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Blood lipids and first-ever ischemic stroke/transient ischemic attack in the Bezafibrate Infarction Prevention (BIP) Registry: high triglycerides constitute an independent risk factor.

BACKGROUND: Despite unclear associations between blood lipids, including fractionated cholesterol and triglycerides, and stroke, recent evidence demonstrates that lipid-modifying agents decrease the risk of stroke in patients with coronary heart disease (CHD). METHODS AND RESULTS: Patients with documented CHD who were screened for but not included in the Bezafibrate Infarction Prevention study and had no history of stroke or transient ischemic attack (TIA) (n=11 177) were followed up. At baseline, medical histories were obtained and blood lipids assessed at a central study laboratory. During a 6- to 8-year follow-up period, 941 patients were identified as having nonhemorrhagic cerebrovascular disease, of whom 487 had verified ischemic stroke (per clinical findings and brain CT) or TIA. Patients experiencing an ischemic stroke/TIA had higher mean levels of triglycerides, lower levels of HDL cholesterol, and lower percentages of cholesterol contained in the HDL cholesterol moiety (%HDL; P<0.01 for all). In a logistic regression model, the adjusted ORs for developing an ischemic stroke/TIA were 1.27 (95% CI 1.01 to 1.60) associated with triglycerides >200 mg/dL and 0.87 (95% CI 0.78 to 0.97) associated with a 5% decrease in %HDL. The increased risk associated with high triglycerides was found across subgroups of age, sex, patient characteristics, and cholesterol fractions. CONCLUSIONS: High triglycerides constitute an independent risk factor for ischemic stroke/TIA across subgroups of age, sex, patient characteristics, and cholesterol fractions, whereas high %HDL was an independent protective factor among patients with CHD. These findings support the role of blood lipids, including triglycerides, as important modifiable stroke risk factors.

Age Factors↗

Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S.

BACKGROUND: Patients with low HDL cholesterol (HDL-C) and elevated triglyceride had an increased risk for coronary heart disease (CHD) events and received the greatest benefit with fibrate therapy in substudy analyses of the Helsinki Heart Study and the Bezafibrate Infarction Prevention Study. METHODS AND RESULTS: In this post hoc analysis of the Scandinavian Simvastatin Survival Study, which enrolled patients with elevated LDL cholesterol (LDL-C) and CHD, subgroups defined by HDL-C and triglyceride quartiles were compared to examine the influence of HDL-C and triglyceride on CHD events and response to therapy. Patients in the lowest HDL-C (<1.00 mmol/L [39 mg/dL]) and highest triglyceride (>1.80 mmol/L [159 mg/dL]) quartiles (lipid triad; n=458) had increased proportions of other features of the metabolic syndrome (increased body mass index, hypertension, diabetes), men, prior myocardial infarction, prior revascularization, and beta-blocker use than patients in the highest HDL-C (>1.34 mmol/L [52 mg/dL]) and lowest triglyceride (<1.11 mmol/L [98 mg/dL]) quartiles (isolated LDL-C elevation; n=545). The major coronary event rate was highest in lipid triad patients on placebo (35.9%), and this subgroup had the greatest event reduction (relative risk 0.48, 95% CI 0.33 to 0.69); a significant treatment-by-subgroup interaction (P=0.03) indicated a greater treatment effect in the lipid triad subgroup than the isolated LDL-C elevation subgroup. CONCLUSIONS: Patients with elevated LDL-C, low HDL-C, and elevated triglycerides were more likely than patients with isolated LDL-C elevation to have other characteristics of the metabolic syndrome, had increased risk for CHD events on placebo, and received greater benefit with simvastatin therapy.

Adult↗

Very low density lipoproteins in intestinal lymph: role in triglyceride and cholesterol transport during fat absorption.

