In 1974, the "Ariadne's thread" (from Greek Mythology, pick one's way through the Labyrinth) of autoimmunity leading to the immunogenetic theory of type 1 diabetes mellitus made it possible to conclude that in this phenotype there exists an unsolved conflict between β-cells and the body's autoreactive immune system. In type 2 diabetes mellitus (T2DM), the "Ariadne's thread" links obesity to pancreatic β-cell biology. Unfortunately, beginning from a wrong interpretation of the relationship between plasma glucose and plasma insulin, the insulin resistance hypothesis was born and claimed as the main defect of T2DM. Overlooking obesity, the understanding of T2DM pathogenesis was delayed by almost half a century. Fortunately, the adipobiology, particularly adipocytes was able to reach the "drawing board" of researchers, and has all the chances these cells to become the "cell of the century", just as the pancreatic β-cell was last the cell of century. The association of diabetes and obesity has motivated us to put pancreatic β-cells and adipocytes head-to-head, that is, we moved from the T2DM-obesity couple to the β-cell-adipocyte couple, appreciating their main secretory products, insulin/proinsulin, C-peptide, amylin (for β-cells), and adiponectin, as well as other numerous adipokines (for adipocytes). We thus propose that the proinsulin-to-adiponectin ratio could become the earliest predictor of dysfunction of these two cell types.
Adipobiology 2012; 4: 41-50.
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