Retarded chylomicron apolipoprotein-B catabolism in type 2 (non-insulin-dependent) diabetic subjects with lipaemia.

To define the kinetics of chylomicron apolipoprotein-B catabolism in diabetic subjects with lipaemia, autologous chylomicrons (Sf 400) harvested from plasma following an oral fat load were radioiodinated and re-injected. The radioactivity in the tetramethylurea-insoluble, non-lipid Sf greater than 400 lipoprotein fraction was followed in serial samples over 60-72 h on a fat-free, isocaloric diet in: (1) five normal subjects; (2) four hypertriglyceridaemic, non-diabetic subjects; and (3) five diabetic patients (one subject, No. 3, was studied twice). The plasma apolipoprotein-B decay curve for the Sf 400 fraction disclosed biphasic disappearance: a rapid first phase (residence time 0.8-1.9 h) accounting for the large majority of removal (60%-95%) and a slower second phase (residence time 3.6-47.6 h), accounting for the remainder. Total chylomicron apolipoprotein-B residence times were similar in normolipidaemic (1.8-7.3 h) and hypertriglyceridaemic (2.3-10.3 h) non-diabetic subjects and the mildly hypertriglyceridaemic diabetic patients (5.6 and 5.8 h). In the untreated lipaemic diabetic subjects (Nos. 1 and 2), only a single, much slower phase was observed (total chylomicron apolipoprotein-B residence time 38.5-58 h). Adipose tissue biopsy in one of these subjects (No. 1) disclosed profoundly low lipoprotein lipase activity. The lipaemic diabetic subject (No. 3) studied early during treatment showed an intermediate pattern. These studies suggest a key role for insulin-dependent, lipoprotein lipase-mediated triglyceride hydrolysis in the removal of chylomicrons from plasma.