LPL and hypertriglyceridemia: These results could explain diabetic hypertriglyceridaemia; additionally, in support of this mechanism, Chen et al. found that hypertriglyceridaemia in STZ rats was not primarily due to VLDL overproduction in liver but to a peripheral VLDL-TAG removal defect [62]: since LPL and VLDL-R are both down-regulated in diabetes, VLDL particles accumulate in the plasma, resulting in hypertriglyceridaemia.