INS and Hypoglycemia: Two are of particular interest; a) the “hindgut hypothesis” suggesting that nutrient delivery to the distal intestine drives the production of “incretins” which enhance insulin secretion (e.g. GLP-1), and b) the “foregut hypothesis.” The foregut hypothesis proposes that foregut bypass reduces the elaboration of nutrient-stimulated intestinal signals (e.g. anti-incretins) that limit insulin secretion, and normally defend against hypoglycemia thereby maintaining homeostasis [18], [19], [20].