Effects of feeding cooked ground beef on plasma lipid and apolipoprotein concentrations in male turkeys.

Two experiments with male turkeys were designed to study the effects of eating cooked ground beef on plasma lipid and lipoprotein levels. In both experiments, cooked ground beef from forage-finished cattle (F-Bf) and grain-finished cattle (G-Bf) were added at an average of 28.1 and 34.5 g of beef per 100 g of ration in order to provide 40% of the protein requirement. The experimental diets formulated to be isocaloric and isonitrogenous were: 1) basal diet (negative control) in which soybean meal and corn oil served as protein and fat sources, respectively; 2) basal plus crystalline cholesterol (positive control) incorporated at 1 and 2% of the diet in trials 1 and 2, respectively; 3) basal plus F-Bf; 4) basal plus G-Bf. The polyunsaturated to saturated fat ratio averaged 3.45 for diets 1 and 2 and 0.17 for diets 3 and 4, respectively. At 16 weeks, consumption of diets 3 and 4 elevated (P less than 0.05) plasma triglyceride levels and phospholipid levels (trial 1). In trial 2, only diet 4 elevated (P less than 0.05) plasma phospholipid levels. In both trials, the beef diets did not significantly elevate plasma cholesterol and high density lipoprotein (HDL) cholesterol levels above the basal diet. However, the major apoprotein in the HDL fraction, apolipoprotein A-I (apoA-I), was increased (P less than 0.05) in the plasma of male turkeys fed the G-Bf diet in both trials and F-Bf diet in trial 1. Plasma apolipoprotein B (apoB), primarily found in low density lipoproteins (LDL), was increased (P less than 0.05) in one of the two trials by the inclusion of beef in the diet. There were no significant differences in plasma cholesterol, HDL-cholesterol, apoA-I and apoB levels between the types of beef (F-Bf vs. G-Bf).

Concurrent inductions of avian hepatic lipogenesis, plasma lipids, and plasma apolipoprotein B by estrogen.

The inductions of hepatic fatty acid synthesis, estrogen-specific plasma proteins, plasma lipids, and apolipoproteins by a single subcutaneous injection of diethylstilbestrol (40 mg/kg body weight) have been examined in immature male turkeys. Estrogen induced the appearance of phosvitin, lipovitellin, and apoVLDL-II in the blood plasma. The highest concentrations of these estrogen-specific plasma proteins were observed 48 hr following hormone administration. Estrogen increased the concentration of triglyceride in the liver, predominantly those molecular species containing 16 carbon fatty acids (triglycerides with 53 and 55 carbon atoms). Liver cholesterol was present predominantly as free cholesterol. Although estrogen did not affect the concentrations of free or esterified cholesterol in the liver, the hormone increased the amount of cholesterol esterified with 20-carbon fatty acids and caused a corresponding decrease in cholesterol esterified with 18 carbon fatty acids. Estrogen treatment elevated the plasma triglycerides 55-fold, tripled the plasma phospholipid, and approximately doubled the plasma cholesterol. The de novo synthesis of fatty acids in the liver in vivo was stimulated by estrogen administration, as exhibited by increased 3H2O incorporation into the phospholipids and triglycerides of both liver and plasma. In contrast, hepatic cholesterol synthesis was unaffected. The amounts of newly synthesized triglyceride in the liver and plasma and the specific radioactivities of the plasma triglyceride following 1-hr in vivo labeling periods, 0, 24, 48, and 72 hr after estrogen injection indicate that increased hepatic fatty acid synthesis is a primary and major casuative factor in the development of estrogen-induced hyperglyceridemia in this avian species. The concentration of apolipoprotein B in the plasma increased in parallel with hepatic fatty acid synthesis and the appearance of newly synthesized triglyceride in the plasma, whereas the plasma apolipoprotein A-I level decreased. These observations indicate that in the avian liver estrogen causes a coordination of inductions in the conversion of carbohydrate to triglyceride and in the production of proteins (apolipoprotein B and apoVLDL-II) involved in the assembly of triglyceride-rich lipoprotein particles, leading to hypersecretion of these lipoproteins into the circulation.

Lipoprotein lipase activity in turkey aorta.

