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Although chylomicron production has only been measured in animal models of diabetes and insulin resistance, VLDL overproduction has been shown in diabetes in humans as well [120–122, 125], the driving force being the non-supressability of FFA postprandially due to the malfunction of adipose tissue by adipose triglyceride lipase (ATGL) leading to an increase in postprandial triglycerides which are taken up by the liver and re-secreted in the VLDL [126]