Effects of a mixture of a saturated with an unsaturated fatty acid on secretion of the very low density lipoprotein by the liver.
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Biomedical subjects
Publications and source records attributed to G D Dunn.
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Diet has a definite role in certain gastrointestinal disorders, and dietary manipulation often is beneficial. In other cases, such as peptic ulcer, traditional dietary therapy cannot be justified by available evidence.
A patient with oat cell carcinoma of the lung which was responsive to radiotherapy developed jaundice. Endoscopic retrograde pancreatocholangiography (ERCP) revealed compression of the distal common bile duct. Radiotherapy to this area produced prompt and prolonged relief of the obstructive jaundice. The use of ERCP which led to significant palliation in a patient with known inoperable cancer makes this case worthy of note.
1. Livers from normal fed male rats were perfused in vitro with a bloodless medium which contained intially 3% bovine serum albumin and 100 mg% glucose. Albumin alone, or myristate (14 : 0), palmitate (16 : 0), palmitoleate (16 : 1), stearate (18 : 0), oleate (18 : 1), or linoleate (18:2) was infused at a constant rate (496 mumol/4 h), as a complex with albumin, during the experiment. 2. The very low density lipoprotein secreted by the liver after infusion of unsaturated fatty acids (16 : 1, 18 :1, 18 : 2) has a faster rate-zonal mobility in the ultracentrifuge and is, therefore, probably a larger particle with fewer moles of phospholipid and cholesterol relative to triacyglycerol (triacyglycerol/phospholipids/cholesterol = 100/25.1/16.4) than the very low density lipoproteins produced after infusion of saturated (14 : 0, 16 : 0, 18 : 0) fatty acids (triacyglycerol/phospholipids/cholesterol = 100/30.1/19.1). The molar ratio of phosphoipids/cholesterol of the very low density lipoprotein was similar regardless of which fatty acid was infused. The predominant fatty acid of the very low density lipoprotein or hepatic triacyglycerol, in all cases, was the infused acid. 3. We conclude that free fatty acid regulates the quantity and proportions of triacyglycerol, phospholipids, and cholesterol secreted by the liver in the very low density lipoprotein, and therefore, may secondarily influence concentrations of lipids in the very low density lipoprotein and other plasma lipoproteins circulating in vivo.
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Male rats were administered 1.5 ml safflower oil by gastric intubation 0, 4, and 8 hr after a 16 hr fast. Plasma, liver, and adipose tissue were collected 16 hr after the last fatty meal. Rats fasted for 16 hr served as controls. Following fat feeding, the fatty acid composition of the very low density lipoprotein, triglyceride, and hepatic triglyceride were similar, as were the percentages of 18:2 in the very low density lipoprotein and hepatic cholesteryl esters. The phospholipids of liver and plasma lipoproteins were similar in the control groups, except that more 16:0 was present in the plasma lipoproteins. After fat feeding, the plasma lipoproein phospholipids were enriched with 18:2 more than were the hepatic phospholipids. Furthermore, the percentage of 18:2 in phospholipid was much less than in triglyceride or cholesteryl esters. Clearly, esterified lipids of liver and plasma lipoproteins (very low density lipoprotein, low density lipoprotein, and high density lipoprotein), and to a lesser extent, adipose tissue, were enriched with 18:2 derived from dietary triglyceride fatty acid even 16 hr after the terminal meal. A major proportion of the very low density lipoprotein isolated by ultracentrifugation in zonal rotors from plasma of fat fed animals had a faster rate-zonal mobility than did the very low density lipoprotein isolated from plasma of control animals. The very low density lipoprotein isolated from plasma of fat fed rats contained fewer moles of phospholipids, cholesterol, and cholesteryl esters, relative to triglyceride than did the very low density lipoprotein from plasma of animals not receiving safflower oil. The molar ratio triglyceride:phospholipid:cholesterol:cholesterol esters in the very low denity lipoprotein was 100:42.0:22.1:44.5 in the control group and 100:35.4:17.8:19.5 in the fat fed animals. It is postulated that an important biochemical mechanism by which dietary triglyceride fatty acids consumed by the animal over a long period of time alter plasma concentrations of triglyceride, phospholipids, and cholesterol esters is the directive influence of plasma free fatty acid, derived from dietary triglyceride, on the secretion of very low density lipoprotein lipids by the liver.
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Fifty patients undergoing upper gastrointestinal fiberoptic endoscopy were studied prospectively for the development of bacteremia by aerobic and anerobic blood cultures obtained before, during, and at 5 and 30 minutes after the procedure. Forty-six patients were culture negative; four had positive cultures at 5 or 30 minutes after the procedure, or at both times. The level of bacteremia as estimated by pour plates was very low. Bacteremia did not correlate with the performance of biopsy or the type of mucosal abnormality found. It is concluded that only very high-risk patients should receive antimicrobial prophylaxis before this procedure. The minor risk of this low-level bacteremia should not be considered a contraindication to the performance of upper gastrointestinal endoscopy.
The objectives of this research were to study effects of dietary neutral fat on the concentration and the fatty acid composition of triglyceride (TG) and other lipid classes in plasma, liver, and adipose tissue and, particularly, to study the temporal and precursor-product relationship among those various lipid pools. Accordingly, male rats were administered 1.5 ml. of safflower oil by gastric intubation at 0, 4, and 8 hours after a 16-hour fast. Samples of plasma, liver, and adipose tissue were collected from groups of rats before fat feeding (0 time, controls), during the period of feeding (4 and 8 hours), and at several times thereafter up to 36 hours (28 hours after the last meal). The esterified lipids in all lipid fractions of liver and plasma became enriched with linoleic acid (18:2) during the experiment. The enrichment of plasma and hepatic TG, and of plasma FFA with 18:2 was substantial, reaching a maximum 8 hours after the third meal, whereas only a modest enrichment of adipose tissue TG was observed. The enrichment with 18:2 of various lipid fractions proceeded in the following sequence: total plasma TG became enriched first with 18:2 of chylomicron TG fatty acids during the period of active absorption of fat. Second, plasma FFA were enriched with 18:2 derived presumably from metabolism of chylomicron TG. Subsequently, enrichment of hepatic TG with 18:2 was observed. After maximum enrichment was attained, the percentage of 18:2 in these various lipid pools decreased in the following order. The percentage of 18:2 in plasma FFA fell rapidly, followed by a slower decrease of the 18:2 content of plasma TG and, finally, by an even slower decline of the 18:2 content of hepatic TG. All lipid fractions except plasma FFA contained an increased content of 18:2 even 28 hours following the last fattly meal. It can be deduced from these temporal relationships that plasma TG is derived indirectly from dietary TG long after active absorption of dietary fat has ceased. The composition of hepatic TG is altered by dietary neutral fat, through the intermediary uptake of plasma FFA derived from metabolism of chylomicron TG; this hepatic TG, which reflects dietary fat, is a significant precursor pool of the plasma TG in the postabsorptive state.
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