Abstract
The Master Course on “Methodologies for Bio-Medical Research in Diabetes” was organized jointly by the University of Bari Aldo Moro, Bari, Italy, and the Italian Society of Diabetology (SID, Società Italiana di Diabetologia). This Course Program has been active throughout the academic year 2011–2012, and engaged selected students in lectures on diabetes research, training in laboratory work, and personal study on selected review articles and original papers. Lecturing activities involved 26 Italian and international experts in the field of diabetes and metabolism and were highly interactive also involving discussion of experimental data sets. The lectures addressed several aspects of diabetes aetiology, pathophysiology, and management, as well methodological and biotechnology topics. At the end of the Course, students were requested to write a review article on a research topic of their choice.
The Master Course on “Methodologies for Bio-Medical Research in Diabetes” was organized jointly by the University of Bari Aldo Moro, Bari, Italy, and the Italian Society of Diabetology (SID, Società Italiana di Diabetologia). This Course Program was approved in July 2011 and has been active throughout the academic year 2011–2012 at the Department of Emergency and Organ Transplantation, Section of Internal Medicine, Endocrinology, Andrology and Metabolic Diseases of the University of Bari. The Course activities engaged selected students in lectures on diabetes research, training in laboratory work, and personal study on selected review articles and original papers. Lecturing activities involved 26 Italian and international experts in the field of diabetes and metabolism and were highly interactive also involving discussion of experimental data sets. The lectures addressed several aspects of diabetes aetiology (genetics and pharmacogenetics of type 2 diabetes; monogenic diabetes), pathophysiology (pancreatic beta-cell and alpha-cell physiology and pathophysiology; mechanisms of insulin resistance; adipose tissue dysfunction; innate immunity and inflammation in diabetes), and management (drugs to preserve beta-cell mass and function; novel markers of microvascular disease; insulin, insulin analogues, and cancer), as well as methodological and biotechnology topics (methods to study endothelial function, oxidative stress, and mitochondrial function; methods to isolate and characterize stem cells and endothelial progenitor cells; various aspects of genomics, proteomics, metabolomics, and bioinformatics applied to diabetes research; development of transgenic animal models; patenting procedures in biomedical research).
At the end of the Course, students were requested to write a review article on a research topic of their choice, stimulated by their participation in the Master Course with the guidance of a faculty member. Five reviews were then selected to undergo a peer review process before appearing in this Special Issue of the Archives of Physiology and Biochemistry.
In the review article “Pharmacologic agents for type 2 diabetes therapy and regulation of adipogenesis”, the authors have addressed the link between type 2 diabetes and excess body weight and, consequently, the need to consider the effects of different anti-hyperglycaemic therapies on body weight and body fat. Currently used diabetes drugs can cause weight gain, i.e. insulin and its analogues, sulphonylureas, and thiazolidinediones, while others, such as metformin and the GLP-1 receptor agonists, may promote weight loss. Excess body weight in patients with diabetes is largely due to expansion of adipose tissue, and these drugs could interfere with the mechanisms underlying the expansion and differentiation of adipocyte precursors. In this review, the available evidence for the specific effects of distinct anti-diabetes drugs on adipose tissue development and function is discussed with the ultimate goal of increasing our understanding of how anti-diabetes medications can modulate energy balance and body fat metabolism.
The review article “‘Browning’ of adipose tissue – regulation and therapeutic perspectives”, deals with the hypothesis that increasing cellular energy expenditure may represent a potentially useful tool to reduce adiposity. Adaptive thermogenesis, a biological process occurring within the brown fat, by which energy is dissipated in mitochondria, results in increased energy expenditure. Based on the recent discovery that brown adipose tissue is present in adult humans, the authors review the mechanisms potentially associated with expansion and activation of brown adipose tissue, and modulation of adaptive thermogenesis. Moreover, they explore the possibility that controlling one or more of these pathways may induce activation of brown fat with potential implications for the treatment of obesity.
The article “Incretin hormones and beta-cell mass expansion: what we know and what is missing” addresses the pathophysiological mechanisms involved in loss of beta-cells and impairment of beta-cell regeneration in type 2 diabetes (T2D). Incretins have been shown to stimulate beta-cell growth and differentiation of pancreas-derived stem/progenitor cells, as well as to exert cytoprotective and anti-apoptotic effects on mature beta-cells. In this article, the authors summarize the current findings and discuss the missing understanding of the effects of incretin hormones on beta-cell mass expansion, with particular emphasis on the discrepancy between pre-clinical in vitro data and the in vivo context.
In the review article “Physiology of incretins and loss of incretin effect in type 2 diabetes and obesity”, the authors emphasize the importance of glucagon-like petide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) in the regulation of glucose homeostasis by reviewing studies assessing GLP-1 and GIP levels and actions in diabetes and obesity and the relationship with glucose intolerance in T2D patients. Several key studies elucidating the association of defective incretin action with T2D and obesity, and the effects of metformin and other anti-diabetes agents on the incretin system are examined here.
Finally, the article “Abnormalities of the cardiac stem and progenitor cell compartment in experimental and human diabetes” emphasizes the concept that a “cardiac stem cell compartment disease” may play an important role in the pathophysiology of diabetic cardiomyopathy. In diabetic hearts, human cardiac stem/progenitor cells are reduced and manifest defective proliferative capacity. Diabetes-associated conditions, such as hyperglycaemia, hyperlipidemia, inflammation, and the consequent oxidative stress, can induce defects in both growth and survival of these cells with an imbalance between cell death and cell replacement, thus favouring the onset of diabetic cardiomyopathy and its progression towards heart failure. This article also reviews studies that have improved our understanding of stem cell biology within the cardiovascular system and of the preservation of the cardiac stem/progenitor cell compartment as a mean to counteract the negative impact of diabetes on the myocardium.
Overall, we believe that the program has been a unique opportunity to educate fellows in the field of diabetes research, by exposing them to a highly qualified and diabetes-focused research faculty, by engaging them in discussions on up-to-date research topics and data sets, and by stimulating their critical review of the relevant papers in the diabetes scientific literature. The review published in the Supplement is a tangible result of this process.
Declaration of interest
The authors report no declarations of interest.