Defect in fatty acid oxidation in moderately obese men with hypertriglyceridaemia
Document Actions
Endogeneous hypertriglyceridaemia could result from 1) re-esterification of excess nonesterified fatty acids entering the liver, 2) activation of hepatic lipogenesis and export of apoB-containing triglyceride-rich lipoproteins, and 3) defective oxidation of hepatic fatty acids leading to greater triglyceride synthesis, a less-documented mechanism. The study used plasma levels of 3-hydroxybutyrate as a marker for fatty acid oxidation and was carried out in hypertriglyceridaemic and normotriglyceridaemic subjects under three conditions: 1) in the fasting state, 2) after a fatty meal designed to enhance fatty acid oxidation, and 3) after an oxandrolone challenge (a synthetic derivative of testosterone) shown to increase fatty acid oxidation. In the fasting state, 3-hydroxybutyrate concentrations in hypertriglyceridaemic patients were only 53% of the levels obtained in the normotriglyceridaemic group. Moderate increases in 3-hydroxybutyrate concentrations were observed after a fatty meal, though values for hypertriglyceridaemic patients remained 62% of the levels observed in normotriglyceridaemic subjects, with a similar pattern noted following oxandrolone challenge. In conclusion, patients with endogeneous hypertriglyceridaemia seem to have a defect in basal and postmeal fatty acid oxidation as reflected by reduced levels of 3-hydroxybutyrate, which contributes to the development of hypertriglyceridaemia.
Abstract
