Chronic kidney disease is characterized by a progressive inability to eliminate toxins from the bloodstream, which causes levels of urea and other toxic metabolites to increase. Although patients with chronic kidney disease often suffer from poor blood sugar regulation, the link between elevations in metabolite levels and glucose metabolism is not clear. In this issue of the JCI, researchers at the University of Montreal demonstrated that high levels of urea may compromise the function of insulin-producing pancreas cells and lead to impaired blood sugar regulation in chronic kidney disease. A team led by Vincent Poitout observed that insulin secretion was impaired in a mouse model of chronic kidney disease. Increasing urea levels in healthy mice led to similar reductions in insulin secretion as well as poor regulation of blood glucose levels. These findings point to a mechanism for blood sugar complications in chronic kidney disease that could potentially be targeted by preventative therapies.
Urea impairs β-cell glycolysis and insulin secretion in chronic kidney disease
Université de Montréal
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