The role of nonchylomicron very low density lipoproteins (VLDL, S(f) 20-400) in the transport of triglyceride and cholesterol was studied during lipid absorption. Various long chain fatty acids were infused intraduodenally in the form of mixed fatty acid-mono-olein-taurocholate micelles; control animals received saline or taurocholate. As compared with controls, all fatty acids (palmitic, oleic, linoleic) resulted in significant increases in chylomicron (S(f) > 400) triglyceride. In addition, palmitic acid resulted in a twofold increase in VLDL triglyceride, whereas with the absorption of oleic or linoleic acid VLDL triglyceride did not change significantly. Differences in triglyceride fatty acid composition between chylomicrons and VLDL were observed during lipid absorption. Although the absolute amount of endogenous cholesterol in intestinal lymph was not significantly affected by lipid absorption under these conditions, its lipoprotein distribution differed substantially among the lipid-infused groups. During palmitate absorption, VLDL cholesterol was similar to that in the taurocholate-infused controls, and was equal to chylomicron cholesterol. In contrast, during oleate and linoleate absorption the VLDL cholesterol fell markedly, and was less than half of the chylomicron cholesterol in these groups. The half-time of plasma survival of VLDL cholesterol-(14)C was found to be twice that of chylomicron cholesterol-(14)C. These studies demonstrate that dietary long chain fatty acids differ significantly in their effects upon the transport of triglyceride and cholesterol by lipoproteins of rat intestinal lymph. These findings, together with the observed differences in rates of removal of chylomicrons and VLDL from plasma, suggest that variations in lipoprotein production at the intestinal level may be reflected in differences in the subsequent metabolism of absorbed dietary and endogenous lipids.

Animals↗

Sex steroid influence on triglyceride metabolism.

Triglyceride metabolism was investigated in groups of fed and fasted rats after 21 days of parenteral estradiol (5 mug daily), progesterone (5 mg daily), or the two steroids in combination. Results were compared with control groups receiving an oil solvent alone. In rats given estradiol separately or combined with progesterone, hypertriglyceridemia was uniformly associated with increased plasma triglyceride entry, estimated with the i.v. Triton WR1339 technique. Progesterone alone had no effect on these parameters. Plasma postheparin lipolytic activity (PHLA), adipose, mammary gland, and protamine-resistant liporotein lipases (LPL) were significantly increased in progesterone-treated rats and significantly decreased in rats receiving estradiol with the exception of mammary gland LPL, which was also increased to a slight extent. The combined regimen reduced plasma PHLA and increased protamine-resistant adipose, and mammary gland LPL activity. Sex steroid treatments had minimal effects on plasma glucose and free fatty acid concentrations, but all increased plasma insulin significantly. Hyperinsulinemia did not parallel changes in body weight or other measured parameters. Linear regression analyses revealed that plasma triglyceride concentrations in all fed, treated rats correlated significantly with triglyceride entry but not very uniformly with plasma or tissue LPL activity. We conclude that estradiol, unlike progesterone, has substantial lipemic effects in the rat which relate best to triglyceride entry. Hyperinsulinemia, changes in body weight, plasma PHLA, and tissue LPL activities did not consistently predict the influence of sex steroid treatment on plasma triglyceride concentrations.

Adipose Tissue↗

Colipase enhances hydrolysis of dietary triglycerides in the absence of bile salts.

This study explores how dietary lipids are digested when intraduodenal bile salts are low or absent. Long-chain triglycerides emulsified with phosphatidylcholine were found to be hydrolyzed very slowly by pancreatic lipase alone, as if the surface layer of phospholipids enveloping the triglycerides impeded the action of the enzyme. Colipase enhanced triglyceride hydrolysis severalfold, both when added before or after the lipase. Hydrolysis became even more rapid when the emulsion was first incubated with pancreatic phospholipase. Hydrolysis of long-chain triglycerides was also severely impeded when other proteins were added to the system, probably because they adsorbed to the oil-water interface of the emulsion droplets. It was previously known that bile salts can relieve such inhibition, presumably by desorbing the adsorbed proteins. Colipase was found to enhance hydrolysis severalfold in a dose-dependent manner even in the absence of bile salts, i.e., it could partially or completely relieve the inhibition depending upon the amount and the type of inhibitory protein added to the system. Prior exposure of a protein-coated triglyceride emulsion to another lipase also enhanced the rate at which pancreatic lipase could then hydrolyze the lipids. Most dietary triglycerides are probably presented for intestinal digestion in emulsions covered by proteins and/or phospholipids. These emulsions would be hydrolyzed slowly by pancreatic lipase alone. However, through the action of the lipase in stomach contents and of pancreatic phospholipase and through the lipolysis-promoting effects of collipase, these triglycerices can be rather efficiently hydrolyzed, even in the absence of bile salts.

