Golden hamsters infected with Spirometra erinacei plerocercoids develop a hypertriglyceridaemia characterized by an increase in very low-density lipoprotein. Acyl-CoA synthetase activity, the rate of fatty acid synthesis in the liver and triglyceride production studies showed that the activation and synthesis of fatty acid and production of triglyceride in plerocercoid-infected hamsters were not significantly different from the controls. Lipase activity in post-heparin plasma was found to be suppressed in plerocercoid-infected golden hamsters. The presence of plerocercoids also resulted in a significant reduction in serum thyroxine, but the hypertriglyceridaemia associated with plerocercoid infection was not reversed by injecting the infected hamsters with 2 micrograms/day doses of L-thyroxine. The levels of serum immunoreactive insulin in plerocercoid-infected hamsters were not significantly different from the controls. We conclude that the hypertriglyceridaemia, associated with plerocercoid infection in hamsters, results predominantly from a suppression of triglyceride degradation, and that the suppression of lipase activity is probably not the result of hypothyroidism or the lack of insulin, but the result of secretion of growth hormone-like substances.