Primary hyperoxaluria type 1 (PH1) is a recessive disease in which an enzyme, alanine:glyoxylate aminotransferase (AGT), is mistargetted from the peroxisomes where it functions in the glyoxylate pathway, to the mitochondia(28) where it is inefficient. It can be caused by defects in at least 2 glyoxylate-metabolizing enzymes and leads to excessive urine oxalate excretion resulting in kidney stones and/or calcification of the kidney which can occur in childhood or adolescence. Patients used to die on average at age 36 (29), however vitamin B12 therapy and dietary changes can help to increase life span in certain forms of the disorder.
According to Birdsey et al., "One molecular adaptation to diet that is spread widely across Mammalia is the differential intracellular targeting of the intermediary metabolic enzyme alanine:glyoxylate aminotransferase(AGT), which tends to be mitochondrial in carnivores, peroxisomal in herbivores, and both mitochondrial and peroxisomal in omnivores."(30)
As we have seen, normal humans express the AGT gene effectively in their peroxisomes, but when AGT is targeted to the mitchondria such as in the PH1 mutation, it cannot operate effectively. It can thus be concluded that humans evolved through a herbivorous lineage, having evolved peroxisomes, but not mitochondria adapted to effective glyoxylate metabolism.