Hepatic carnitine palmitoyltransferase (CPT) turnover was studied in control and in non-ketotic hyperlycaemic streptozotocin-diabetic rate. The degradation constant (k(d)) and half-life (t( 1/2 )) did not appear to be altered by mild diabetes. The hepatic CPT (μg/g of liver) was not increased by the mild, non-ketotic, diabetes. However, the total hepatic CPT (μg/liver) was 37% greater in the diabetic animals, owing to the increased liver weight. This resuylted from a 405 increase in the synthesis constant (k(s)). Hepatic CPT activity (total detergent-solubulized) and translation rates were measured in fed, starved (48h), and non-ketotic diabetic, ketotic diabetic and diethylhexyl phthalate (DEHP)-treated rats. CPT activity (munits/mg of mitochondrial protein) was not significantly increased with non-ketotic diabetes (44% increase, but non-significant), but was increased approx. 2-fold with starvation and ketotic diabetes, and 3.5-fold with DEHP treatment. CPT expressed as units/liver was increased non-significantly (23%) in non-ketotic and starved rats, similar to the turnover study, but was significantly iocnreased with ketotic diabetes and with DEHP treatment. mRNA-translation activity for CPT was elevated in all states to a somewhat greater extent than was activity. It was concluded that protein synthesis as a product of increased CPT-mRNA translation activity is a major means of long-term regulation.