Animals↗

Differing uptake of emulsion triglyceride by the fed and fasted rat liver.

The recycling perfusion of a fasted rat liver with an apoprotein E-enriched synthetic triglyceride emulsion revealed a significantly greater hepatic uptake of both the apoprotein and the triglyceride than did the liver of a chow-fed animal. This greater hepatic triglyceride uptake by the perfused fasted liver in comparison to the fed was also noted for emulsions containing no added apoprotein or supplemented with both the E and CIII-1 proteins. However, no difference in the uptake of the triglyceride emulsion was seen for the fed and fasted livers when evaluated by a nonrecycling single pass perfusion. The isolated hepatocyte plasma membranes from fasted rats failed to demonstrate enhanced binding of apoprotein or lipid when compared to those from fed animals. If the residual E loaded triglyceride emulsion was recovered from the recycling perfusates of fed and fasted livers and evaluated in a non-recycling single-pass system, the emulsion from the fasted perfusion was cleared as facilely as previously, whereas that from the fed was less actively cleared. The emulsions retrieved from the perfusion of the fed liver contained significantly more protein than did the fasted; in particular apo C. This apparent alteration of emulsion apoproteins by the fed liver possibly results in a less active hepatic retrieval and may be important in downregulating the entry of lipoprotein triglyceride in the postabsorptive liver.

Animals↗

Interleukin-6 stimulates hepatic triglyceride secretion in rats.

Interleukin-6 (IL-6) not only regulates a variety of immune functions, but also is the most potent cytokine in inducing the hepatic acute phase proteins. We determined the effect of IL-6 on serum lipid levels and the mechanism of IL-6-induced hypertriglyceridemia in rats. Intravenous administration of IL-6 (0.1-10 micrograms/200 g BW) increased serum triglyceride levels in a dose-dependent manner. One hour after IL-6 administration, serum triglyceride levels were increased, with peak values at 2 h (2.2-fold increase). Serum cholesterol levels also increased, but the effect was delayed, first occurring at 4 h and peaking at 8 h (1.24-fold increase). IL-6 treatment increased hepatic triglyceride secretion without decreasing the clearance of triglyceride-rich lipoproteins, indicating that the hypertriglyceridemia was due to increased secretion by the liver. Furthermore, IL-6 stimulates lipolysis, and the increased delivery of FFA to the liver significantly contributed to the IL-6-induced hypertriglyceridemia. Neither alpha 1- nor beta-adrenergic receptor antagonists affected the hypertriglyceridemia induced by IL-6, whereas previous studies have shown that endotoxin-induced hypertriglyceridemia was blocked by alpha-adrenergic receptor antagonists. These results demonstrate that IL-6 induces hypertriglyceridemia by stimulating hepatic triglyceride secretion independent of endogenous catecholamines. Thus, changes in hepatic triglyceride metabolism are another acute phase response that can be induced by IL-6.

Animals↗

CREB activation induced by mitochondrial dysfunction triggers triglyceride accumulation in 3T3-L1 preadipocytes.

