Reviews
| Rev Diabet Stud,
2011,
8(2):230-244 |
DOI 10.1900/RDS.2011.8.230 |
Association Between Genetics of Diabetes, Coronary Artery Disease, and Macrovascular Complications: Exploring a Common Ground Hypothesis
André G. Sousa1,2, Lívia Selvatici1, José E. Krieger1, Alexandre C. Pereira1
1Laboratory of Genetics and Molecular Cardiology, Heart Institute, University of Sao Paulo Medical School, Sao Paulo, Brazil
2Clinical Medicine Department, Federal University of Rio Grande do Norte, Natal, Brazil
Address correspondence to: Alexandre C. Pereira, e-mail: alexandre.pereira@incor.usp.br
Abstract
Type 2 diabetes and coronary artery disease (CAD) are conditions that cause a substantial public health burden. Since both conditions often coexist in the same individual, it has been hypothesized that they have a common effector. Insulin and hyperglycemia are assumed to play critical roles in this scenario. In recent years, many genetic risk factors for both diabetes and CAD have been discovered, mainly through genome-wide association studies. Genetic aspects of diabetes, diabetic macrovascular complications, and CAD are assumed to have intersections leading to the common effector hypothesis. However, only a few genetic risk factors could be identified that modulate the risk for both conditions. Polymorphisms in TCF7L2 and near the CDKN2A/B genes seem to be of great importance in this regard since they appear to modulate both conditions, and they are not necessarily related to insulinism, or hyperglycemia, for CAD development. Other issues related to this hypothesis, such as the problems of phenotype heterogeneity, are also of interest. Recent studies have contributed to a better understanding of the complex genetics of diabetic macrovascular complications. Much effort is still needed to clarify the associations in the genetics of diabetes, and cardiovascular disease. At present, there is little genetic evidence to support a common effector hypothesis, other than insulin or hyperglycemia, for the association between these conditions.
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| Rev Diabet Stud,
2011,
8(2):245-253 |
DOI 10.1900/RDS.2011.8.245 |
Modeling Chick to Assess Diabetes Pathogenesis and Treatment
Savita P. Datar1, Ramesh R. Bhonde2
1Department of Zoology, Sir Parshurambhau College, Pune 411030, India
2Manipal Institute of Regenerative Medicine, Manipal University, Bangalore, India
Address correspondence to: Ramesh R. Bhonde, e-mail: rrbhonde@gmail.com
Abstract
Animal models have been used extensively in diabetes research. Studies on animal models have contributed to the discovery and purification of insulin, development of new therapeutic approaches, and progress in fundamental and clinical research. However, conventional rodent and large animal mammalian models face ethical, practical, or technical limitations. Therefore, it would be beneficial developing an alternative model for diabetes research which would overcome these limitations. Amongst other vertebrates, birds are phylogenically closer to mammals, and amongst birds, the chick has been used as one of the favored models in developmental biology, toxicology, cancer research, immunology, and drug testing. Chicken eggs are readily available, have a short incubation period and easily accessible embryos. Based on these inimitable advantages, the present review article aims to discuss the suitability of the chick as a model system to study specific aspects of diabetes. The review focuses on the application of i) chick pancreatic islets for screening of antidiabetic agents and for islet banking, (ii) shell-less chick embryo culture as a model to study hyperglycemia-induced malformations observed in mammalian embryos, and (iii) chick chorioallantoic membrane (CAM) to examine glucose-induced endothelial damage leading to inhibition of angiogenesis.
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