Fatty Acid Incorporation into Human Adipose Tissue in Hypertrigiyceridaemia*

AbstractThe fatty acid and glucose incorporation into glycerides and glycerol release from adipose tissue were determined in a middle‐aged population of 109 men and 41 women. 43 men and 19 women were rrormolipidaemic. The same analysis was also carried out in 13 male and 9 female normolipidaemic students. Needle biopsy specimens of adipose tissue were incubated in vitro in an albumin medium containing 3H‐fatty acids and 14C‐glucose. After two hours of incubation values for fatty acid and glucose incorporation were calculated from the incorporation of 3H‐activity into the fatty acids and 14C‐activity into the glycerol moiety of extracted glycerides. The mean values for fatty acid incorporation were lower in all types of hypertriglyceridaemic subjects (II B, III, IV and V) than in the normolipidaemic control subjects. In the male hypertriglyceridaemic population 36 % had values for fatty acid incorporation below the 5th percentile of the normolipidaemic group and 14 % had values below the lowest normal value. The rate of fatty acid incorporation was negatively correlated with the serum triglyceride concentration. This correlation remained unchanged when partial correlation was performed when the influence of body weight was eliminated. Fatty acid and glucose incorporation correlated positively. Incorporation of glucose behaved in the same way as described above for incorporation of fatty acids. Glycerol and fatty acid release was the same in the normo‐ and hypertriglyceridaemic groups. It is likely that the removal of plasma triglycerides from blood requires hydrolysis of triglycerides to fatty acids and the subsequent removal of the fatty acids. The hypothesis has been formulated that when the former process is normal, a defect of fatty acid removal (a low rate of fatty acid incorporation into glycerides) may be responsible for an impaired removal of plasma triglyceride‐fatty acids. A low rate of fatty acid incorporation may contribute to the development of hypertrigiyceridaemia, according to this hypothesis.