Browsing by Author "Argilés, Josep M."

Studies were performed to determine whether and/ or how dietary lipids participate in maternal hypertriglyceridemia during late gestation in the rat. After oral administration of glycerol-tri(1-14C)-palmitate, total radioactivity in plasma increased more rapidly in 20-day pregnant rats than in either 19-day pregnant rats or virgin controls. At the peak of plasma radioactivity. four hours after the tracer was administered. most of the plasma label corresponded to 14C-lipids in triglyceride-rich lipoproteins (d < 1.006). and when expressed per micromol of triglyceride, values were higher in pregnant than in virgin rats. The difference was less after 24 hours, although at this time the level of 14C-lipids in d < 1.006 lipoproteins was still higher in 20-day pregnant rats than in virgins. Tissue 14C-lipids. as expressed per gram of fresh weight, were similar in pregnant and virgin rats. but the values in mammary glands were much higher in the former group. Estimated recovery of administered radioactivity four hours after tracer in total white adipose tissue. mammary glands. and plasma lipids was higher in pregnant than in virgin rats. No difference was found between 20-day pregnant and virgin rats either in the label retained in the gastrointestinal tract or in that exhaled as 14C-CO2 during the first four hours following oral administration of 14C-tripalmitate. These findings plus the known maternal hyperphagia, indicate that in the rat at late pregnancy triglyceride intestinal absorption is unchanged or even enhanced and that dietary lipids actively contribute to both maternal hypertriglyceridemia and lipid uptake by the mammary gland.

Lipidic composition of plasma lipoproteins were determined at different times after total hepatectomy in the rat and compared with those in sham-operated animals. After hepatectomy there was a progressive decrease in the plasma triglycerides amounts corresponding to changes in the content of very low density lipoproteins (VLDL) triglycerides. Phospholipid concentrations in both low density lipoproteins (LDL) and VLDL decreased after hepatectomy but these lipids were unchanged in high density lipoproteins (HDL) which are the main contributors to plasma phospholipid content. Contrary to the other lipid components, plasma cholesterol leveis increased after hepatectomy, due mainly to the increment in HDL-esterified cholesterol. Modifications in plasma triglyceride levels after hepatectomy are interpreted as the result of total reduced synthesis and the effect of extrahepatic lipoprotein lipase activity on VLDL-triglycerides. Changes in cholesterol are considered due to its enhanced production by extrahepatic tissues.

In sham-operated rats, intravenous administration of 14C-very low density lipoprotein triglycerides (with labelled esterified fatty acids) caused an initial decrease and subsequent increase in plasma 14C-lipids of both very low density lipoproteins (VLDL) (density < 1.006) and lipoproteins of density > 1.019. There was a similar change in 14C-lipids in adipose tissue and heart whereas in kidney, spleen and liver, 14C-lipids increased initially and then decreased. Insulin treatment in sham-operated animals decreased circulating 14C-lipids in VLDL and in lipoproteins of density > 1.019, while intermediate density (1.006-1.019) lipoproteins increased. Insulin also enhanced the radioactivity retained in spleen. In functionally hepatectomized rats, 14C-lipids progressively increased in heart. Insulin treatment in these rats enhanced the disappearance from circulation of 14C-VLDL and of lipoproteins of density > 1.019, as well as the appearance of 14C-intermediate density lipoproteins. Toe appearance of 14C-lipids in white adipose tissue also was augmented, while it decreased in heart and lung. Thus, in sham-operated animals, insulin apparently stimulates the uptake of products of VLDL metabolism by cells in the reticuloendothelial system, while in functionally hepatectomized rats there is increased heart utilization of VLDL triglycerides, and insulin enhances the net extrahepatic catabolism of these lipoproteins.