Apolipoprotein B metabolism in hypertriglyceridemic diabetic patients administered either a fish oil- or vegetable oil-enriched diet

Abstract

The effect on apolipoprotein B kinetics of a diet enriched in either fish oil or safflower oil was investigated in five hypertriglyceridemic (HTG), non-insulin-dependent diabetic subjects. The fish oil diet decreased plasma triglycerides and VLDL-apoB but increased LDL-apoB and LDL-cholesterol. Total plasma apoB concentration did not change, nor did the increased VLDL-apoB secretion present in these HTG subjects, which, accompanied by impaired lipolysis, accounted for their elevated VLDL. The fish oil-induced fall in VLDL resulted from a decrease in secretion without a change in residence time. The IDL fraction, which also contained small VLDL, was the primary site for the secretion of apoB particles in the HTG subjects. On the fish oil diet there was a further, compensatory increase in the secretion of these lipoproteins such that the transport of apoB in IDL remained the same, as did its mass. In the HTG subjects the major portion of IDL lipoproteins was catabolized, with LDL-apoB production comprising the lesser quantity. On the fish oil diet, a shift in the channeling of the lipoprotein output from IDL resulted in a decrease in the catabolic pathway and an increase in conversion to LDL. As the residence time of LDL did not change, this increased input gave rise to the larger mass of LDL-apoB seen in these hypertriglyceridemic subjects when receiving a fish oil diet.-Fisher, W. R., L. A. Zech, and P. W. Stacpoole. Apolipoprotein B metabolism in hypertriglyceridemic diabetic patients administered either a fish oil-or vegetable oilenriched diet.

Hypertriglyceridemia Results From an Impaired Catabolism of Triglyceride-Rich Lipoproteins in PLIN1 -Related Lipodystrophy

“…30 On the contrary, the hypotriglyceridemic treatment with omega-3 fatty acids seems less appropriate since the reduction of plasma triglyceride levels with omega-3 fatty acids mainly results from a reduction of VLDL production. [31][32][33] Moreover, because PLIN1-related FPL leads progressively to diabetes, the choice of an antidiabetic treatment that also improves the catabolism of triglyceride-rich lipoproteins may be considered. For instance, liraglutide has been shown to significantly increase the catabolism of VLDL and IDL, 12 suggesting that the class of GLP-1R (glucagon-like peptide-1 receptor) agonists could be a good option to both reduce insulin resistance and also accelerate the catabolism of triglyceride-rich lipoproteins.…”