Several mitochondrial pathologies are characterized by lipid redistribution and microvesicular cell phenotypes resulting from triglyceride accumulation in lipid-metabolizing tissues. However, the molecular mechanisms underlying abnormal fat distribution induced by mitochondrial dysfunction remain poorly understood. In this study, we show that inhibition of respiratory complex III by antimycin A as well as inhibition of mitochondrial protein synthesis trigger the accumulation of triglyceride vesicles in 3T3-L1 fibroblasts. We also show that treatment with antimycin A triggers CREB activation in these cells. To better delineate how mitochondrial dysfunction induces triglyceride accumulation in preadipocytes, we developed a low-density DNA microarray containing 89 probes, which allows gene expression analysis for major effectors and/or markers of adipogenesis. We thus determined gene expression profiles in 3T3-L1 cells incubated with antimycin A and compared the patterns obtained with differentially expressed genes during the course of in vitro adipogenesis induced by a standard pro-adipogenic cocktail. After an 8-day treatment, a set of 39 genes was found to be differentially expressed in cells treated with antimycin A, among them CCAAT/enhancer-binding protein alpha (C/EBPalpha), C/EBP homologous protein-10 (CHOP-10), mitochondrial glycerol-3-phosphate dehydrogenase (GPDmit), and stearoyl-CoA desaturase 1 (SCD1). We also demonstrate that overexpression of two dominant negative mutants of the cAMP-response element-binding protein CREB (K-CREB and M1-CREB) and siRNA transfection, which disrupt the factor activity and expression, respectively, inhibit antimycin-A-induced triglyceride accumulation. Furthermore, CREB knockdown with siRNA also downregulates the expression of several genes that contain cAMP-response element (CRE) sites in their promoter, among them one that is potentially involved in synthesis of triglycerides such as SCD1. These results highlight a new role for CREB in the control of triglyceride metabolism during the adaptative response of preadipocytes to mitochondrial dysfunction.

3T3-L1 Cells↗

Plasma triglyceride-decreasing components of pine needles.

An ultrafiltrate (M.W. < 10000) of 0.1 M acetic acid extract from Japanese red pine needles was treated with Sep-Pak Vac C18, and an absorbable fraction (pine aqueous components fraction, PAC) was obtained. Since the intraperitoneal administration of PAC to rats decreased plasma triglyceride in a screening test for bioactivity, we tried to further isolate the active substances with respect to this triglyceride-decreasing action. Active substances were precipitated by acid, and we then divided them into fractions using reversed phase HPLC. The active fractions were hydrolyzed, then the hydrolysate was re-separated by the same HPLC system. Negative ion mode FAB-LC/MS of the bioactive fractions of this hydrolysate revealed an [M-H] molecular ion peak at m/z 169 and 321. The 13C-NMR spectra were consistent with those of authentic gallic acid and galloyl gallic acid, a dimer of gallic acid. Authentic gallic acid also showed a triglyceride-decreasing action, and galloyl gallic acid even more markedly decreased triglyceride. These findings suggest that the triglyceride-decreasing action of Japanese red pine needles is due to these polyphenol compounds. In addition, amino acids were also detected in the hydrolysate of PAC, indicating that the components in Japanese red pine needles that decrease triglycerides are complexes of a hydrolyzable tannin, which contains gallic acid and galloyl gallic acid as components and peptides.

Amino Acids↗

Effect of serum triglyceride concentration on the fluctuation of whole blood concentration of cyclosporin A in patients.

The methodology to distinguish the patients showing considerable fluctuation of the whole blood concentration of cyclosporin A (CYA) was investigated from a viewpoint of laboratory test values. First, we retrospectively examined the CYA trough blood concentrations monitored continuously. The patients were classified into three groups by the fluctuation of CYA trough blood concentrations during the examination period (Cmax/Cmin): Group 1 (Cmax/Cmin=100-200%; n=21), Group 2 (Cmax/Cmin=200-300%; n=25), and Group 3 (Cmax/Cmin=more than 300%; n=32). In the laboratory tests examined, the serum triglyceride concentrations were considerably different among the groups, and it was the highest in Group 3. Next, to elucidate the effect of serum triglyceride concentration on the CYA blood concentration, in vivo pharmacokinetic studies after single intravenous or repetitive oral administration of CYA were conducted in the model rats with pseudo-hypertriglyceridemia, hypocythemia, and acute renal failure. Only in pseudo-hypertriglyceridemia rats, the CYA blood concentration after a single intravenous injection was significantly higher than that in normal rats because of the restriction of CYA distribution to the extravascular tissues. On the other hand, the increase in the serum triglyceride concentration did not affect the fluctuation of CYA trough blood concentration after repetitive oral administration. Taken together, the fluctuation of CYA trough blood concentrations observed in the clinical situation could be due to the fluctuation of serum triglyceride concentration, and the patients with such fluctuation of serum triglyceride concentrations might also be distinguishable by the higher concentration of serum triglyceride in laboratory tests.

