The relative risk of type 2 diabetes is higher in individuals of low birth weight, and programming of the metabolic axis is influenced by the intrauterine nutritional environment. The β-cells of the pancreatic islets develop from precursor cells and islet development is controlled by the interactions of transcription factors and peptide growth factors. Both are modulated by fetal nutrition. Fetal programming of adult glucose intolerance has been studied using rodent models, including administration of a low protein (LP) diet. Long-term changes are found in insulin action within target tissues, as well as in the development and function of the endocrine pancreas. Intrauterine growth restriction in rat or man results in a reduced islet and β-cell mass at birth. A reduction of dietary protein to 8% throughout gestation caused relative growth restriction at birth with reduced β-cell mass and islet size. If LP diet is extended to weaning the changes are irreversible, and include an altered β-cell ontogeny, decreased cell replication but increased apoptosis, a reduced expression of insulin-like growth factors, and a reduction in islet vascularity and the number of endothelial precursor cells. The net result is a population of islets with limited plasticity and an inability to adapt to the associated insulin resistance. Studies with supplementation of selected amino acids in early life showed that the altered pancreatic morphology, and glucose intolerance, is reversible by taurine. Both LP diet and taurine are able to delay the onset of type 1 diabetes in the non-obese diabetic mouse.