As the incidence of diabetes increases worldwide, the need for recommendations on how to prevent and treat the condition grows exponentially, and so does the need for an authoritative source for information on the appropriate models to study the condition. The new edition of Animal Models of Diabetes is that source. The book presents updated and expanded information regarding the use of models in experiments with both Type 1 and Type 2 diabetes.
The new edition compiles relevant time-saving information on well-recognized models, including various mice, rats, minipigs, and Rhesus monkeys, and provides extensive references for more in-depth study. It contains new and updated referenced reviews on animals with induced obesity as well as observations on retinopathy in spontaneous diabetes resembling human lesions. The book discusses nutritionally diabetes-prone animals and considerations of insulin resistance and obesity. The contributors also address the importance of recent findings on the pathogenesis of diabetes and its complications in relation to human disease.
Including contributions from prominent experts in the field, the book brings together scattered data and lucidly presents it. This promotes the understanding of the etiopathology of diabetes and offers a new grasp of the insulin action, its negative feedback leading to insulin resistance, and its detrimental outcomes. The book also includes new knowledge on specific complications of diabetes, offering an incentive to test advanced modalities to prevent and inhibit their occurrence.
A timely collection of research papers by 18 leading scientists in the area of biochemical genetics of diabetes mellitus, these contributions focus on a well defined class of monogenic forms of the disease (i.e. MODYs 1-5) all caused by specific mutations or deletion of genes that control pancreatic beta-cell functions: HNF-4alpha, glucokinase, HNF-1alpha, IDX-1 and HNF-1beta. This volume offers a historical perspective of MODYs, and it also contains contributions which deal with the fundamental questions of pancreas and liver development, critical for the understanding of the syndrome complex discussed. Attempts have been made to highlight results and concepts that may be relevant for understanding type-II diabetes in general, exemplified by contributions that connect the field of pancreatic islet cell biology and pathology with the newest findings in the area of insulin action, e.g. the role of the insulin receptor and insulin receptor substrates (IRS 1-3).