Acute Kidney Injury↗

Basal and postprotein insulin and glucagon levels during a high and low carbohydrate intake and their relationships to plasma triglycerides.

The effects of acute and chronic differences in the carbohydrate content of the diet on plasma insulin, glucagon, insulin-glucagon molar ratio (I/G), and triglycerides were studied. Acute effects were studied by varying the carbohydrate content of a single test meal, while chronic effects were determined by varying the carbohydrate content of the diet for a week. A test meal containing 0.6 gm of gelatin per kilogram plus 0.6 gm. per kilogram of glucose resulted in much higher levels of insulin and I/G (p smaller than 0.005), lower glucagon levels (p smaller than 0.05), and slightly higher triglycerides (N.S.) than did a meal of 1.2 gm, per kilogram of gelatin alone. One week of a 12 gm. carbohydrate, 2870-calorie diet lowered insulin (p smaller than 0.001), I/G (p smaller than 0.05), and triglycerides (p smaller than 0.001) and increased glucagon (N.S.), whereas a 390-gm. carbohydrate, 2784-calorie intake significantly increased insulin, I/G, and triglycerides (p smaller than 0.005) and lowered glucagon (p smaller than 0.02) within two days; even greater changes in hormones were observed on a 510-gm. carbohydrate intake. Of those patients in whom a high carbohydrate intake induced a triglyceride rise of at least 40 mg. per deciliter, a significant correlation between the change in I/G and the change in triglycerides was noted (r equals 0.85; p smaller than 0.01). The results are compatible with but do not prove the proposal that pancreatic alpha and beta cells play a mediating role in carbohydrate induction of hyperlipidemia.

Adult↗

Use of a nonionic detergent (Triton WR 1339) in healthy cats to assess hepatic secretion of triglyceride.

OBJECTIVE: To determine whether a nonionic detergent (Triton WR 1339) can be used in cats to assess hepatic secretion of triglyceride. ANIMALS: 28 healthy cats. PROCEDURE: Triton WR 1339 was administered IV according to the following schedule: 5, 50, 150, and 250 mg/kg of body weight. Control cats did not receive an injection or received 0.9% NaCl or PBS solutions at the same osmolarity and volume as the 250 mg/kg group. Blood samples were collected throughout the 48-hour period after administration for determination of triglyceride and cholesterol concentrations and for RBC morphology and osmotic fragility studies. RESULTS: Administration of Triton WR 1339 at 150 and 250 mg/kg caused profound hypertriglyceridemia. Triglyceride concentrations increased in a curvilinear fashion for the first 2 hours and remained increased for approximately 24 hours. Area under the time-concentration curve for triglyceride at 5 hours differed significantly among groups. At 12 and 24 hours, cholesterol was significantly higher in cats receiving 250 mg/kg. The most dramatic changes in osmotic fragility and RBC morphology were in cats receiving 250 mg/kg; 1 of these cats developed severe icterus and died 5 days later. Feeding rice and casein before administering Triton WR 1339 at 150 mg/kg did not appear to affect the hypertriglyceridemia response. CONCLUSIONS AND CLINICAL RELEVANCE: Triton WR 1339 can be administered IV to cats at a rate of 150 mg/kg to assess hepatic triglyceride secretion, although some cats may have increased RBC osmotic fragility. Higher dosages caused substantial adverse effects, whereas lower dosages did not alter plasma triglyceride concentration.

Animals↗

Health-based reference values of the Mini-Finland Health Survey: 3. Triglycerides in total serum and in different lipoprotein fractions.

