Type 1 and type 2 diabetes are growing public health problems. As iPS cells retain the same genetic make-up as the somatic cell targeted for reprogramming, these cells hold tremendous promise for uncovering novel genetic and biochemical factors that underlie diseases with complex and poorly understood genetic influences, such as diabetes. However, while the role of endothelial cells in supporting beta-cell homeostasis is vastly investigated, the role of pericytes remains largely unknown. For those who have Type 1 diabetes, the body’s immune system destroys cells that make insulin, the hormone needed to regulate blood sugar. “There really is only one competitor in this field who has been working as long as we have, and have made similar innovations, and that is BetaLogics,” ViaCyte CEO Paul Laikind said yesterday in an interview. Therefore, even modest levels of beta-cell activity at entry in the DCCT were associated with reduced incidences of retinopathy and nephropathy. Clinical studies incorporating indirect measures of beta-cell function also support a protective effect with some agents.
Such mechanisms are related to those of the insulin secreted beta-cell. Thus, β-cell death and cell death-associated inflammation through innate immune receptors could be important in both T1D and T2D. Blockage of multiple pathways, rather than a single pathway, of beta cell-death may, therefore be necessary to fully protect beta cells from destruction and thereby prevent type 1 diabetes.