prevention of diabetes is crucial to lowering disease incidence, and thus minimizing the individual, familial, and public health burden. The purpose of this review is to gather current information from meta-analyses on dietary and lifestyle practices concerning reduction of risk to develop type 2 diabetes. Low glycemic index dietary patterns reduce both fasting blood glucose and glycated proteins independent of carbohydrate consumption. Diets rich in whole-grain, cereal high fiber products, and non-oil-seed pulses are beneficial. Whereas, frequent meat consumption has been shown to increase risk. Regarding non-alcoholic beverages, 4 cups/day of filtered coffee or tea are associated with a reduced diabetes risk. In contrast, the consumption of alcoholic beverages should not exceed 1-3 drinks/day. Intake of vitamin E, carotenoids, and magnesium can be increased to counteract diabetes risk. Obesity is the most important factor accounting for more than half of new diabetes' cases; even modest weight loss has a favorable effect in preventing the appearance of diabetes. Also, physical exercise with or without diet contributes to a healthier lifestyle, and is important for lowering risk. Finally, there is a positive association between smoking and risk to develop type 2 diabetes. As far as secondary and tertiary prevention is concerned, for persons already diagnosed with diabetes, there is limited evidence of the effectiveness of diet or lifestyle modification on glycemic control, but further studies are necessary.

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