The reference values for triglyceride concentrations in total serum and in its VLDL, LDL and HDL fractions have been produced based on the data obtained in the Mini-Finland Health Survey. The lipoprotein fractions were separated with ultracentrifugation. Efforts were made to obtain reference values for the healthy ambulatory population. Two health-derived selection criteria were used for inclusion of persons into the reference population: those based on the literature available and those based on the recommendations published by the Committee on Reference Values of the Scandinavian Society for Clinical Chemistry and Clinical Physiology, with minor modifications. The frequency distributions of triglycerides especially in total serum and in VLDL fraction were very skewed. Because of that the data were transformed before the calculation of the reference ranges according to the method of Box and Cox [1]. This transformation method appeared to be the best one of many tested methods in obtaining the distributions closer to the normal ones. The 95% inner reference intervals of total serum triglycerides in all subjects and in the two selection groups were 0.5-4.0, 0.5-2.8, and 0.5-3.2 mmol l-1 for men and 0.5-3.4, 0.5-2.3, and 0.5-2.4 mmol l-1 for women, respectively. The age dependence of triglyceride level was prominent in women after the early middle age. The distribution and age dependence of VLDL triglycerides resembled those of total triglycerides. In LDL and HDL fractions the skewness was not as clear as in the whole serum or in VLDL fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Stereospecific analysis of high melting triglycerides of bovine milk fat and their biosynthetic origin.

Fatty acid composition, triglyceride molecular weight distributions, melting ranges, amount of cis and trans isomers, and stereospecific fatty acid distributions were determined for high melting triglyceride fractions and bovine milk fat free of them. Distributions of fatty acids on the high melting triglycerides differed from distributions of fatty acids in the rest of the milk fat triglycerides. The significance of these results is evaluated in relation to the biosynthetic origin of high melting triglycerides. Stereospecific distributions of these fatty acids support previous speculations that the monoglyceride pathway may play a significant role in biosynthesis of high melting triglyceride in bovine milk fat.

Animals↗

Effect on days of lactation and methionine hydroxy analog on incorporation of plasma fatty acids into plasma triglycerides.

Methionine hydroxy analog has been proposed to stimulate hepatic lipoprotein synthesis and incorporation of plasma fatty acids into plasma triglyceride. Seven cows were fed diets containing 0 or 30 g analog/d starting 14 d prepartum. At approximately 30 and 60 d postpartum, cows were continuously infused intravenously with 1-[14C] palmitic acid for 160 min to achieve steady-state labeling of plasma fatty acid and triglyceride. Turnover of fatty acid and transfer quotients for triglyceride and CO2 were 3.3 and 2.7 mmol min-1; 13.0 and 10.0%; and 8.0 and 5.0%, for control and analog, respectively. Proportion of fatty acid turnover incorporated into triglyceride and CO2 were 14.0 and 15.0%; and 21.0 and 18.0, respectively, for control and analog. Analog increased 14C recovered in milk fat (52 vs. 36%). Plasma concentration of fatty acids, percent oxidized to CO2, and percent of CO2 from fatty acids decreased with increasing lactation days. Milk fat percent and yield, fatty acid turnover, and oxidation were positively correlated with concentration of plasma fatty acids, whereas fatty acid incorporated into plasma triglyceride was negatively correlated with fatty acid concentration. The data suggest that hepatic triglyceride secretion is not increased in early lactation; further, no effects of analog on lipid metabolism were detected.

Animals↗

Relationship of triglyceride accumulation to insulin clearance and hormonal responsiveness in bovine hepatocytes.