Lipoprotein lipase activity was measured in heparin extracts of aortic intima and adventitia from normal and cholesterol-fed turkeys. This lipolytic activity showed typical characteristics of lipoprotein lipase i.e., requirement of serum for activity and a 92% inhibition by protamine sulfate. The highest lipoprotein lipase activity was found in the adventitia of the abdominal aorta. Lipoprotein lipase activity was greater in the intima of the thoracic aorta than in the intima of the abdominal aorta. This higher activity of thoracic intima was not correlated with development of fibrous plaques which were found only in abdominal aorta. Cholesterol-feeding resulted in plasma very low density lipoproteins enriched in cholesterol-ester but had no effect on the level of lipoprotein lipase activity of aortic intima. Cholesterol-feeding, although altering lipoprotein composition, did not increase aortic intima lipoprotein lipase activity.

Lipid metabolism in laying hens. The relationship of plasma lipids and liver fatty acid synthetase activity to changes in liver composition.

Plasma and liver samples were taken from a random sample of caged commercial hybrid layer hens which had been in egg production for fifteen months. The concentration of plasma and liver lipids and the activity of liver fatty acid synthetase (FAS) were measured in laying hens with liver weight of 20 to 53 g. Liver total lipid, water, non-lipid, and cytosolic fractions, which are the four major liver components, increased linearly with respect to wet liver weight. FAS activity increased with all liver components. Accumulation of lipid in the liver did not inhibit FAS activity. Total cholesterol, free cholesterol, esterified cholesterol, triglycerides, and phosphorous were measured on each plasma sample. Multiple regression analysis showed that all plasma lipids, except cholesterol esters, were related cubically with increasing wet liver weight and cytosolic protein.

Effect of estrogen on triacylglycerol metabolism: inhibtion of post-heparin plasma lipoprotein lipase by phosvitin, an estrogen-induced protein.

PIP: The effects of phosvitin and lipovittelin on partially purified postheparin plasma levels of lipoprotein lipase (LPL) and triacylglycerol (TGL) and adipose tissue LPL were studied in laying and nonlaying female turkeys and estrogen-treated male turkeys. Postheparin plasma lipolytic activities and those of LPL and TGL decreased 2- to 3-fold after the onset of egg production, while a 24-fold increase in triacylglycerol (TG) was observed. Lipovittelin had no effect on either TGL or LPL, while phosvitin, in a dose of 3 mcg protein/ml assay mixture, had a strong inhibitory effect on plasma LPL and chicken adipose tissue LPL. TGL was not affected by phosvitin. The results suggest that phosvitin may have a role in the regulation of adipose tissue and plasma levels of TG in laying birds.^ieng

Mercury inhibition of fatty acid synthesis in chicks.

Male chicks were fed a commercial ration and were given drinking water which contained 0, 50, 100, 150, 200 or 300 mug of mercury/ml as mercuric chloride from hatching to 3 weeks of age. In one experiment, the mercuric chloride was administered by injection into the abdominal cavity rather than in the drinking water. At 3 weeks the chicks were killed, and the livers were removed and weighed. The activity of fatty acid synthetase in the 800 X gav supernatant fractions of the liver homogenates and in vivo incorporation of [14C]acetate into liver and carcass fatty acids and respiratory 14CO2 was determined as indicated. Administration of mercury at a treatment level of 300 mug/ml of drinking water depressed growth, feed and water consumption, liver weight, hepatic fatty acid synthetase activity, and in vivo incorporation of [14C]acetate into liver and carcass fatty acids, and increased the production of respiratory 14CO2 as compared with controls. In experiments in which graded doses of mercury were administered, body weights, liver weights, and feed and water intakes of the chicks receiving 0, 50 and 100 mug of mercury/ml of drinking water were similar to each other, but these parameters were severely depressed by 200 mug of mercury/ml of drinking water. Mercury caused a dose-related decrease of fatty acid synthetase activity. Incorporation of [14C]acetate into carcass fatty acid was depressed by 50 and 200 mug of mercury/ml of drinking water; incorporation into liver fatty acids and production of respiratory 14CO2 was not affected by mercury. Intra-abdominal injection of 6 mg of mercury/100 g body weight (as mercuric chloride) into well alimented chicks depressed hepatic fatty acid synthetase activity at 1 h post-injection. The data are consistent with the hypothesis that a portion of the effects of mercury on fatty acid synthesis are direct rather than a secondary effect of inanition.