Nevertheless, the findings in human bariatric patients indicate not only that endogenous GLP‐1 and PYY reserves are sufficient to sustain high post‐prandial plasma concentrations even months and years post‐surgery and often after prolonged presurgical history of diabetes, but also that at least in the context of preserved beta cell function and insulin sensitivity, the elevated GLP‐1 levels can promote insulin secretion and lowering of plasma glucose. The gene discussed is GLP1R; the disease is diabetes mellitus.