The accumulation of triglycerides in the liver has been associated with reduced hepatic function; however, direct evidence that fat accumulation causes decreased liver function is lacking. Hepatocyte monolayers isolated from ruminating calves with an initial low triglyceride concentration were either loaded or not loaded with triglycerides by incubation with 1.5 or 0 mM exogenous nonesterified fatty acids from 12 to 48 h after plating. Basal rates of synthesis of albumin and protein were not affected by triglycerides in the cell. Inclusion of insulin and glucagon from 12 to 72 h after plating increased rates of albumin and protein synthesis. Hepatocytes loaded with triglycerides were less sensitive to the hormonal stimulation of albumin and protein synthesis than were normal hepatocytes. Insulin clearance rates were also lower in hepatocytes loaded with triglycerides than in normal hepatocytes. Decreased insulin clearance and hormonal control of protein synthesis could contribute to the etiology of metabolic disorders that are associated with periparturient fatty liver in dairy cows.

Albumins↗

Effects of induced parturition and estradiol on feed intake, liver triglyceride concentration, and plasma metabolites of transition dairy cows.

The effect of induced parturition and estradiol on feed intake, liver triglyceride, plasma metabolites, and milk yield was evaluated in fifty-six Holstein cows and heifers. Cows were assigned to treatments on d 260 of gestation and were on trial until d 10 postpartum for measurement of dry matter intake (DMI), plasma metabolites, and liver triglyceride and until d 31 postpartum to measure milk yield. Fourteen animals per group (9 cows and 5 heifers) received either a placebo, 1 mg of fenprostalene, 50 mg of estradiol-17 beta benzoate, or both on d 276 of gestation. Cows that received fenprostalene consumed more dry matter (DM) for the last 8 d prepartum than did cows that did not receive fenprostalene (9.6 kg/d vs. 8.5 kg/d, respectively) but consumed less DM for the first 10 d postpartum (10.9 kg/d vs. 13.1 kg/d, respectively). Cows injected with estradiol-17 beta benzoate tended to consume less DM postpartum than did cows not injected with estradiol-17 beta benzoate (11.3 kg/d vs. 12.7 kg/d, respectively). There was no effect of treatment on milk yield; however, a fenprostalene by day interaction resulted from lower milk yield on d 3, 4, 5, 7, and 10 relative to calving in cows that received fenprostalene. Administration of fenprostalene resulted in a delay in the peak plasma nonesterified fatty acid (NEFA) concentration until 2 d after calving. Plasma glucose concentrations were greatest 1 d prior to calving for cows that received fenprostalene, whereas plasma glucose concentrations peaked on the day of calving for cows that did not receive fenprostalene. Liver triglyceride increased over time; however, there was no effect of treatment on liver triglyceride. Calving induction improved DMI for the last 8 d prepartum, but a concomitant decrease in liver triglyceride after calving did not result. Estradiol-17 beta benzoate had no effect on plasma metabolites or liver triglyceride, indicating that the physiological rise in estradiol prior to calving does not have a primary role in lipolysis or hepatic fatty acid metabolism in the dairy cow.

Abortifacient Agents, Nonsteroidal↗

Digestion and absorption of lipids in chicks fed triglycerides or free fatty acids: synthesis of monoglycerides in the intestine.

Digestion and absorption of lipids were determined in 3-week-old chicks fed diets containing triglycerides, free fatty acids, or free fatty acids with added glycerol. The 91YCl3 was present as a non-absorbed reference substance. Overall absorption of total fatty acids was highest in triglyceride-fed chicks and lowest in chicks receiving fatty acids. Net secretion of endogenous fatty acids from biliary phospholipids was observed in the duodenum of triglyceride fed chicks, whereas in the other treatments net absorption was observed at this site. Fractionation of the intestinal lipids by thin layer chromatography showed that triglycerides were almost completely hydrolyzed in the duodenum. Monoglycerides were present at high levels in the duodenum of triglyceride fed chicks and at lower levels in chicks receiving free fatty acids and glycerol and at trace levels in free fatty acid-fed chicks. Total micellar fatty acids were lowest in the duodenum of free fatty acid-fed chicks. In vitro incubation of pancreatic homogenate with oleic acid, glycerol, phosphatidyl choline, and taurocholate revealed synthesis of monoglycerides. The poorer fat absorption observed on feeding acidulated soapstock instead of triglycerides is partially explained by less efficient micellarization when free fatty acids are fed.

Animals↗