Little is known on the molecular mechanisms of deterioration in aging edible nuts. Proteomic differences between aging and germinating nuts may unravel these mechanisms. Walnut (Juglans regia) kernels have physiological dormancy which can be alleviated by cyanide accompanying with enhanced gluconeogenesis. Warm/moist conditions however, promote kernel deterioration marked by reduced germination associated with increased lipase activity. The hypotheses that aging i) brings about increased lipase activity and enhanced lipid mobilization through increased abundance of lipase protein, ii) compromises gluconeogenesis of lipid reserves, iii) enhances proteolysis and amino acid catabolism, and finally iv) leads to oxidative stress were tested in a proteomic study of kernels aged by controlled deterioration, and those dormant non-aged and cyanide-treated ones all with 15% moisture content; having low, medium and high germination potentials, respectively. This revealed 155 differentially abundant proteins out of 930 identified ones compared to dry (6% moisture content) kernels. In deteriorated nuts, proteins with increased abundance were mainly involved in protein folding, translation and degradation, stress response/detoxification and glycolysis, but those with decreased abundance were related to gluconeogenesis and amino acid metabolism. Contrastingly, in non-aged cyanide-treated kernels, the proteins belonged to gluconeogenesis and oxidative pentose phosphate pathway showed increased abundance. Unlike aging seeds of many other plants, the deteriorated kernels accumulated various chaperons and detoxification proteins. Thus, deteriorating kernels experienced perturbations in lipid gluconeogenesis and amino acid metabolism associated with enhanced respiration and oxidative stress. As no lipase protein increased during kernel aging, the aging-induced lipase activation is possibly regulated by post-translational mechanisms.